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Childhood Treatment
Childhood Esthesioneuroblastoma Treatment
Childhood Laryngeal Tumors Treatment
Childhood Nasopharyngeal Cancer Treatment
Childhood Oral Cavity Cancer Treatment
Childhood Salivary Gland Tumors Treatment
Hypopharyngeal Cancer Treatment
Laryngeal Cancer Treatment
Lip & Oral Cavity Treatment
Metastatic Squamous Neck Cancer with Occult Primary Treatment
Nasopharyngeal Cancer Treatment
Oropharyngeal Cancer Treatment
Paranasal Sinus & Nasal Cavity Cancer Treatment
Salivary Gland Cancer Treatment
Oral Cavity, Pharyngeal, and Laryngeal Cancer Prevention
Oral Cavity, Pharyngeal, and Laryngeal Cancer Screening
Laryngeal Cancer Treatment (Adult) (PDQ®)–Health Professional Version
General Information About Laryngeal Cancer
Cellular Classification of Laryngeal Cancer
Stage Information for Laryngeal Cancer
Treatment Option Overview for Laryngeal Cancer
Stage I Laryngeal Cancer Treatment
Stage II Laryngeal Cancer Treatment
Stage III Laryngeal Cancer Treatment
Stage IV Laryngeal Cancer Treatment
Recurrent and Metastatic Laryngeal Cancer
Changes to This Summary (10/03/2019)
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Incidence and Mortality
Estimated new cases and deaths from laryngeal cancer in the United States in 2019:[1]
New cases: 12,410.
Deaths: 3,760.
The larynx is divided into the following three anatomical regions:
The supraglottic larynx includes the epiglottis, false vocal cords, ventricles, aryepiglottic folds, and arytenoids.
The glottis includes the true vocal cords and the anterior and posterior commissures.
The subglottic region begins about 1 cm below the true vocal cords and extends to the lower border of the cricoid cartilage or the first tracheal ring.
The supraglottic area is rich in lymphatic drainage. After penetrating the pre-epiglottic space and thyrohyoid membrane, lymphatic drainage is initially to the jugulodigastric and midjugular nodes. About 25% to 50% of patients present with involved lymph nodes. The precise figure depends on the T (tumor) stage. The true vocal cords are devoid of lymphatics. As a result, vocal cord cancer confined to the true cords rarely, if ever, presents with involved lymph nodes. Extension above or below the cords may, however, lead to lymph node involvement. Primary subglottic cancers, which are quite rare, drain through the cricothyroid and cricotracheal membranes to the pretracheal, paratracheal, and inferior jugular nodes, and occasionally to mediastinal nodes.[2]
A clear association has been made between smoking, excess alcohol ingestion, and the development of squamous cell cancers of the upper aerodigestive tract.[3] For smokers, the risk of the development of laryngeal cancer decreases after the cessation of smoking but remains elevated even years later when compared with that of nonsmokers.[4] If a patient who has had a single cancer continues to smoke and drink alcoholic beverages, the likelihood of a cure for the initial cancer, by any modality, is diminished, and the risk of second tumor is enhanced. Because of clinical problems related to smoking and alcohol use in this population, many patients succumb to intercurrent illness rather than to the primary cancer.
Supraglottic cancers typically present with sore throat, painful swallowing, referred ear pain, change in voice quality, or enlarged neck nodes. Early vocal cord cancers are usually detected because of hoarseness. By the time they are detected, cancers arising in the subglottic area commonly involve the vocal cords; thus, symptoms usually relate to contiguous spread.
Prognostic Factors
The most important adverse prognostic factors for laryngeal cancers include increasing T stage and N (regional lymph node) stage. Other prognostic factors may include sex, age, performance status, and a variety of pathologic features of the tumor, including grade and depth of invasion.[5]
Prognosis for small laryngeal cancers that have not spread to lymph nodes is very good with cure rates of 75% to 95% depending on the site, tumor bulk,[6] and degree of infiltration. Although most early lesions can be cured by either radiation therapy or surgery, radiation therapy may be reasonable to preserve the voice, leaving surgery for salvage. Patients with a preradiation hemoglobin level higher than 13 g/dL have higher local control and survival rates than patients who are anemic.[7]
Locally advanced lesions are treated with combined modality treatment involving radiation and chemotherapy with or without surgery, the aim of which is laryngeal preservation in appropriately selected candidates.[8] Distant metastases are also common, even if the primary tumor is controlled.
Intermediate lesions have intermediate prognoses, depending on site, T stage, N stage, and performance status. Therapy recommendations for patients with these lesions are based on a variety of complex anatomic, clinical, and social factors, which should be individualized and discussed in multidisciplinary consultation (surgery, radiation therapy, and dental and oral surgery) prior to prescribing therapy.
Follow-up and Survivorship
Second primary tumors, often in the aerodigestive tract, have been reported in as many as 25% of patients whose initial lesion is controlled. A study has shown that daily treatment of these patients with moderate doses of isotretinoin (i.e., 13-cis-retinoic acid) for 1 year can significantly reduce the incidence of second tumors.[9] No survival advantage has been demonstrated, partially because of recurrence and death from the primary malignancy.
Patients treated for laryngeal cancers are at the highest risk of recurrence in the first 2 to 3 years. Recurrences after 5 years are rare and usually represent new primary malignancies. Close, regular follow-up is crucial to maximize the chance for salvage. Careful clinical examination and repetition of any abnormal staging study are included in follow-up, along with attention to any treatment-related toxic effect or complication.
American Cancer Society: Cancer Facts and Figures 2019. Atlanta, Ga: American Cancer Society, 2019. Available online. Last accessed December 12, 2019.
Spaulding CA, Hahn SS, Constable WC: The effectiveness of treatment of lymph nodes in cancers of the pyriform sinus and supraglottis. Int J Radiat Oncol Biol Phys 13 (7): 963-8, 1987. [PUBMED Abstract]
Spitz MR: Epidemiology and risk factors for head and neck cancer. Semin Oncol 21 (3): 281-8, 1994. [PUBMED Abstract]
Bosetti C, Garavello W, Gallus S, et al.: Effects of smoking cessation on the risk of laryngeal cancer: an overview of published studies. Oral Oncol 42 (9): 866-72, 2006. [PUBMED Abstract]
Yilmaz T, Hoşal S, Gedikoglu G, et al.: Prognostic significance of depth of invasion in cancer of the larynx. Laryngoscope 108 (5): 764-8, 1998. [PUBMED Abstract]
Reddy SP, Mohideen N, Marra S, et al.: Effect of tumor bulk on local control and survival of patients with T1 glottic cancer. Radiother Oncol 47 (2): 161-6, 1998. [PUBMED Abstract]
Fein DA, Lee WR, Hanlon AL, et al.: Pretreatment hemoglobin level influences local control and survival of T1-T2 squamous cell carcinomas of the glottic larynx. J Clin Oncol 13 (8): 2077-83, 1995. [PUBMED Abstract]
Forastiere AA, Zhang Q, Weber RS, et al.: Long-term results of RTOG 91-11: a comparison of three nonsurgical treatment strategies to preserve the larynx in patients with locally advanced larynx cancer. J Clin Oncol 31 (7): 845-52, 2013. [PUBMED Abstract]
Hong WK, Lippman SM, Itri LM, et al.: Prevention of second primary tumors with isotretinoin in squamous-cell carcinoma of the head and neck. N Engl J Med 323 (12): 795-801, 1990. [PUBMED Abstract]
The clear majority of laryngeal cancers are of squamous cell histology. Squamous cell subtypes include keratinizing and nonkeratinizing and well-differentiated to poorly differentiated grade. A variety of nonsquamous cell laryngeal cancers also occur.[1] These are not staged using the American Joint Cancer Committee staging system, and their management, which is not discussed here, can differ from that of squamous cell laryngeal cancers. In situ squamous cell carcinoma of the larynx is usually managed by a conservative surgical procedure such as mucosal stripping or superficial laser excision. Radiation therapy may also be appropriate treatment of selected patients with in situ carcinoma of the glottic larynx.
Mendenhall WM, Werning JW, Pfister DG: Treatment of head and neck cancer. In: DeVita VT Jr, Lawrence TS, Rosenberg SA: Cancer: Principles and Practice of Oncology. 9th ed. Philadelphia, Pa: Lippincott Williams & Wilkins, 2011, pp 729-80.
The staging system for laryngeal cancer is clinical and based on the best possible estimate of the extent of disease before treatment. The assessment of the primary tumor is based on inspection and palpation when possible and by fiberoptic laryngoscopy. Panendoscopy under anesthesia ensures careful clinical examination to determine clinical extent of local disease. The tumor must be confirmed histologically, and any other pathological data obtained on biopsy may be included. Head and neck magnetic resonance imaging, computed tomography, or positron emission tomography-computed tomography should be done before therapy to supplement inspection and palpation.[1] Additional radiographic studies may be included. The appropriate nodal drainage areas in the neck should be examined by careful palpation.
Definitions of TNM
The American Joint Committee on Cancer (AJCC) has designated staging by TNM (tumor, node, metastasis) classification to define laryngeal cancer.[2]
Table 1. Definition of Supraglottis, Glottis, and Subglottis Primary Tumor (T) for Laryngeal Cancera,b
T Category
T Criteria
aReprinted with permission from AJCC: Larynx. In: Amin MB, Edge SB, Greene FL, et al., eds.: AJCC Cancer Staging Manual. 8th ed. New York, NY: Springer, 2017, pp 149–61.
TX Primary tumor cannot be assessed.
Tis Carcinoma in situ.
Supraglottis
T1 Tumor limited to one subsite of supraglottis with normal vocal cord mobility.
T2 Tumor invades mucosa of more than one adjacent subsite of supraglottis or glottis or region outside the supraglottis (e.g., mucosa of the base of the tongue, vallecula, medial wall of pyriform sinus) without fixation of the larynx.
T3 Tumor limited to larynx with vocal cord fixation and/or invades any of the following: postcricoid area, pre-epiglottic space, paraglottic space, and/or inner cortex of thyroid cartilage.
T4 Moderately advanced or very advanced.
–T4a Moderately advanced local disease. Tumor invades through the outer cortex of the thyroid cartilage and/or invades tissues beyond the larynx (e.g., trachea, soft tissues of the neck including deep extrinsic muscle of the tongue, strap muscles, thyroid, or esophagus).
–T4b Very advanced local disease. Tumor invades prevertebral space, encases carotid artery, or invades mediastinal structures.
Glottis
T1 Tumor limited to the vocal cord(s) (may involve anterior or posterior commissure) with normal mobility.
–T1a Tumor limited to one vocal cord.
–T1b Tumor involves both vocal cords.
T2 Tumor extends to supraglottis and/or subglottis, and/or with impaired vocal cord mobility.
T3 Tumor limited to the larynx with vocal cord fixation and/or invasion of paraglottic space and/or inner cortex of the thyroid cartilage.
–T4a Moderately advanced local disease. Tumor invades through the outer cortex of the thyroid cartilage and/or invades tissues beyond the larynx (e.g., trachea, cricoid cartilage, soft tissues of the neck including deep extrinsic muscle of the tongue, strap muscles, thyroid, or esophagus).
Subglottis
T1 Tumor limited to the subglottis.
T2 Tumor extends to vocal cord(s) with normal or impaired mobility.
–T4a Moderately advanced local disease. Tumor invades cricoid or thyroid cartilage and/or invades tissues beyond the larynx (e.g., trachea, soft tissues of the neck including deep extrinsic muscles of the tongue, strap muscles, thyroid, or esophagus).
Table 2. Definition of Clinical (cN) Regional Lymph Nodes (N) for Laryngeal Cancer a,b
N Category
N Criteria
ENE = extranodal extension.
bA designation of "U" or "L" may be used for any N category to indicate metastasis above the lower border of the cricoid (U) or below the lower border of the cricoid (L). Similarly, clinical and pathological ENE should be recorded as ENE(–) or ENE(+).
NX Regional lymph nodes cannot be assessed.
N0 No regional lymph node metastasis.
N1 Metastasis in a single ipsilateral lymph node ≤3 cm in greatest dimension and ENE(–).
N2 Metastasis in a single ipsilateral node, >3 cm but not >6 cm in greatest dimension and ENE(–); or metastases in multiple ipsilateral lymph nodes, none >6 cm in greatest dimension and ENE(–); or metastases in bilateral or contralateral lymph nodes, none >6 cm in greatest dimension and ENE(–).
–N2a Metastasis in a single ipsilateral node >3 cm but not >6 cm in greatest dimension and ENE(–).
–N2b Metastases in multiple ipsilateral nodes, none >6 cm in greatest dimension and ENE(–).
–N2c Metastases in bilateral or contralateral lymph nodes, none >6 cm in greatest dimension and ENE(–).
N3 Metastasis in a lymph node >6 cm in greatest dimension and ENE(–); or metastasis in any lymph nodes(s) with clinically overt ENE(+).
–N3a Metastasis in a lymph node >6 cm in greatest dimension and ENE(–).
–N3b Metastasis in any lymph node(s) with clinically overt ENE(+).
Table 3. Definition of Pathological (pN) Regional Lymph Nodes (N) for Laryngeal Cancera,b
N2 Metastasis in a single ipsilateral lymph node, ≤3 cm in greatest dimension and ENE(+); or metastasis in a single ipsilateral lymph node, >3 cm but not >6 cm in greatest dimension and ENE(–); or metastases in multiple ipsilateral lymph nodes, none >6 cm in greatest dimension and ENE(–); or metastases in bilateral or contralateral lymph nodes, none >6 cm in greatest dimension and ENE(–).
–N2a Metastasis in a single ipsilateral node ≤3 cm in greatest dimension and ENE(+); or metastasis in a single ipsilateral node >3 cm but not >6 cm in greatest dimension and ENE.
–N2c Metastases in bilateral or contralateral lymph node(s), none >6 cm in greatest dimension and ENE(–).
N3 Metastasis in a lymph node >6 cm in greatest dimension and ENE(–); or metastasis in a single ipsilateral node >3 cm in greatest dimension and ENE(+); or metastases in multiple ipsilateral, contralateral, or bilateral lymph nodes and any with ENE(+); or a single contralateral node of any size and ENE(+).
–N3a Metastasis in a lymph node, >6 cm in greatest dimension and ENE(–).
–N3b Metastasis in a single ipsilateral node >3 cm in greatest dimension and ENE(+); or metastases in multiple ipsilateral, contralateral, or bilateral nodes and any with ENE(+); or a single contralateral node of any size and ENE(+).
Table 4. Definition of Distant Metastasis (M) for Laryngeal Cancera
M0 No distant metastasis.
M1 Distant metastasis.
AJCC Prognostic Stage Groups
Table 5. Definition of TNM Stage 0a
T = primary tumor; N = regional lymph node; M = metastasis.
0 Tis, N0, M0 Tis = Carcinoma in situ.
N0 (cN and pN) = No regional lymph node metastasis.
M0 = No distant metastasis.
Table 6. Definition of TNM Stage Ia
T = primary tumor; N = regional lymph node; M = metastasis; cN = clinical N; pN = pathological N.
I T1, N0, M0 Supraglottis
T1 = Tumor limited to one subsite of supraglottis with normal vocal cord mobility.
T1 = Tumor limited to the vocal cord(s) (may involve anterior or posterior commissure) with normal mobility.
–T1a = Tumor limited to one vocal cord.
–T1b = Tumor involves both vocal cords.
T1 = Tumor limited to the subglottis.
Table 7. Definition of TNM Stage IIa
II T2, N0, M0 Supraglottis
T2 = Tumor invades mucosa of more than one adjacent subsite of supraglottis or glottis or region outside the supraglottis (e.g., mucosa of the base of the tongue, vallecula, medial wall of pyriform sinus) without fixation of the larynx.
T2 = Tumor extends to supraglottis and/or subglottis, and/or with impaired vocal cord mobility.
T2 = Tumor extends to vocal cord(s) with normal or impaired mobility.
Table 8. Definition of TNM Stage IIIa
T = primary tumor; N = regional lymph node; M = metastasis; cN = clinical N; ENE = extranodal extension; pN = pathological N.
III T3, N0, M0 Supraglottis
T3 = Tumor limited to larynx with vocal cord fixation and/or invades any of the following: postcricoid area, pre-epiglottic space, paraglottic space, and/or inner cortex of thyroid cartilage.
T3 = Tumor limited to the larynx with vocal cord fixation and/or invasion of paraglottic space and/or inner cortex of the thyroid cartilage.
T3 = Tumor limited to larynx with vocal cord fixation and/or invasion of paraglottic space and/or inner cortex of the thyroid cartilage.
N0 (cN or pN) = No regional lymph node metastasis.
T1, T2, T3, N1, M0 Supraglottis
N1 (cN or pN) = Metastasis in a single ipsilateral node, ≤3 cm in greatest dimension and ENE (–).
Table 9. Definition of TNM Stage IVA, IVB, and IVCa
IVA T4a, N0, N1, M0 Supraglottis
–T4a = Moderately advanced local disease. Tumor invades through the outer cortex of the thyroid cartilage and/or invades tissues beyond the larynx (e.g., trachea, soft tissues of the neck including deep extrinsic muscle of the tongue, strap muscles, thyroid, or esophagus).
–T4a = Moderately advanced local disease. Tumor invades through the outer cortex of the thyroid cartilage and/or invades tissues beyond the larynx (e.g., trachea, cricoid cartilage, soft tissues of the neck including deep extrinsic muscle of the tongue, strap muscles, thyroid, or esophagus).
–T4a = Moderately advanced local disease. Tumor invades cricoid or thyroid cartilage and/or invades tissues beyond the larynx (e.g., trachea, soft tissues of the neck including deep extrinsic muscles of the tongue, strap muscles, thyroid, or esophagus).
N0 (cN and pN) = Metastasis in a single ipsilateral node, ≤3 cm in greatest dimension and ENE (–).
T1, T2, T3, T4a, N2, M0 Supraglottis
cN2 = Metastasis in a single ipsilateral node >3 cm but not >6 cm in greatest dimension and ENE(–); or metastases in multiple ipsilateral lymph nodes, none >6 cm in greatest dimension and ENE(–); or metastases in bilateral or contralateral lymph nodes, none >6 cm in greatest dimension and ENE(–).
‒cN2a = Metastasis in a single ipsilateral node, larger than 3 cm but not larger than 6 cm in greatest dimension and ENE(–).
‒cN2b = Metastases in multiple ipsilateral nodes, none larger than 6 cm in greatest dimension and ENE(–).
‒cN2c = Metastasis in bilateral of contralateral lymph nodes, none larger than 6 cm in greatest dimension and ENE(–).
pN2 = Metastasis in a single ipsilateral lymph node, ≤3 cm in greatest dimension and ENE(+); or metastasis in a single ipsilateral lymph node >3 cm but not >6 cm in greatest dimension and ENE(–); or metastases in multiple ipsilateral lymph nodes, none >6 cm in greatest dimension and ENE(–); or metastases in bilateral or contralateral lymph nodes, none >6 cm in greatest dimension and ENE(–).
‒pN2a = Metastasis in a single ipsilateral or contralateral node, 3 cm or smaller in greatest dimension and ENE(+); or metastasis in a single ipsilateral node, larger than 3 cm but not larger than 6 cm in greatest dimension and ENE(–).
‒pN2b = Metastases in multiple ipsilateral nodes, none larger than 6 cm in greatest dimension and ENE(–).
‒pN2c = Metastasis in bilateral or contralateral lymph nodes, none larger than 6 cm in greatest dimension and ENE(–).
IVB Any T, N3, M0 Any T = See Table 1.
cN3 = Metastasis in a lymph node >6 cm in greatest dimension and ENE(–); or metastasis in any lymph node(s) with clinically overt ENE(+).
–cN3a = Metastasis in a lymph node >6 cm in greatest dimension and ENE(–).
–cN3b = Metastasis in any lymph node(s) with clinically overt ENE(+).
pN3 = Metastasis in a lymph node >6 cm in greatest dimension and ENE(–); or metastasis in a single ipsilateral node >3 cm in greatest dimension and ENE(+); or metastases in multiple ipsilateral, contralateral, or bilateral lymph nodes and any with ENE(+).
–pN3a = Metastasis in a lymph mode >6 cm in greatest dimension and ENE(–).
–pN3b = Metastasis in a single ipsilateral node >3 cm in greatest dimension and ENE(+); or metastases in multiple ipsilateral, contralateral, or bilateral lymph nodes and any with ENE(+).
T4b, Any N, M0 Supraglottis
–T4b = Very advanced local disease. Tumor invades prevertebral space, encases carotid artery or invades mediastinal structures.
–T4b = Very advanced local disease. Tumor invades prevertebral space, encases carotid artery, or invades mediastinal structures.
Any N = See Table 2 and Table 3.
IVC Any T, Any N, M1 Any T = See Table 1.
M1 = Distant metastasis.
Thabet HM, Sessions DG, Gado MH, et al.: Comparison of clinical evaluation and computed tomographic diagnostic accuracy for tumors of the larynx and hypopharynx. Laryngoscope 106 (5 Pt 1): 589-94, 1996. [PUBMED Abstract]
Larynx. In: Amin MB, Edge SB, Greene FL, et al., eds.: AJCC Cancer Staging Manual. 8th ed. New York, NY: Springer, 2017, pp 149-61.
Surgery and/or Radiation Therapy
Surgery and radiation therapy have been the standards for treatment of laryngeal cancer; however, outcome data from randomized trials are limited. Studies have attempted to address the question of whether to use surgery or radiation, but the studies have been underpowered.[1] Selection of primary surgery versus radiation therapy-based treatment should be made in a multidisciplinary setting with consideration of disease stage, comorbidities, and functional status, including voice and swallowing outcomes and lung capacity.
Small superficial cancers without laryngeal fixation or lymph node involvement are successfully treated by radiation therapy or surgery alone, including laser excision surgery. Radiation therapy may be selected to preserve the voice and to reserve surgery for salvaging failures. The radiation field and dose are determined by the location and size of the primary tumor. A variety of curative surgical procedures are also recommended for laryngeal cancers, some of which preserve vocal function. An appropriate surgical procedure must be considered for each patient, given the anatomic problem, performance status, and clinical expertise of the treatment team. Advanced laryngeal cancers are often treated by combining radiation with concurrent chemotherapy for larynx preservation and total laryngectomy for bulky T4 disease or salvage.[2-4]
Evaluation of treatment outcome can be reported in various ways: locoregional control, disease-free survival, determinate survival, and overall survival (OS) at 2 to 5 years. Preservation of voice is an important parameter to evaluate. Outcome should be reported after initial surgery, initial radiation, planned combined treatment, or surgical salvage of radiation failures. Primary source material should be consulted to review these differences.
A review of published clinical results of definitive radiation therapy for head and neck cancer suggests a significant loss of local control when the administration of radiation therapy was prolonged; therefore, lengthening of standard treatment schedules should be avoided whenever possible.[5,6]
Direct comparison of the results of radiation therapy versus endolaryngeal surgery (with or without laser) has not been made for patients with early-stage laryngeal cancer. The evidence is insufficient to show a clear difference in the results between treatment options regarding local control or OS. Retrospective data suggest that in comparison with surgery, radiation therapy might cause less perturbation of voice quality without a significant difference in patient perception.[7]
Concurrent Chemoradiation Therapy
Concurrent chemoradiation therapy is a standard treatment option for patients with locally advanced (stage III and stage IV) laryngeal cancer.
Evidence (concurrent chemoradiation therapy):
A meta-analysis of 93 randomized, prospective head and neck cancer trials published between 1965 and 2000 showed the following:[8][Level of evidence: 2A]
The subset of patients receiving chemotherapy and radiation therapy had a 4.5% absolute survival advantage.
Patients who received concurrent chemotherapy had a greater survival benefit than those who received neoadjuvant chemotherapy.
In a randomized trial of patients with locally advanced head and neck cancer, curative-intent radiation therapy alone (213 patients) was compared with radiation therapy plus weekly cetuximab (211 patients).[9] The initial dose of cetuximab was 400 mg/m2 of body-surface area 1 week before radiation therapy was started, followed by a weekly dose of 250 mg/m2 of body-surface area for the duration of the radiation therapy. This study allowed altered-fractionation regimens to be used in both arms.[9,10][Level of evidence: 1iiA]
At a median follow-up of 54 months, patients treated with cetuximab and radiation therapy demonstrated significantly higher progression-free survival (PFS) (hazard ratio [HR] for disease progression or death, 0.70; P = .006).
Patients in the cetuximab arm experienced higher rates of acneiform rash and infusion reactions, although the incidence of other grade 3 or higher toxicities, including mucositis, did not differ significantly between the two groups.
(Refer to the PDQ summary on Oral Complications of Chemotherapy and Head/Neck Radiation for more information about oral toxicities.)
Neoadjuvant Chemotherapy Followed by Concurrent Chemoradiation Therapy
In a meta-analysis of five randomized trials, a total of 1,022 patients with locally advanced head and neck squamous cell cancer were randomly assigned to receive either neoadjuvant chemotherapy with TPF (docetaxel, cisplatin, and fluorouracil) followed by concurrent chemoradiation therapy or concurrent chemoradiation therapy alone. The analysis failed to show an OS (HR, 1.01; 95% confidence limits [CLs], 0.84, 1.21; P = .92) or PFS (HR, 0.91; 95% CLs, 0.75, 1.1; P = .32) advantage for neoadjuvant chemotherapy using the TPF regimen over concurrent chemoradiation therapy alone.[11][Level of evidence: 1iA]
Evidence (neoadjuvant chemotherapy followed by concurrent chemoradiation therapy):
A direct comparison of chemotherapy followed by radiation therapy versus upfront surgery was made by The Department of Veterans Affairs (VA) Laryngeal Cancer Study Group in a trial in which 332 patients were randomly assigned to three cycles of chemotherapy (cisplatin and fluorouracil) and radiation therapy or surgery and radiation therapy.[12]
After two cycles of chemotherapy, the clinical tumor response was complete in 31% of the patients, and there was a partial response in 54% of the patients. Survival was similar in both arms; however, larynx preservation was possible in 64% of the patients in the chemotherapy-followed-by-radiation therapy arm.
The VA study was followed up in a randomized study, RTOG 9111 (NCT00002496), in which the laryngeal preservation arm of the VA study was compared with the concurrent chemoradiation therapy and radiation therapy-alone arms, and the primary endpoint was laryngectomy-free survival.[4] The RTOG 9111 study evaluated 547 patients with locally advanced laryngeal cancer who were enrolled between August 1992 and May 2000, with a median follow-up for surviving patients of 10.8 years (range, 0.07–17 years). Three regimens were compared, including neoadjuvant chemotherapy plus radiation therapy, concurrent chemoradiation therapy, and radiation therapy alone.
Both chemotherapy regimens improved laryngectomy-free survival compared with radiation therapy alone (neoadjuvant chemotherapy vs. radiation therapy alone, HR, 0.75; 95% confidence interval [CI], 0.59–0.95; P = .02; concurrent chemotherapy vs. radiation therapy alone, HR, 0.78; 95% CI, 0.78–0.98; P = .03).
Concurrent radiation therapy plus cisplatin resulted in a statistically significantly higher percentage of patients with an intact larynx at 10 years (67.5% for patients who had neoadjuvant chemotherapy; 81.7% for patients who had concurrent chemotherapy; and 63.8% for patients who received radiation therapy alone); 80% of laryngectomies were performed during the first 2 years (84 laryngectomies during year 1 and 35 laryngectomies during year 2).
Concurrent cisplatin with radiation therapy resulted in a 41% reduction in risk of locoregional failure compared with radiation therapy alone (HR, 0.59; 95% CI, 0.43–0.82; P = .0015) and a 34% reduction in risk compared with neoadjuvant chemotherapy (HR, 0.66; 95% CI, 0.48–0.92; P = .004). Both chemotherapy regimens had a lower incidence of distant metastases, although this did not reach statistical significance compared with radiation therapy alone.
The 10-year cumulative rates of late toxicity (grades 3–5) were 30.6% for neoadjuvant chemotherapy, 33.3% for concurrent chemotherapy, and 38% for radiation therapy alone, and were not significantly different between the arms.
OS was not significantly different between the groups, although there was possibly a worse outcome in the concurrent groups compared with the neoadjuvant chemotherapy group (HR, 1.25; 95% CI, 0.98–1.61; P = .08). The OS rates were 58% (5 year) and 39% (10 year) for neoadjuvant chemotherapy, 55% (5 year) and 28% (10 year) for concurrent chemoradiation therapy, and 54% (5 year) and 32% (10 year) for radiation therapy alone.
The number of deaths not attributed to larynx cancer or treatment were higher with concurrent chemotherapy (30.8% vs. 20.8% with neoadjuvant chemotherapy and 16.9% with radiation alone), because after approximately 4.5 years, the survival curves began to separate and favor neoadjuvant chemotherapy, although the difference was not statistically significant.
Altered Fractionation Versus Standard Fractionation Radiation Therapy
Radiation therapy alone with altered fractionation may be used for patients with locally advanced laryngeal cancer who are not candidates for chemotherapy. Altered fractionation radiation therapy yields a higher locoregional control rate compared with standard fractionated radiation therapy for patients with stage III and stage IV head and neck cancer.
Evidence (altered fractionation vs. standard fractionation radiation therapy):
The randomized trial RTOG-9003 (NCT00771641) included four radiation therapy treatment arms:[13,14][Level of evidence: 1iiA]
Standard fractionation (SFX) to 70 Gy in 35 daily fractions for 7 weeks.
Hyperfractionation (HFX) to 81.6 Gy in 68 twice-daily fractions for 7 weeks.
Accelerated fractionation split course (AFX-S) to 67.2 Gy in 42 fractions for 6 weeks with a 2-week rest after 38.4 Gy.
Accelerated concurrent boost fractionation (AFX-C) to 72 Gy in 42 fractions for 6 weeks.
In a long-term analysis, the three investigational arms were compared with SFX.
Only the HFX arm showed superior locoregional control and survival at 5 years compared with the SFX arm (HR, 0.79; 95% CI, 0.62–1.00; P = .05).
AFX-C was associated with increased late toxicity compared with SFX.
The following results were shown in a meta-analysis of 15 randomized trials with a total of 6,515 patients and a median follow-up of 6 years involving the assessment of HFX or AFX-S for patients with stage III and stage IV oropharyngeal cancer:[15][Level of evidence: 1iiA]
There was a significant survival benefit with altered-fractionated radiation therapy and a 3.4% absolute benefit at 5 years (HR, 0.92; 95% CI, 0.86–0.97; P = .003).
Altered-fractionation radiation therapy improves locoregional control, with greater benefit shown in younger patients.
HFX demonstrated a greater survival benefit (8% at 5 years) than did AFX-S (2% with accelerated fractionation without total dose-reduction and 1.7% with total dose-reduction at 5 years, P = .02).
An additional late effect from radiation therapy is hypothyroidism, which occurs in 30% to 40% of patients who have received external-beam radiation therapy to the entire thyroid gland. Thyroid function testing of patients is a consideration before therapy and as part of posttreatment follow-up.[16,17]
Prospective data of two randomized controlled trials reported the incidence of hypothyroidism.[18]
At a median follow-up of 41 months, 55.1% of the patients developed hypothyroidism (39.3% subclinical, 15.7% biochemical).
Patients who underwent intensity-modulated radiation therapy (IMRT) had higher subclinical hypothyroidism (51.1% vs. 27.3%; P = .021), peaking around 1 year after radiation therapy.
Younger age, hypopharynx/larynx primary, node positivity, higher dose/fraction (IMRT arm), and D100 were statistically significant factors for developing hypothyroidism.[18][Level of evidence: 1iiC]
For patients with well-lateralized oropharyngeal cancer, such as a T1 or T2 tonsil primary tumor with limited extension into the palate or tongue base and limited ipsilateral lymph node involvement without extracapsular extension, elective treatment to the ipsilateral lymph nodes results in only minimal risk of spread to the contralateral neck.[19] For T3 and T4 tumors that are midline or approach the midline, bilateral nodal treatment is a consideration. In addition to the cervical lymph node chain, retropharyngeal lymph nodes can also be encompassed in the elective nodal treatment.
Surgery Followed by Postoperative Radiation Therapy (PORT) With or Without Chemotherapy for Patients With Locally Advanced Disease
New surgical techniques for resection and reconstruction that provide access and functional preservation have extended the surgical options for patients with stage III or stage IV laryngeal cancer. Specific surgical procedures and their modifications are not described here because of the wide variety of surgical approaches, the variety of opinions about the role of modified neck dissections, and the multiple reconstructive techniques that may give the same results. This group of patients is managed by head and neck surgeons who are skilled in the multiple procedures available and are actively and frequently involved in the care of these patients.
Depending on pathological findings after primary surgery, PORT with or without chemotherapy is used in the adjuvant setting for the following histological findings:
T4 disease.
Perineural invasion.
Lymphovascular invasion.
Positive margins or margins less than 5 mm.
Extracapsular extension of a lymph node.
Two or more involved lymph nodes.
The addition of chemotherapy to PORT for laryngeal cancer squamous cell carcinoma demonstrates a locoregional control and OS benefit compared with radiation therapy alone in patients who have high-risk pathological risk factors, extracapsular extension of a lymph node, or positive margins, based on a pooled analysis of the EORTC-22931 [NCT00002555] and RTOG-9501 [NCT00002670] studies.[20-23][Level of evidence: 1iiA]
For patients with intermediate pathological risk factors, the addition of cisplatin chemotherapy given concurrently with PORT is unclear. Intermediate pathologic risk factors include:
T3 and T4 disease (or stage III and stage IV disease).
Perineural infiltration.
Vascular embolisms.
Clinically enlarged level IV–V lymph nodes secondary to tumors arising in the oral cavity or oropharynx.
Two or more histopathologically involved lymph nodes without extracapsular extension.
Close margins less than 5 mm.
The addition of cetuximab with radiation therapy in the postoperative setting for these intermediate pathological risk factors is being tested in a randomized trial (RTOG-0920 [NCT00956007]).
The risk of lymph node metastases in patients with stage I glottic cancer ranges from 0% to 2%, and for more advanced disease, such as stage II, the incidence is 10%, and for stage III glottic, the incidence is 15%. Thus, there is no need to treat glottic cancer cervical lymph nodes electively in patients with stage I tumors and small stage II tumors. Elective neck radiation is a consideration for T3 or T4 glottic tumors or T1 to T4 supraglottic tumors.[24]
For patients with cancer of the subglottis, combined modality therapy is generally preferred for the uncommon small lesions (i.e., stage I or stage II); however, radiation therapy alone may be used.
Patients who smoke during radiation therapy appear to have lower response rates and shorter survival durations than those who do not;[25] therefore, patients should be counseled on smoking cessation before beginning radiation therapy.
Iyer NG, Tan DS, Tan VK, et al.: Randomized trial comparing surgery and adjuvant radiotherapy versus concurrent chemoradiotherapy in patients with advanced, nonmetastatic squamous cell carcinoma of the head and neck: 10-year update and subset analysis. Cancer 121 (10): 1599-607, 2015. [PUBMED Abstract]
Silver CE, Ferlito A: Surgery for Cancer of the Larynx and Related Structures. 2nd ed. Philadelphia, Pa: Saunders, 1996.
Fowler JF, Lindstrom MJ: Loss of local control with prolongation in radiotherapy. Int J Radiat Oncol Biol Phys 23 (2): 457-67, 1992. [PUBMED Abstract]
Hansen O, Overgaard J, Hansen HS, et al.: Importance of overall treatment time for the outcome of radiotherapy of advanced head and neck carcinoma: dependency on tumor differentiation. Radiother Oncol 43 (1): 47-51, 1997. [PUBMED Abstract]
Yoo J, Lacchetti C, Hammond JA, et al.: Role of endolaryngeal surgery (with or without laser) compared with radiotherapy in the management of early (T1) glottic cancer: a clinical practice guideline. Curr Oncol 20 (2): e132-5, 2013. [PUBMED Abstract]
Pignon JP, le Maître A, Maillard E, et al.: Meta-analysis of chemotherapy in head and neck cancer (MACH-NC): an update on 93 randomised trials and 17,346 patients. Radiother Oncol 92 (1): 4-14, 2009. [PUBMED Abstract]
Bonner JA, Harari PM, Giralt J, et al.: Radiotherapy plus cetuximab for squamous-cell carcinoma of the head and neck. N Engl J Med 354 (6): 567-78, 2006. [PUBMED Abstract]
Curran D, Giralt J, Harari PM, et al.: Quality of life in head and neck cancer patients after treatment with high-dose radiotherapy alone or in combination with cetuximab. J Clin Oncol 25 (16): 2191-7, 2007. [PUBMED Abstract]
Budach W, Bölke E, Kammers K, et al.: Induction chemotherapy followed by concurrent radio-chemotherapy versus concurrent radio-chemotherapy alone as treatment of locally advanced squamous cell carcinoma of the head and neck (HNSCC): A meta-analysis of randomized trials. Radiother Oncol 118 (2): 238-43, 2016. [PUBMED Abstract]
Induction chemotherapy plus radiation compared with surgery plus radiation in patients with advanced laryngeal cancer. The Department of Veterans Affairs Laryngeal Cancer Study Group. N Engl J Med 324 (24): 1685-90, 1991. [PUBMED Abstract]
Fu KK, Pajak TF, Trotti A, et al.: A Radiation Therapy Oncology Group (RTOG) phase III randomized study to compare hyperfractionation and two variants of accelerated fractionation to standard fractionation radiotherapy for head and neck squamous cell carcinomas: first report of RTOG 9003. Int J Radiat Oncol Biol Phys 48 (1): 7-16, 2000. [PUBMED Abstract]
Beitler JJ, Zhang Q, Fu KK, et al.: Final results of local-regional control and late toxicity of RTOG 9003: a randomized trial of altered fractionation radiation for locally advanced head and neck cancer. Int J Radiat Oncol Biol Phys 89 (1): 13-20, 2014. [PUBMED Abstract]
Baujat B, Bourhis J, Blanchard P, et al.: Hyperfractionated or accelerated radiotherapy for head and neck cancer. Cochrane Database Syst Rev (12): CD002026, 2010. [PUBMED Abstract]
Turner SL, Tiver KW, Boyages SC: Thyroid dysfunction following radiotherapy for head and neck cancer. Int J Radiat Oncol Biol Phys 31 (2): 279-83, 1995. [PUBMED Abstract]
Constine LS: What else don't we know about the late effects of radiation in patients treated for head and neck cancer? Int J Radiat Oncol Biol Phys 31 (2): 427-9, 1995. [PUBMED Abstract]
Murthy V, Narang K, Ghosh-Laskar S, et al.: Hypothyroidism after 3-dimensional conformal radiotherapy and intensity-modulated radiotherapy for head and neck cancers: prospective data from 2 randomized controlled trials. Head Neck 36 (11): 1573-80, 2014. [PUBMED Abstract]
O'Sullivan B, Warde P, Grice B, et al.: The benefits and pitfalls of ipsilateral radiotherapy in carcinoma of the tonsillar region. Int J Radiat Oncol Biol Phys 51 (2): 332-43, 2001. [PUBMED Abstract]
Cooper JS, Pajak TF, Forastiere AA, et al.: Postoperative concurrent radiotherapy and chemotherapy for high-risk squamous-cell carcinoma of the head and neck. N Engl J Med 350 (19): 1937-44, 2004. [PUBMED Abstract]
Bernier J, Domenge C, Ozsahin M, et al.: Postoperative irradiation with or without concomitant chemotherapy for locally advanced head and neck cancer. N Engl J Med 350 (19): 1945-52, 2004. [PUBMED Abstract]
Bernier J, Cooper JS, Pajak TF, et al.: Defining risk levels in locally advanced head and neck cancers: a comparative analysis of concurrent postoperative radiation plus chemotherapy trials of the EORTC (#22931) and RTOG (# 9501). Head Neck 27 (10): 843-50, 2005. [PUBMED Abstract]
Cooper JS, Zhang Q, Pajak TF, et al.: Long-term follow-up of the RTOG 9501/intergroup phase III trial: postoperative concurrent radiation therapy and chemotherapy in high-risk squamous cell carcinoma of the head and neck. Int J Radiat Oncol Biol Phys 84 (5): 1198-205, 2012. [PUBMED Abstract]
Browman GP, Wong G, Hodson I, et al.: Influence of cigarette smoking on the efficacy of radiation therapy in head and neck cancer. N Engl J Med 328 (3): 159-63, 1993. [PUBMED Abstract]
Standard treatment options:
External-beam radiation therapy (EBRT) therapy alone.
Supraglottic laryngectomy. Total laryngectomy may be reserved for patients unable to tolerate potential respiratory complications of surgery or the supraglottic laryngectomy.
(Refer to the Treatment Option Overview for Laryngeal Cancer section of this summary for more information.)
Radiation therapy.[1-4]
Endoscopic CO2 laser excision.[5]
Cordectomy for very carefully selected patients with limited and superficial T1 lesions.[6,7]
Partial or hemilaryngectomy or total laryngectomy, depending on anatomic considerations.
Lesions can be treated successfully by radiation therapy alone with preservation of normal voice.
Surgery is reserved for failure of radiation therapy or for patients who cannot be easily assessed for radiation therapy.
Selection of treatment should include an evaluation of voice function and quality after treatment. Endoscopic CO2 laser resections may also achieve similar results in terms of local control and function [8] compared with radiation therapy, although no randomized studies have been performed.[9]
A meta-analysis of 22 consecutive case series to examine oncologic control demonstrated no clear differences between transoral CO2 laser excision and external beam radiation therapy (EBRT) in terms of local control (odds ratio [OR], 0.81; 95% confidence interval [CI], 0.51–1.3 and laryngectomy-free survival [OR, 0.84, 95% CI, 0.42–1.66]).
There was a trend for improved posttreatment voice quality with radiation therapy. Transoral CO2 laser–excision surgery dominates radiation therapy from a cost-utility standpoint.[5][Level of Evidence: 2C]
Conventional and hypofractionated regimens have been studied regarding radiation-dose fractionation for patients with early-stage larynx cancer. In a randomized study of patients with early-stage larynx cancer, patients were randomly assigned to standard fractionation in 2 Gy daily fractions compared with a hypofractionated regimen of 2.25 Gy daily; 82 patients were allocated to a conventional fractionation (CONV) arm (66 Gy/33 fractions for T1 and 70 Gy/35 fractions for T2), with 74 patients to the hypofractionation (HYPO) arm (63 Gy/28 fractions for T1 and 67.5 Gy/30 fractions for T2).[10] The study was underpowered and closed early because of a lack of accrual, although no statistically significant differences were seen between treatment arms in terms of local progression-free survival (PFS).
With a median follow-up of 67 months (range, 2–122 months), the 5-year local PFS was 77.8% for the CONV arm and 88.5% for the HYPO arm (hazard ratio [HR], 1.55; P = .213).
No significant difference was observed in the toxicity profile between the two arms.
In a subgroup exploratory analysis for T1a disease, the 5-year local PFS trended positively in the HYPO arm (76.7% vs. 93.0%; HR, 3.65; P = .056).[10][Level of evidence: 1iiDiii]
Earlier single-institution reports support hypofractionated regimens using 2.25 Gy per fraction for early T1 and T2 larynx cancer with high local control rates.[11][Level of Evidence: 3iiDiv]
Current Clinical Trials
Use our advanced clinical trial search to find NCI-supported cancer clinical trials that are now enrolling patients. The search can be narrowed by location of the trial, type of treatment, name of the drug, and other criteria. General information about clinical trials is also available.
Mittal B, Rao DV, Marks JE, et al.: Role of radiation in the management of early vocal cord carcinoma. Int J Radiat Oncol Biol Phys 9 (7): 997-1002, 1983. [PUBMED Abstract]
Wang CC: Factors influencing the success of radiation therapy for T2 and T3 glottic carcinomas. Importance of cord mobility and sex. Am J Clin Oncol 9 (6): 517-20, 1986. [PUBMED Abstract]
Mendenhall WM, Amdur RJ, Morris CG, et al.: T1-T2N0 squamous cell carcinoma of the glottic larynx treated with radiation therapy. J Clin Oncol 19 (20): 4029-36, 2001. [PUBMED Abstract]
Foote RL, Olsen KD, Kunselman SJ, et al.: Early-stage squamous cell carcinoma of the glottic larynx managed with radiation therapy. Mayo Clin Proc 67 (7): 629-36, 1992. [PUBMED Abstract]
Higgins KM: What treatment for early-stage glottic carcinoma among adult patients: CO2 endolaryngeal laser excision versus standard fractionated external beam radiation is superior in terms of cost utility? Laryngoscope 121 (1): 116-34, 2011. [PUBMED Abstract]
Steiner W: Results of curative laser microsurgery of laryngeal carcinomas. Am J Otolaryngol 14 (2): 116-21, 1993 Mar-Apr. [PUBMED Abstract]
Olsen KD, Thomas JV, DeSanto LW, et al.: Indications and results of cordectomy for early glottic carcinoma. Otolaryngol Head Neck Surg 108 (3): 277-82, 1993. [PUBMED Abstract]
Agrawal A, Moon J, Davis RK, et al.: Transoral carbon dioxide laser supraglottic laryngectomy and irradiation in stage I, II, and III squamous cell carcinoma of the supraglottic larynx: report of Southwest Oncology Group Phase 2 Trial S9709. Arch Otolaryngol Head Neck Surg 133 (10): 1044-50, 2007. [PUBMED Abstract]
Dey P, Arnold D, Wight R, et al.: Radiotherapy versus open surgery versus endolaryngeal surgery (with or without laser) for early laryngeal squamous cell cancer. Cochrane Database Syst Rev (2): CD002027, 2002. [PUBMED Abstract]
Fein DA, Mendenhall WM, Parsons JT, et al.: T1-T2 squamous cell carcinoma of the glottic larynx treated with radiotherapy: a multivariate analysis of variables potentially influencing local control. Int J Radiat Oncol Biol Phys 25 (4): 605-11, 1993. [PUBMED Abstract]
Moon SH, Cho KH, Chung EJ, et al.: A prospective randomized trial comparing hypofractionation with conventional fractionation radiotherapy for T1-2 glottic squamous cell carcinomas: results of a Korean Radiation Oncology Group (KROG-0201) study. Radiother Oncol 110 (1): 98-103, 2014. [PUBMED Abstract]
External-beam radiation therapy alone for the smaller lesions encompassing the primary disease and regional elective nodes.[1]
Supraglottic laryngectomy with bilateral neck dissections, depending on location of the lesion, clinical status of the patient, and expertise of the treatment team. Careful selection must be made to ensure adequate pulmonary and swallowing function postoperatively.
Postoperative radiation therapy (PORT) is indicated for positive or close surgical margins or other adverse pathological risk factors.
Radiation should be preferred because of the good results, preservation of the voice, and the possibility of surgical salvage in patients whose disease recurs locally. (Refer to the Treatment Option Overview for Laryngeal Cancer section of this summary for more information.)
Partial or hemilaryngectomy or total laryngectomy, depending on anatomic considerations. Under certain circumstances, laser microsurgery may be appropriate.[6]
Lesions can be treated successfully by radiation therapy alone with preservation of normal voice.[1]
Surgery is reserved for failure of radiation therapy or for patients in whom follow-up is likely to be difficult.
Mittal B, Marks JE, Ogura JH: Transglottic carcinoma. Cancer 53 (1): 151-61, 1984. [PUBMED Abstract]
Medini E, Medini I, Lee CK, et al.: Curative radiotherapy for stage II-III squamous cell carcinoma of the glottic larynx. Am J Clin Oncol 21 (3): 302-5, 1998. [PUBMED Abstract]
Concurrent chemoradiation therapy can be considered for patients who would require total laryngectomy for control of disease.[1]
Neoadjuvant chemotherapy followed by concurrent chemoradiation therapy. Laryngectomy is reserved for patients with less than a 50% response to chemotherapy or who have persistent disease following radiation.[1-6][Level of evidence: 1iiC]
Definitive radiation therapy alone with altered fractionation in patients who are not candidates for concurrent chemotherapy and surgery (total laryngectomy) for salvage of radiation failures.[7]
Surgery with or without postoperative radiation therapy (PORT).[8]
Neoadjuvant chemotherapy followed by concurrent chemoradiation therapy. Laryngectomy is reserved for patients with less than a 50% response to chemotherapy or who have persistent disease after radiation.[1-6]
Surgery with or without PORT.[8]
Treatment options under clinical evaluation:
Clinical trials exploring novel targeted therapy, immunotherapy, novel chemotherapy, radiosensitizers, or particle beam-radiation therapy.[9]
Laryngectomy plus isolated thyroidectomy and tracheoesophageal node dissection usually followed by PORT.[10]
Treatment by radiation therapy alone is indicated for patients who are not candidates for surgery. Patients should be closely followed, and surgical salvage should be planned for recurrences that are local or in the neck.
Definitive radiation therapy alone with altered fractionation in patients who are not candidates for concurrent chemotherapy and surgery (total laryngectomy) for salvage of radiation failures.[6,7]
Induction chemotherapy followed by concomitant chemotherapy and radiation. Laryngectomy is reserved for patients with less than a 50% response to chemotherapy or who have persistent disease after radiation.[6]
Clinical trials exploring novel targeted therapy, immunotherapy, novel chemotherapy, radiosensitizers, or particle-beam radiation therapy.[9]
Role of Neck Dissection in the Post Radiation Therapy Setting
In a prospective randomized trial, 564 head and neck cancer patients with N2 or N3 disease were randomly assigned to planned neck dissection versus surveillance with positron emission tomography/computed tomography (PET/CT). With a median follow-up of 36 months, PET/CT resulted in fewer neck dissections compared with the surgical arm (54 vs. 221), with a 2-year survival of 84.9% versus 81.5%, respectively. The hazard ratio (HR)death slightly favored PET/CT-guided surveillance and indicated noninferiority (upper boundary, 95% confidence interval for HR, <1.50; P = .004).[11][Level of evidence: 1iiA]
Spaulding MB, Fischer SG, Wolf GT: Tumor response, toxicity, and survival after neoadjuvant organ-preserving chemotherapy for advanced laryngeal carcinoma. The Department of Veterans Affairs Cooperative Laryngeal Cancer Study Group. J Clin Oncol 12 (8): 1592-9, 1994. [PUBMED Abstract]
Adelstein DJ, Saxton JP, Lavertu P, et al.: A phase III randomized trial comparing concurrent chemotherapy and radiotherapy with radiotherapy alone in resectable stage III and IV squamous cell head and neck cancer: preliminary results. Head Neck 19 (7): 567-75, 1997. [PUBMED Abstract]
Jeremic B, Shibamoto Y, Milicic B, et al.: Hyperfractionated radiation therapy with or without concurrent low-dose daily cisplatin in locally advanced squamous cell carcinoma of the head and neck: a prospective randomized trial. J Clin Oncol 18 (7): 1458-64, 2000. [PUBMED Abstract]
Lefebvre JL, Pointreau Y, Rolland F, et al.: Induction chemotherapy followed by either chemoradiotherapy or bioradiotherapy for larynx preservation: the TREMPLIN randomized phase II study. J Clin Oncol 31 (7): 853-9, 2013. [PUBMED Abstract]
MacKenzie RG, Franssen E, Balogh JM, et al.: Comparing treatment outcomes of radiotherapy and surgery in locally advanced carcinoma of the larynx: a comparison limited to patients eligible for surgery. Int J Radiat Oncol Biol Phys 47 (1): 65-71, 2000. [PUBMED Abstract]
Adelstein DJ, Lavertu P, Saxton JP, et al.: Mature results of a phase III randomized trial comparing concurrent chemoradiotherapy with radiation therapy alone in patients with stage III and IV squamous cell carcinoma of the head and neck. Cancer 88 (4): 876-83, 2000. [PUBMED Abstract]
Mehanna H, Wong WL, McConkey CC, et al.: PET-CT Surveillance versus Neck Dissection in Advanced Head and Neck Cancer. N Engl J Med 374 (15): 1444-54, 2016. [PUBMED Abstract]
Concurrent chemoradiation therapy can be considered for patients who would require total laryngectomy for control of disease, including those with nonbulky T4a disease.[1]
Definitive radiation therapy alone in patients who are not candidates for concurrent chemotherapy and surgery (total laryngectomy) for salvage of radiation failures.[7]
For patients with bulky T4 disease, surgery followed by postoperative radiation therapy (PORT) with or without concurrent chemotherapy based on pathological risk factors for large volume T4 disease.[8]
Neoadjuvant chemotherapy followed by concurrent chemoradiation therapy. Laryngectomy is reserved for patients with less than a 50% response to chemotherapy or who have persistent disease following radiation.[1-6]
For patients with bulky T4 disease, surgery (total laryngectomy) followed by PORT with or without concurrent chemotherapy based on pathological risk factors for large volume T4 disease.[8]
Laryngectomy plus total thyroidectomy and bilateral tracheoesophageal node dissection usually followed by PORT with or without concurrent chemotherapy based on pathological risk factors.[10]
Clinical trials exploring novel targeted therapy, immunotherapy, novel chemotherapy, radiosensitizers, or particle-beam radiation therapy.
Bernier J, Cooper JS: Chemoradiation after surgery for high-risk head and neck cancer patients: how strong is the evidence? Oncologist 10 (3): 215-24, 2005. [PUBMED Abstract]
Treatment of recurrent and metastatic supraglottic, glottic, and subglottic cancer includes further surgery or clinical trials.[1-3]
Surgery [4] and/or radiation therapy. Salvage is possible for failures of surgery alone or of radiation therapy alone, and further surgery [4] and/or radiation therapy should be attempted, as indicated. Selected patients may be candidates for partial laryngectomy after high-dose radiation therapy has failed.[5]
Radiation therapy. Re-irradiation for laryngeal salvage following radiation therapy failure has resulted in long-term survival in a small number of patients; it may be considered for small recurrences after radiation therapy, especially in patients who refuse or are not candidates for laryngectomy.[6]
Chemotherapy. A response of variable duration may be achieved after systemic chemotherapy.[7]
Immunotherapy. Immunotherapy (inhibitor of the programmed death-ligand 1 [PD-L1] pathway) can be used after platinum-based failure in the locally recurrent or metastatic setting.[8,9]
Platinum-based chemotherapy is often used as first-line treatment for patients with recurrent or metastatic squamous cell carcinoma (SCC) of the head and neck.
Evidence (chemotherapy):
In a phase III randomized trial of 442 patients with untreated recurrent or metastatic SCC of the head and neck, adding cetuximab to platinum plus fluorouracil compared with platinum plus fluorouracil alone improved overall survival (OS), with a median survival of 10.1 months versus 7.4 months (hazard ratio [HR] for death [HRdeath], 0.80; 95% confidence interval [CI], 0.64–0.99; P = .04).[10]
Quality of life (QOL) was not adversely affected by adding cetuximab to this platinum-based regimen.[11]
Tumor EGFR gene copy number was not found to be a predictive biomarker for the efficacy of cetuximab plus platinum and fluorouracil as first-line therapy for patients with recurrent or metastatic SCC of the head and neck.[12][Level of evidence: 1iiA]
An open-label phase III randomized trial demonstrated improvements in progression-free survival (PFS) for patients who received afatinib compared with patients who received methotrexate.[13]
After a median follow-up of 6.7 months, the median PFS was 2.6 months (95% CI, 2.0–2.7) for the afatinib group and 1.7 months (95% CI, 1.5–2.4) for the methotrexate group (HR, 0.80; 95% CI, 0.65–0.98; P = .030).
The most frequent grade 3 or grade 4 drug-related adverse events for patients treated with afatinib or methotrexate included the following:
Rash or acne (10% for afatinib vs. 0% for methotrexate).
Diarrhea (9% for afatinib vs. 2% for methotrexate).
Stomatitis (6% for afatinib vs. 8% for methotrexate).
Fatigue (6% for afatinib vs. 3% for methotrexate).
Neutropenia (<1% for afatinib vs. 7% for methotrexate).
Overall serious adverse events occurred in 14% of patients treated with afatinib and 11% of patients treated with methotrexate.
Pembrolizumab is a monoclonal antibody and an inhibitor of the programmed death (PD-1) pathway.
Evidence (pembrolizumab):
In a randomized phase III trial, patients with incurable recurrent or metastatic head and neck SCC who had received platinum-based treatment within 3 to 6 months were eligible.[8] Patients were randomly assigned to the pembrolizumab arm (200 mg every 3 weeks [247 patients]) or to the standard therapy arm of the investigator's choice (methotrexate, docetaxel, or cetuximab [248 patients]). Patients received treatment until progression or toxicity. The maximum duration of pembrolizumab was 24 months. The primary endpoint was overall survival (OS) in the intention-to-treat population.
The median OS was 8.4 months in the pembrolizumab arm versus 6.9 months in the standard therapy arm (HR, 0.80 [0.65–0.98]; nominal P = .0161).[8][Level of evidence: 1iiA]
Pembrolizumab was associated with fewer grade 3 or higher adverse events (pembrolizumab, 13% vs. standard therapy, 36%). The most common treatment-related adverse events were hypothyroidism (13%) in the pembrolizumab arm and fatigue (18%) in the standard therapy arm.
In patients receiving pembrolizumab, there were four treatment-related deaths resulting from large intestinal perforation, Stevens-Johnson syndrome, and unspecified, malignant progression; two treatment-related deaths in the standard therapy arm resulted from malignant progression and pneumonia.
The PD-L1 combined positive score was 1 or higher in 79% of the patients in the pembrolizumab arm and 77% of the patients in the standard therapy arm.
Patients with PD-1 expression on their tumors or in the tumor microenvironment as noted by the PD-L1 combined positive score of 1 or higher (HR, 0.74; 95% CI, 0.58–0.93; nominal P = .0049) or a PD-L1 tumor proportion score of 50% or higher (HR, 0.53; 95% CI, 0.35–0.81; nominal P = .0014), and treated with pembrolizumab had reduced HRdeath when compared with patients treated with standard therapy.
Nivolumab is a fully human immunoglobulin G4 (IgG4) anti–PD-1 monoclonal antibody.
Evidence (nivolumab):
In an open-label, phase III trial, randomized in a 2:1 ratio, 361 patients with recurrent SCC of the head and neck and disease progression within 6 months after platinum-based chemotherapy were randomly assigned to receive nivolumab (at a dose of 3 mg/kg of body weight) every 2 weeks or standard, single-agent systemic therapy (methotrexate, docetaxel, or cetuximab) with a primary endpoint of OS.[9]
The median OS was 7.5 months (95% CI, 5.5–9.1) in the nivolumab group versus 5.1 months (95% CI, 4.0–6.0) in the standard therapy arm. OS was significantly longer with nivolumab than with the standard therapy (HRdeath, 0.70; 97.73% CI, 0.51–0.96; P = .01), and the estimates of the 1-year survival rate were approximately 19% higher with nivolumab (36.0%) than with standard therapy (16.6%).[9][Level of evidence: 1iiA]
There was no difference in median PFS between arms. The rate of PFS at 6 months was 19.7% with nivolumab versus 9.9% with standard therapy.
The response rate was 13.3% in the nivolumab group versus 5.8% in the standard therapy group.
Grade 3 or 4 treatment-related adverse events occurred in 13.1% of the patients in the nivolumab group compared with 35.1% in the standard therapy group.
QOL using the European Organisation for Research and Treatment of Cancer Quality of Life Questionnaire (QLQ), Core Module (QLQ-C30) and the Head and Neck Module (QLQ-H&N35) domains—including physical, role, social functioning, pain, sensory, and social contact problems—were stable in the nivolumab arm, but QOL was worse in the standard therapy arm.
In the subgroup of patients with a PD-L1 expression level of 1% or higher, the HRdeath among the patients treated with nivolumab versus standard therapy was 0.55 (95% CI, 0.36–0.83) compared with the subgroup of patients with a PD-L1 expression level of lower than 1% for whom the HR was 0.89 (95% CI, 0.54–1.45; P = .17 for interaction).
Salvage after previous combined total laryngectomy and radiation therapy is poor.
Patients whose disease does not respond to combined radiation therapy and surgery should be considered for clinical trials.
Million RR, Cassisi NJ, eds.: Management of Head and Neck Cancer: A Multidisciplinary Approach. Philadelphia, Pa: Lippincott, 1994.
Vikram B, Strong EW, Shah JP, et al.: Intraoperative radiotherapy in patients with recurrent head and neck cancer. Am J Surg 150 (4): 485-7, 1985. [PUBMED Abstract]
Jacobs C, Lyman G, Velez-García E, et al.: A phase III randomized study comparing cisplatin and fluorouracil as single agents and in combination for advanced squamous cell carcinoma of the head and neck. J Clin Oncol 10 (2): 257-63, 1992. [PUBMED Abstract]
Wong LY, Wei WI, Lam LK, et al.: Salvage of recurrent head and neck squamous cell carcinoma after primary curative surgery. Head Neck 25 (11): 953-9, 2003. [PUBMED Abstract]
Paleri V, Thomas L, Basavaiah N, et al.: Oncologic outcomes of open conservation laryngectomy for radiorecurrent laryngeal carcinoma: a systematic review and meta-analysis of English-language literature. Cancer 117 (12): 2668-76, 2011. [PUBMED Abstract]
Wang CC, McIntyre J: Re-irradiation of laryngeal carcinoma--techniques and results. Int J Radiat Oncol Biol Phys 26 (5): 783-5, 1993. [PUBMED Abstract]
Al-Sarraf M: Head and neck cancer: chemotherapy concepts. Semin Oncol 15 (1): 70-85, 1988. [PUBMED Abstract]
Cohen EEW, Soulières D, Le Tourneau C, et al.: Pembrolizumab versus methotrexate, docetaxel, or cetuximab for recurrent or metastatic head-and-neck squamous cell carcinoma (KEYNOTE-040): a randomised, open-label, phase 3 study. Lancet 393 (10167): 156-167, 2019. [PUBMED Abstract]
Ferris RL, Blumenschein G, Fayette J, et al.: Nivolumab for Recurrent Squamous-Cell Carcinoma of the Head and Neck. N Engl J Med 375 (19): 1856-1867, 2016. [PUBMED Abstract]
Vermorken JB, Mesia R, Rivera F, et al.: Platinum-based chemotherapy plus cetuximab in head and neck cancer. N Engl J Med 359 (11): 1116-27, 2008. [PUBMED Abstract]
Mesía R, Rivera F, Kawecki A, et al.: Quality of life of patients receiving platinum-based chemotherapy plus cetuximab first line for recurrent and/or metastatic squamous cell carcinoma of the head and neck. Ann Oncol 21 (10): 1967-73, 2010. [PUBMED Abstract]
Licitra L, Mesia R, Rivera F, et al.: Evaluation of EGFR gene copy number as a predictive biomarker for the efficacy of cetuximab in combination with chemotherapy in the first-line treatment of recurrent and/or metastatic squamous cell carcinoma of the head and neck: EXTREME study. Ann Oncol 22 (5): 1078-87, 2011. [PUBMED Abstract]
Machiels JP, Haddad RI, Fayette J, et al.: Afatinib versus methotrexate as second-line treatment in patients with recurrent or metastatic squamous-cell carcinoma of the head and neck progressing on or after platinum-based therapy (LUX-Head & Neck 1): an open-label, randomised phase 3 trial. Lancet Oncol 16 (5): 583-94, 2015. [PUBMED Abstract]
The PDQ cancer information summaries are reviewed regularly and updated as new information becomes available. This section describes the latest changes made to this summary as of the date above.
Editorial changes were made to this summary.
This summary is written and maintained by the PDQ Adult Treatment Editorial Board, which is editorially independent of NCI. The summary reflects an independent review of the literature and does not represent a policy statement of NCI or NIH. More information about summary policies and the role of the PDQ Editorial Boards in maintaining the PDQ summaries can be found on the About This PDQ Summary and PDQ® - NCI's Comprehensive Cancer Database pages.
Purpose of This Summary
This PDQ cancer information summary for health professionals provides comprehensive, peer-reviewed, evidence-based information about the treatment of adult laryngeal cancer. It is intended as a resource to inform and assist clinicians who care for cancer patients. It does not provide formal guidelines or recommendations for making health care decisions.
Reviewers and Updates
This summary is reviewed regularly and updated as necessary by the PDQ Adult Treatment Editorial Board, which is editorially independent of the National Cancer Institute (NCI). The summary reflects an independent review of the literature and does not represent a policy statement of NCI or the National Institutes of Health (NIH).
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The lead reviewers for Laryngeal Cancer Treatment (Adult) are:
Ann W. Gramza, MD (Georgetown Lombardi Comprehensive Cancer Center)
Minh Tam Truong, MD (Boston University Medical Center)
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PDQ® Adult Treatment Editorial Board. PDQ Laryngeal Cancer Treatment (Adult). Bethesda, MD: National Cancer Institute. Updated <MM/DD/YYYY>. Available at: https://www.cancer.gov/types/head-and-neck/hp/adult/laryngeal-treatment-pdq. Accessed <MM/DD/YYYY>. [PMID: 26389189]
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Uganda Vs. Olar James (Crim. Case No. 97 Of 2008) ((Crim. Case No. 97 Of 2008)) [2010] UGHC 98 (28 October 2010);
IN THE HIGH COURT OF UGANDA HOLDEN AT ARUA
CRIMINAL SESSION CASE NO. 0097 OF 2008
UGANDA ::::::::::::::::::::::::::::::::::: PROSECUTOR
=VERSUS=
OLAR JAMES ::::::::::::::::::::::::::::::::::: ACCUSED
BEFORE HON. JUSTICE J.W. KWESIGA
OLAR JAMES, the Accused person is indicted for Murder contrary to sections 188 and 189 of the Penal Code Act. It is alleged in the particulars of the offence tat on 18th April, 2008 at Nyibola Alisi Tungu in Nebbi District the accused person murdered Arua Charles.
The Accused person pleaded Not guilty to the indictment. It is settled that the moment an accused person pleads not guilty to a criminal charge, he shall be presumed not guilty until the prosecution proves that he is guilty. The burden of proof falls upon the prosecution and shall remain upon the prosecution throughout the trial. The prosecution can only discharge the burden of proof by adducing sufficient evidence that proves the essential elements of the offence and in the instant case they are the following:-
That the person named as the deceased is actually dead.
b) That the death was caused unlawfully.
c) That the death was caused with malice aforethought.
d) That the accused person participated in causing the death.
See Uganda Vs Okello [1992 – 1993] HCB 68.
The moment any of the above setout ingredients of the offence is not proved, the accused person would be entitled to being acquitted. The standard of proof must be beyond reasonable doubt.
PW 6 MORRIS NGAGENO a clinical officer at Nebbi Hospital, a holder of a certificate in Pharmacology, Diploma in Clinical Medicine with experience in post-mortem examinations, examined the dead body identified to him as that of ARUA CHARLES by Kerwegi Florence. He observed multiple cut wounds on the face, the head and a broken skull. He assessed the cause of death as the severe head injury with circulatory fracture. The Postmortem report was admitted as prosecution exhibit P.IV.
PW 1 TABU HASSAN knew the deceased as a workmate at the same boda boda transport stage or station and that on 18th April 2008 he saw the deceased alive, left the stage at 8.00pm to transport the accused. The next thing is that he was among the people that went to the scene where a dead body was reported. He identified the body as that of Arua Charles. He saw the body lying on its back, it had a cut wound on the central front part of the head.
PW.2 Onencan Sadik also observed the wounds and identified Arua Charles' dead body.
The above evidence of PW.1, PW.2 and PW.6 leaves no doubt that Arua Charles died on 18th April, 2008 as stated in the particulars of the offence.
It is a settled principle in our Criminal Law that every homicide is presumed unlawful unless there is evidence to show that it was caused accidentally, or under excusable circumstances. See R Vs BUSAMBIZA s/o Wesonga [1948] 15 EACA 65.
PW.1 and PW.2 testified that the deceased left them at their station of work at 8.00 pm on the 18th day of April, 2008 when he was well. He was next seen the next day when he was dead. The wounds that were found on his body were fatal injuries that had been inflicted on him. The weapon used was found near the body. This was a small hoe with a sharp edge. He was found, by PW.6 to have died from the severe head injuries which included a broken skull. The nature of injuries and the presence of the weapon or implement used to kill the deceased when considered together, it is clear that this was an unlawful homicide.
It is not every criminal homicide that amount to murder. Malice aforethought must be proved by the prosecution.
Malice aforethought is a state of mind which must be established from the circumstances and the evidence as a whole that establishes how the offence was committed.
The court of Appeal in AKOL PATRICK & ANOTHER Vs UGANDA [2006] 1 HCB held that in determining the presence of malice aforethought the court must consider the weapon used, the manner in which the weapon was used and the part of the body injured. Similar holding is found in Uganda Vs Ochieng [1992 – 1993] HCB 80 and Uganda Vs Okello [1992 – 1993] HCB 68.
The test is that once a deadly weapon is used, excessive violence is used, and injuries are inflicted on the most vulnerable parts of a human body such as the heart, head, neck and stomach, and once it is proved that multiple injuries were inflicted, it will lead to one conclusion that the assailant intended to cause death of the deceased.
In the instant case, the deceased suffered severe multiple injuries on the head. The fractured skull must have been due to use of severe violent assault on the head to lead to the broken skull. The weapon recovered at the scene, a hoe adds to the circumstantial evidence of use of a lethal weapon in the assault that led to the deceased's death. The assault concentrated on the head, a very sensitive part of a human being that contains the brain a vital organ.
The above evidence clearly proves to the satisfaction of this court that whoever assaulted the late Arua Charles intended to cause his death and therefore had malice aforethought.
Having found that Arua Charles died on 18th April 2008 and that his death was caused unlawfully and with malice aforethought, this court has a duty to examine the evidence as a whole to establish whether or not the accused person is responsible for the murder.
The accused person pleaded not guilty and throughout the trial he maintained that he did not participate in or have anything to do with the murder of Arua Charles.
In his sworn evidence as DW 1, OLAR JAMES (Accused). He testified that on 18th April 2008, he was at Adupare village in Paidha. He left the home at 8.30 am to Paidha to book a bus ticket to go to Kampala after which he went to Nyapea and at 5.30 pm he returned to Paidha. That he spent a night at Paidha police barracks until 5.00pm when he left for Kampala by bus. He returned from Kampala on 20th April 2008 and on reaching Nebbi he was arrested. He denied knowledge of the deceased. He denied participation in the murder. That he spent the night of 18/4/2008 at Nyapea. That he spent the night of 17/4/2008 at Paidha and booked a bus ticket on 18/4/2008 at 8.30 am.
On cross examination he stated that he spent the night of 18/4/2008 at Paidha and left for Kampala on 19/4/2008. He confirmed that among the prosecution witnesses he was well known to TABU (PW.1) with whom they had a pending assault case hence a grudge.
DW 2 ODAGAWUN ALFRED testified that he knew the accused. He saw him on 17/4/2008 at 9.30 pm when he went to change clothes in the house of one LUPINYI. The accused was sleeping and he talked to him. The following morning at 6.20 am he did not find the accused. On 18/4/2008 he was on night duty up to next morning at 6.00 am.
The effect of the accused person's defence is that he was not near the scene of crime between 18th April, 2008 8.00 pm and the next morning when he left for Kampala at 6.30 am, he left on 19th April 2008. This is a defence of ALIBI.
The accused person has no duty to prove his ALIBI. The duty is upon the prosecution to adduce evidence that puts the accused person at the scene of crime. However, once the accused person, on his own offers evidence to support his ALIBI, that evidence must be closely and critically examined to determine its credibility. Once evidence to support the ALIBI is on record it must be examined together with the evidence in the case as a whole without shifting the burden of proof upon the accused.
As stated in Bogere Moses and Another Vs Uganda [1976] HCB 5, the principal is that in criminal cases, a part from certain limited exceptions the burden of proof throughout the trial is on the prosecution.
This was earlier stated in R Vs SIMS [1946] 1 KB 5 that the moment the accused person pleaded not guilty to a criminal charge the burden of proof entirely falls on the prosecution to adduce evidence to prove beyond reasonable doubt that the offence was committed by the accused person.
I will proceed to examine the evidence of the accused person's participation. There is no direct evidence that proves the participation. The prosecution seeks to rely purely on the circumstantial evidence based on the testimonies that the accused person is the person who was last seen with the deceased alive at 8.00 pm on the fateful night.
PW1 TABU Hassan testified that he knew the accused person before and he saw him on 18th April 2008 while he negotiated with the deceased to take him to NYIBOLA. It was at 8.00 pm but this was at GAPCO Petrol station which was lit and there was street electric light so he was able to see the accused talk to the deceased.
The deceased took the accused on his motorcycle at 8.00 pm and he never came back. He never heard of the deceased until next morning when he was found dead, PW1 further testified that at the scene of crime he saw a hoe, a shirt and a jumper. He recognized the shirt and the jumper as those he knew belonged to the accused. The accused denied ownership of items. He alleged he had a grudge with PW1 over a case of assault in court and that PW1 was telling lies due to the grudge.
PW2 Onencan said accused was a common person in Paidha town. He worked with the deceased, he had last seen the deceased on 18/4/2008. He went in the team that to recover the body of the deceased, he saw a hoe in form of a hummer near the dead body which was lying in a pool of blood. He saw a shirt and jumper which were blood stained at the scene. After postmortem the body was given to the family members for burial while it was dressed in the shirt and the jumper. The family members rejected the clothes that they did not belong to the deceased. PW2 took the clothes to the police from the deceased's home. PW2 confirmed that on 18/4/2008 he had not seen the accused anywhere. He confirmed the recovery team which included PW1 dressed the body in the very clothes found at the scene since the body was found naked.
PW 3 Ocangiu, custom check-point attendant, testified that he knew both the deceased and the accused. That on 18/4/2008 at 8.00 pm he stopped a boda boda rider at the crossing point between Congo and Uganda. He recognized the rider as Arua Charles (deceased) he did not recognize the passenger. They crossed the boarder and after about 30 minutes he saw a motorcycle at a high speed which refused to stop and came into Uganda. He did not recognize this motorcycle or its rider. The next day he called the boda boda rider's leader to tell him of a report that a person was found dead. He confirmed that he knew both Arua Charles and the accused for over 4 years. When he stopped the motorcycle he recognized Arua Charles and did not recognize the passenger.
PW4 Odongo Kizito also recognized accused from the boda boda stage on 18/4/2008 and saw the accused and deceased ride off at about 8.00pm. He testified he participated in recovering Arua's body from the scene. At the scene he saw a whitish shirt and a reddish jumper about 1 meter from the body. The body was dressed up at the scene with the clothes. But the relatives removed them at the burial that they did not belong to the deceased. He said he saw the accused put them on on 18/4/2008 at 8.00pm.
PW 5 D/Cpl John Onencan, testified on 19/4/2008 he was at the police station when a dead body was delivered by a group of boda boda riders, it was dressed up then. PW 6 P/C Drani Alfred the store man at the police received and kept:-
A small hoe looking like a hummer P.3
2) A blue long sleeved shirt P.1
3) A red jumper P.2
4) Unregistered motorcycle.
Circumstantial evidence is very often the best evidence, it is evidence of surrounding circumstances which must be intensively examined and before drawing inference of accused's guilt from the circumstantial evidence, court must be sure that there are no other circumstantial which would weaken or destroy the inference. The circumstances must produce moral certainty to the exclusion of every reasonable doubt. See Taper Vs R. [1952] A.C 489.
To convict the accused person in this case would depend on the truthfulness of the evidence of witnesses who allegedly saw the accused go away with the deceased and in addition the circumstances must rule out a possibility that anyone else could have killed the deceased after 8.00 pm on the 18th day of April 2008.
PW.1 and PW.4 testified that they saw the accused talk to the deceased at 8.00 pm and they left together at about that time.
PW.3 Ocangiu testified that at 8.00 pm on 18/4/2008 while at the boarder crossing point he stopped a motorcyclist whom he recognized as Arua Charles, the deceased. He did not recognize the passenger he carried. He testified that he knew the accused person for four years before. This creates a presumption that if the accused person had been the passenger, PW.3 would have recognized him like he recognized the deceased.
He allowed the deceased and his passenger to cross into Congo. The deceased was found the following day dead, on the Congo side of boarder. There is no evidence to prove that the motorcycle he saw riding into Uganda after that meeting is the same he saw the deceased on. There is no evidence that the rider who crossed into Uganda was the passenger the deceased had or was in anyway connected with the deceased.
The prosecution evidence talks of a recovered motorcycle sometime much later on the Ugandan side of the river Nyibola. There is no proof that it was the deceased's motorcycle or that the accused had anything to do with it. The accused was arrested on 20th April 2008 as he came from Kampala. The motorcycle was found 5 miles away from the scene by undisclosed person and on undisclosed date.
Apart from the questionable movement of the clothes attributed to the accused their existence and value is doubtful. PW.1 and PW.4 who recovered the body participated in dressing the deceased in these clothes, delivered the body to police in the clothes, took the body for post-mortem in these clothes, delivered the body to the relatives for burial. It is alleged the relatives rejected these clothes as not belonging to the deceased and up to this point these witnesses who knew the deceased very well had not noted this. They claim to have known the accused very well and to have known his clothes very well and surprisingly they were prepared to burry their friend in these clothes they knew belonged to the suspect! This is unbelievable.
These clothes were an attempt to link the accused to the scene of crime. There is no independent or credible proof of ownership of those clothes.
I have examined the accused person's defence of ALIBI together with the prosecution evidence, notwithstanding the weak nature of the accused person's ALIBI in that not all the hours of the night of 18/4/2008 are fully accounted faor, the prosecution evidence does not squarely put the accused person at the scene of crime.
The accused person cannot be convicted on the weakness of his defence, it must be on the strength of the prosecution evidence. The Assessors advised me to convict the accused person. However, from my appreciation of the evidence as examined above, I am unable to agree with their advice. The accused person is hereby acquitted and set free.
J.W. KWESIGA
Uganda Vs Kapere & 3 Ors (CRIMINAL CASE No. 0013 OF 2013) [2016] UGHCCRD 71 (31 August 2016);
Uganda v Wanican & Anor (CRIMINAL SESSIONS CASE No. 0153 OF 2015) [2018] UGHCCRD 111 (10 May 2018);
Uganda v Kaweesi & 2 Ors (CRIMINAL SESSION CASE NO.0528 OF 2017) [2018] UGHCCRD 76 (20 February 2018);
Uganda v Aliomuke & Anor (CRIMINAL CASE No. 0146 OF 2016) [2017] UGHCCRD 35 (10 February 2017);

redpajama_set_name: RedPajamaCommonCrawl


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Economy on bumpy road, Republicans end benefits
By Masao Suzuki |
Read more articles in Capitalism and Economy
San José, CA - On Friday June 4, the U.S. Department of Labor monthly report on the job market for May 2021 showed that 559,000 new jobs were created, bouncing back from the poor showing the month before. But the economy remained down 7.6 million jobs from February 2020, when the recession began. If job creation continues at the same rate as in May, it would still take until summer of 2022 to reach the pre-pandemic level.
But this is unlikely, given all the shortages showing up in the economy. Shortages of computer chips have slowed car production. Shortages of lumber are crimping housing construction and driving up prices.
One thing that is not rising rapidly are wages, with a gain of 2% over the last year. This is less than half the overall inflation rate for consumers reported in April of 4.2%. This means that the actual purchasing power of workers' wages are going down on average.
Nevertheless, businesses across the country are complaining about a shortage of labor, even as they drag their feet on increasing wages, in an effort to further fatten their bottom line. The big corporations and the richest 1% made out like bandits during the recession, and now they are doing the same.
Businesses are showing their control of both political parties, as 25 Republican-led states are ending the $300 a week supplement to unemployment benefits and also the Pandemic Unemployment Assistance or PUA for the self-employed and gig workers. President Joe Biden defended their "right" to end the aid and emphasized that they are temporary programs.
But the PUA in particular is needed as a permanent program, as a growing number of businesses like Uber and Lyft convert their workforce to "independent contractors" to save on taxes and benefits. These workers are not covered by traditional unemployment insurance, and the PUA actually is paying benefits to more jobless workers than the regular state unemployment program.
Last month, when the job creation number was only about one-quarter of what economists predicted, businesses launched a campaign to blame unemployment benefits. This month, with twice as many jobs created, they are still singing the same tune. What they really want is to reduce unemployment benefits as much as possible to force the jobless to work for lower wages. Another sign of the businesses chasing lower wages is that the unemployment rate for teenagers fell to a historic low in records going back to 1953.
The same jobs report also said that the official national unemployment rate fell in May to 5.8%, from 6.1% in April. While most of this improvement came from the unemployed finding jobs, almost one-third came from people leaving the labor force by giving up their search for a job. Over the last three months the unemployment rate has only dropped by 0.2%. At this rate is would take almost three years to get the rate down to the pre-recession level of 3.5% last seen in February 2020.
The official unemployment rate understates the economic hardship workers have faced. Counting all the people who have given up looking for working or working, the unemployment rate would be closer to 7.6%, more than twice the level before the recession. The rising tide of job creation, as usual, is very unequal, with Latinos and African Americans having unemployment rates 50 to 100% more than that of whites.
Another challenge for jobless workers is that the federal eviction moratorium is ending on June 30. More than 10 million tenants are behind on their rent and could face evictions once this protection is dropped. The federal government is spending billions to try to aid tenants and landlords. But not only is the amount too little; only part of the money has been spent. A handful of states have enacted their own moratoriums but many more will need to do this.
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On the good days, you feel brighter and lighter.
Find out how others make the most of the good days and manage the bad ones.
Most people told us they do have good days despite COPD. Even if they couldn't forget about the condition completely, on a good day people felt able to 'get on with life'. "It's like clean air, free, a clear sky … you can breathe it in deeper".
The consensus was that the goal was often just to live as close to a normal life as possible, so "I do everything everyone else does". Many wanted to lead healthier lifestyles to help them manage the more difficult times, which they explained as a weight or a darkness: "… like a cloud hanging over you, a big heavy cloud".
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It can feel like you're always carrying COPD around with you.
But it doesn't need to weigh you down.
COPD can make you feel vulnerable, or even isolated at times.
But the people around you can be a big help.
At times COPD can feel like a storm raging around you.
But it doesn't need to wash away all the positive things in life.
It isn't always easy balancing COPD on one side and normal life on the other.
The right help can help you stay steady.


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Home Entertainment Syleena Johnson Shares Why She Thinks White People Aren't Concerned About The...
Syleena Johnson Shares Why She Thinks White People Aren't Concerned About The Buffalo Mass Shooting Like They Were About The Will Smith Oscars Slap
Back in March the infamous Oscars slap involving Will Smith and Chris Rock was the talk of the news for weeks after the incident. However, after the recent mass shooting in Buffalo, that left 10 Black people deceased, many people are questioning why that incident hasn't drawn the same amount of attention.
During the latest episode of the Fox Soul show "Cocktails With Queens," Syleena Johnson shared why she thinks white people are not as outraged about the mass shooting in Buffalo as they were about this year's unforgettable Oscars moment.
She said, "Sorry guys, white people are used to seeing us get killed. It's not news anymore to them, we're always getting shot down either by them or by each other. So for them, this is run-of-the-mill news. They're not outraged anymore, they're used to seeing this type of thing happen. They're watching the show like every other nationality is watching the show in terms of Black people and death."
Media personality Scottie Beam recently spoke on the matter as well. However, she called out Amy Schumer and Judd Apatow in particular and said,
"Remember when the celebrities were traumatized over a smack between two grown a** men… How loud are they now that an anti-Black hate crime killed 10 people? Specifically @amyschumer @JuddApatow. Quickly."
She added, "When it comes to policing Black people you haven't hesitated.. but when Black people are killed by a racist demon.. where is your pleather pale ass tears."
As previously reported, Payton S. Gendron was identified as the shooter responsible for the mass shooting at Tops Friendly Market in Buffalo, NY. He was charged with first-degree murder in the shooting. Officials say he showed up at the supermarket dressed in tactical gear and live-streamed the mass shooting with a camera attached to his helmet.
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The post Syleena Johnson Shares Why She Thinks White People Aren't Concerned About The Buffalo Mass Shooting Like They Were About The Will Smith Oscars Slap appeared first on The Shade Room.
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BREAKING: 6th Memphis Police Officer 'Relieved Of Duty' Following Fatal Arrest Of Tyre Nichols
A sixth Memphis police officer has been relieved of duty following footage of the fatal arrest of Tyre Nichols being made public. According to CNN, the individual is named Officer… [...]
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Knoc-turn'al Ft. Meezy Mays – "Ain't Enough Time".


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Pacquiao camp predicting "short and sweet" WBO title fight
Originally published June 28, 2017 at 2:37 am
BRISBANE, Australia (AP) — Manny Pacquiao isn't saying it publicly, preferring not to dwell too much on landing a knockout blow.
His trainer, Freddie Roach, isn't pulling any punches, though. Roach reckons the WBO welterweight world championship fight against Jeff Horn on Sunday will be "short and sweet."
"Manny is in great shape," Roach said. "He doesn't like to predict knockouts, but I do. It's going to be short and sweet.
"If Horn comes out likes he says he's gonna, Manny will fire back. I think it's going to be a great fight but it won't last too long — someone will get knocked out."
Pacquiao, who hasn't won by knockout since 2009, said he has a few strategies to handle Horn, who is unbeaten in 17 fights since turning pro in 2013. The 38-year-old Philippines senator has knocked sparring partners down in training and said he's feeling better than he has in a while.
Roach said the training camp has been more like a vintage Pacquiao preparation.
"The thing is, in sparring, we haven't had knockdowns and knockouts in a long time. This time we did," the legendary trainer said. "Manny has been his old self, having fun and doing what he does best."
Pacquiao said he likes to fight boxers in front of their home crowd, and recalled a similar bout with Marco Antonio Barrera at San Antonio, Texas, in 2003.
"I feel excited for the fight. Everything is all set," he said. "I like to fight a home advantage of my opponent so that there are a lot of fans cheering for him. That gives me a lot of motivation, determination and focus to win the fight.
"I'm not taking it lightly. I'm seriously focused."
The afternoon fight is being dubbed the "Battle of Brisbane" and will be staged at the outdoor Suncorp Stadium, with an expected crowd of more than 50,000 and in forecast sunny skies and a high of about 22 degrees Celsius (72 Fahrenheit).
It will be broadcast live on the U.S. east coast at 9 p.m. on Saturday by ESPN, with Pacquiao's handlers expecting the timing to expose the Filipino boxer to millions of new fans.
Horn's trainer, Glenn Rushton, believes Pacquiao's camp has underestimated the Australian boxer by talking already about future rematches with Floyd Mayweather.
"I believe this fight will end in a stoppage. As much as I respect (Roach) for his wealth of experience — he's trained more world champions than most boxers have had professional fights — I think he's wrong," Rushton said. "Where he's talking about an early stoppage I don't see that at all.
"I see this going deep. I think it'll be a late stoppage after a torrid war. I do think Freddie and Manny are underestimating Jeff … (and) when they get out there, it's going to be so different."
Horn's promotor Dean Lonergan also picked up on the theme, highlighting Pacquiao's continual attention to his cell phone during Wednesday's official news conference and describing the 11-time world champion Filipino fighter as a "world champion texter."
For his part, the 29-year-old Horn didn't mind it if Roach and Co. are expecting a knockout.
"I was surprised to hear them say that, actually," the former school teacher said. "If he's looking for a knockout it always makes you vulnerable. If you look for a knockout, it usually doesn't come and you leave lots of openings."
Pacquiao said he never predicted how he'd win a fight, and said he only spoke about a potential rematch with Mayweather because he was answering questions about it from the media.
Pacquiao (59-6-2, 38 knockouts) explained that he was preparing notes on his phone regarding who to thank during the news conference and didn't mean any offense.
He rejected any suggestion he was taking Horn lightly, saying he'd worked so hard in training at times that Roach had ordered him to stop, and he was ready to put his WBO belt and his reputation on the line.


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