A 65-year-old male; was a heavy smoker from 15 or 16 to 42 years old and did not have relevant co-morbidities. When he was 58 years old, he underwent a left nephrectomy for the occasional detection of the absence of the left urinary duct. On 5 May 2010, he underwent subtotal esophagectomy with intra-thoracic esophago-plastic surgery; post-operative histology showed adeno-carcinoma of the esophageal–gastric junction, intestinal type by Lauren’s classification. pT2 N0 M0 was the post-operative TNM classification, and cells were HER2 negative. He did not receive any adjuvant therapy. This patient remained disease-free until September 2016, when he went to an emergency department because of heavy abdominal cramps. On this occasion, no pathological signs were ascertained by clinical-radiological assessment, and the patient was discharged without symptoms following anti-inflammatory and anti-spastic therapy. Two months later (in November), the same signs and sialorrhoea occurred; again, he went to the same emergency department, where WB CT showed pelvic ascites and mesenteric fat thickness with small nodules suspected for peritoneal metastases. This diagnosis was confirmed at the National Institute of Cancer in Milan, where the patient was sent for consultation. From 24 November 2016 to 1 February 2017, he received four cycles of 2000/sqm/day capecitabine given orally plus 130 mg/sqm oxaliplatin by i.v. infusion (the Xelox regimen) with complete response (CR); after that, on 1 April 2017, he started maintenance cyclic IT. This patient was disease-free at the last clinical-radiological assessment on 20 May 2019. To date, 35 months from the diagnosis of metastases, he is doing well.\nThe median OS of gastrointestinal cancer patients with moderate metastatic peritoneal ascites was reported to be 9.6 and 13.5 months [,].\nDuring IT in all four cases, the mean basal values of IL-2 increased. In patients 4 and 2, the difference was significant (** p = 0.046 and * p = 0.049, respectively) or close to significant (** p = 0.083). In patient 1, it was close to significant (* p = 0.061 and ** p = 0.083). The mean total number of lymphocytes decreased in two of the four cases. The difference was close to significant in patients 1 (* p = 0.076, ** p = 0.083) and 4 (* p = 0.079, ** p = 0.083). Accordingly, CD3+, CD4+, and NK basal values decreased during IT in three (75%) of the four examined patients. In particular, in contrast to NK, for which no significant difference occurred, the difference in CD3+ was significant (* p = 0.040) or close to significant (* p = 0.083) in patient 1 and close to significant (** p = 0.088) in patient 4. The difference in CD4+ was close to significant in both patients 1 (* p = 0.053, ** p = 0.083) and 3 (** p = 0.083). Basal VEGF, IL-12, and CD19+ values decreased in three (75%) patients. The difference in VEFG was close to significant (** p = 0.083) in patients 1 and 3. IL-12 was significant (* p = 0.040) or close to significant (** p = 0.083) in patient 2 and it was close to significant (** p = 0.083) in patient 1. In patients 1 (p = 0.063, ** p = 0.083) and 4 (* p = 0.071, ** p = 0.077), the difference in CD19+ was close to significant (). No significance was found for IL-6. An increase in three patients with only one close to significant was found for IL-10 and IL-2R. Conflicting results were obtained for CD8+; Treg; CD4+45RO; IL-1R; TNF alpha; TGF beta1; FGF; EGF; IGF1; and IL-1, IL-8, and CMP1 inflammatory cytokines (see ).
On 9 October 2002, a 57-year-old male underwent nerve-sparing radical prostatectomy (RP), orchidectomy, vesiculectomy, and bilateral lymphadenectomy for prostate adenocarcinoma. The pre-operative serum PSA was >30 ng/mL. pT3a No Mo was the post-operative TNM classification, G2, 4-5 Gleason, stage III. On 27 January 2003, biochemical recurrence (BCR) (two consecutive values higher than 0.2 ng/mL) was detected [,] with a serum PSA level of 0.60 ng/mL. On 1 April 2003, a PSA level of 1.17 ng/mL was found. From 19 April 2003 to 3 June 2012, intermittent androgen deprivation therapy (IAD) was administered with 250 mg flutamide pills, three pills/day, and an luteinizing hormone-releasing hormone (LHRH) agonist was given subcutaneously once every four weeks. From 3 June 2012 to 12 October 2013, because of increasing serum PSA levels (on 29 May 2012, a PSA of 2.24 ng/mL was found), flutamide was replaced with 50 mg bicalutamide, one pill/day, and an LHRH agonist was given subcutaneously once every four weeks. Because PSA levels continued to increase (on 7 October 2013, a PSA value of 9.85 ng/mL was found), from 12 October 2013 to 15 April 2014, bicalutamide was replaced by 300 mg of cyproterone acetate, which was administered i.m. once a week, and an LHRH agonist was given subcutaneously once every four weeks. A trans-rectal ultrasound on 4 November 2013 and whole body (WB) computed tomography (CT) on 30 November 2013 detected a 27 × 26 mm nodule adherent to the bladder wall, and it was suspected to be local recurrence; this suspicion was confirmed by biopsy. On 17 December 2013, the serum PSA level was 18.28 ng/mL. From 18 April 2014 to 18 June 2014, he received external beam radiotherapy (EBRT; 7000 cGray in total). Following the fractioned EBRT, the serum PSA levels continuously decreased and, on 5 May 2016, the PSA value was 0.24 ng/mL. On 1 June 2016, the patient started cyclic IT, which was consistently administered according to the above-reported schedule. The serum PSA levels further and progressively decreased. On 27 August 2018, 50 months after EBRT, serum PSA was undetectable, and then it fluctuated between 0 and 0.01 ng/mL. The last PSA observation on 5 August 2019 was 0.01 ng/mL.\nA study [] recruited 35 prostate cancer patients submitted to RP. Ten of these patients were pT2a-b N0M0 and 24 pT3a-b N0M0. All 35 patients with a macroscopic histologically-proven local recurrence received 30 Gy (21 patients) or 40 Gy (14 patients) of intensity-modulated brachytherapy (IMBT), combined with 30 Gy of EBRT. In the subgroup of 21 patients, after a mean follow-up of 29 months, PSA progression-free survival (PFS) was 24%, and the mean time interval to a PSA increase was 16 months. In the other subgroup of 14 patients, the mean follow-up was 26 months, the PSA progression-free survival (PFS) was 43%, and the mean time interval to a PSA increase was 10 months. Rising PSA values of <2 to 4 ng/mL have been reported to be predictive factors for successful radiotherapy of local recurrences after RP [,]. In the above-mentioned study, the mean rising PSA prior to salvage radiotherapy was 5.02 ng/mL, while it was 18.28 ng/mL in our reported patient. Moreover, the serum PSA nadir has been reported in the literature to occur 12–24 months after radiotherapy (RT) []; in our patient, it was reached after 50 months and maintained at 62 months.