***TASK*** the task is to summarize an input biomedical literature in six sentences 
    ***INPUT*** the input is a biomedical literature 
    ***OUTPUT*** the output is the summary of an input biomedical literature in six sentences 
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    Input: AIMS Fluid retention is a phenomenon associated with taxoids . The principal objective of this study was to investigate the pathophysiological mechanism of docetaxel-induced fluid retention in advanced cancer patients . METHODS Docetaxel was administered as a 1 h intravenous infusion every 3 weeks , for at least 4 - 6 consecutive cycles , to patients with advanced breast ( n = 21 ) or ovarian ( n = 3 ) carcinoma , who had received previous chemotherapy , 21 for advanced disease . Phase II clinical trials have shown that 5 day corticosteroid comedication , starting 1 day before docetaxel infusion , significantly reduces the incidence and severity of fluid retention . This prophylactic corticosteroid regimen is currently recommended for patients receiving docetaxel but was not permitted in this study because of its possible interference with the underlying pathophysiology of the fluid retention . RESULTS Fluid retention occurred in 21 of the 24 patients but was mainly mild to moderate , with only five patients experiencing severe fluid retention .  Eighteen patients received symptomatic flavonoid treatment , commonly prescribed after the last cycle . Specific investigations for fluid retention confirmed a relationship between cumulative docetaxel dose and development of fluid retention . Capillary filtration test analysis showed a two-step process for fluid retention generation , with progressive congestion of the interstitial space by proteins and water starting between the second and the fourth cycle , followed by insufficient lymphatic drainage . CONCLUSIONS A vascular protector such as micronized diosmine hesperidine with recommended corticosteroid premedication and benzopyrones may be useful in preventing and treating docetaxel-induced fluid retention Background : As cancer treatments evolve , it is important to reevaluate their effect on lymphedema risk in breast cancer survivors . Methods : A population -based r and om sample of 631 women from metropolitan Philadelphia , Pennsylvania , diagnosed with incident breast cancer in 1999 to 2001 , was followed for 5 years . Risk factor information was obtained by question naire and medical record review . Lymphedema was assessed with a vali date d question naire . Using Cox proportional hazards models , we estimated the relative incidence rates [ hazard ratios ( HR ) ] of lymphedema with st and ard adjusted multivariable analyses ignoring interactions , followed by models including clinical ly plausible treatment interactions . Results : Compared with no lymph node surgery , adjusted HRs for lymphedema were increased following axillary lymph node dissection [ ALND ; HR , 2.61 ; 95 % confidence interval ( 95 % CI ) , 1.77 - 3.84 ] but not sentinel lymph node biopsy ( SLNB ; HR , 1.04 ; 95 % CI , 0.58 - 1.88 ) . Risk was not increased following irradiation [ breast/chest wall only : HR , 1.18 ( 95 % CI , 0.80 - 1.73 ) ; breast/chest wall plus supraclavicular field ( + /− full axilla ) : HR , 0.86 ( 95 % CI , 0.48 - 1.54 ) ] . Eighty-one percent of chemotherapy was anthracycline based . The HR  for anthracycline chemotherapy versus no chemotherapy was 1.46 ( 95 % CI , 1.04 - 2.04 ) , persisting after stratifying on stage at diagnosis or number of positive nodes . Treatment combinations involving ALND or chemotherapy result ed in approximately 4- to 5-fold increases in HRs for lymphedema [ e.g. , HR of 4.16 ( 95 % CI , 1.32 - 12.45 ) for SLNB/chemotherapy/no radiation ] compared with no treatment . Conclusion : With st and ard multivariable analyses , ALND and chemotherapy increased lymphedema risk whereas radiation therapy and SLNB did not . However , risk varied by combinations of exposures . Impact : Treatment patterns should be considered when counseling and monitoring patients for lymphedema . Cancer Epidemiol Biomarkers Prev ; 19(11 ) ; 2734–46 . © 2010 AACR PURPOSE Docetaxel is highly active in the treatment of patients with breast cancer . The principal dose-limiting toxicities of the 3-weekly regimen are neutropenia and febrile neutropenia . In a previous phase I dose-escalation study with granulocyte colony-stimulating factor ( G-CSF ) support , the recommended dose was determined to be docetaxel 160 mg/m(2 ) 3-weekly . The objectives of this phase II study were to determine the response rate and toxicity of this dose and schedule , given as first-line in patients with advanced breast cancer . Mobilisation of peripheral blood stem cells ( PBSCs ) was also investigated . PATIENTS AND METHODS Eligible women had metastatic breast cancer and were aged 18 - 75 years with ECOG performance status < or = 2 . Strict criteria for liver function were followed , and  adjuvant chemotherapy  must have been completed at least 6 months previously . Treatment was docetaxel 160 mg/m(2 ) over 60 - 90 min every 21 days with G-CSF 5 micro g/kg/day until neutrophil recovery , for up to six cycles . A 3-day corticosteroid prophylaxis was given . Bloods sample s to determine PBSC levels [ CD34 + , granulocyte-macrophage colony-forming cells ( GM-CFC ) and burst-forming units-erythroid ( BFU-E ) ] were taken on days 6 , 8 , 9 and 11 following docetaxel . RESULTS Twenty-five women with median age 50 years ( range 35 - 66 ) were included . Seventeen ( 68 % ) had previously received adjuvant chemotherapy . In total , 112 cycles were delivered ( median four per patient ) , with dose reductions required in 12.5 % of cycles . G-CSF was given for a median of 6 days . The median neutrophil nadir was 0.5 x 10(9)/l and occurred a median 5 days after treatment . The median duration of grade 3 or 4 neutropenia was 2 days ( range 1 - 7 ) . Grade 4 neutropenia occurred in 44 % of patients , but there was only one episode of febrile neutropenia .  Five patients were taken off study due to toxicities that included oedema , neurosensory toxicity and asthenia . Confirmed partial response was seen in nine patients ( 37.5 % ; 95 % confidence interval 19 % to 59 % ) . CD34 + cells , GM-CFC and BFU-E levels peaked at day 8 following docetaxel administration . The median CD34 + cell peak was 6.5 x 10(4)/ml , with only 20 % of patients < 2 x 10(4)/ml , a level below which leukapheresis is not usually attempted . CONCLUSIONS Docetaxel 160 mg/m(2 ) was delivered with G-CSF support with a very low rate of febrile neutropenia . Non-haematological toxicity was significant , causing five patients to go off study . Effective mobilisation of PBSCs was seen . The response rate of 37.5 % was less than that obtained in first-line studies using st and ard-dose docetaxel 100 mg/m(2 ) , suggesting that there is no additional benefit in dose escalation of this cytotoxic agent in breast cancer patients using this schedule The aim of this study was to compare the efficacy and tolerability of docetaxel to methotrexate and 5-fluorouracil in advanced breast cancer after anthracycline failure . A r and omised multicentre trial was conducted in 283 patients with advanced breast cancer who had failed previous anthracycline treatment .  Docetaxel at a dose of 100 mg/m2 every 3 weeks ( n = 143 ) was compared with sequential methotrexate and 5-fluorouracil ( MF ; n = 139 ) given at day 1 and 8 every 3 weeks at dosages of 200 mg/ m2 and 600 mg/m2 , respectively . After progression , crossover to the alternative treatment group was recommended . There was a significantly higher overall response rate in the docetaxel 42 % ( CR 8 % + PR 34 % ) than in the MF arm 21 % ( CR 3 % + PR 18 % ) ( P < 0.001 ) . The median time to progression ( TTP ) was 6.3 months in the docetaxel arm and 3.0 months in the MF arm ( P < 0.001 ) . Docetaxel also had a significantly higher response rate of 27 % following crossover compared with MF ( 12 % ) . Significantly more side-effects ( leucopenia , infections , neuropathy , oedema , asthenia , skin , nail changes , alopecia ) were seen in the docetaxel than in the MF group . However , grade 3 and 4 side-effects were infrequent with both drugs , with the exception of fatigue , alopecia and infections . Median overall survival ( OS ) including crossover phase was 10.4 months in the docetaxel and 11.1 months in the MF arm ( P = 0.79 ) . Based on the response rate and the primary endpoint of TTP , docetaxel is superior to sequential methotrexate and 5-fluorouracil in advanced breast cancer after anthracycline failure Purpose A single-arm phase II multicenter trial of the combination of cyclophosphamide ( C ) , epirubicin ( E ) , and 5-fluorouracil ( F ) followed by docetaxel as neoadjuvant chemotherapy is being conducted by the Japan Breast Cancer Research Group . This report describes an interim analysis of the clinical response and safety of 79 patients who finished preoperative chemotherapy and surgery . Patients and Methods Patients with operable breast cancer received C at 500 mg/m2 , E at 100 mg/m2 , and F at 500 mg/m2 every 21 days for 4 cycles followed by docetaxel at 75 mg/m2 every 21 days for 4 cycles . Results Of the 79 patients evaluable for analysis the median age was 46 years ( 28–59 ) . and 61 patients ( 77.2 % ) had T2 tumors . A total of 312 of 316 ( 98.7 % ) cycles of CEF and 296 of 312 ( 94.9 % ) cycles of docetaxel were administered . Average total cumulative dose was 92 % and 95 % for CEF and docetaxel , respectively . The rate and grade of edema , neuropathy , arthralgia and myalgia were higher with docetaxel than with CEF .  The overall clinical response rate was 70.9 % . Breast conserving surgery was performed in 31 of 42 patients ( 73.8 % ) with a base-line tumor size of more than 3 cm . Conclusions Interim data suggest that CEF followed by docetaxel is an active and tolerable neoadjuvant chemotherapy regimen . A final analysis is planned for 2005 PURPOSE The aim of our study was to eluci date whether the fluid retention syndrome induced by docetaxel is caused by capillary protein leakage or by other mechanisms . PATIENTS AND METHODS Twenty-four patients with advanced or metastatic non-small-cell lung cancer ( NSCLC ; 23 patients ) or metastatic head and neck cancer ( one patient ) were included on this prospect i ve , nonr and omized trial . Docetaxel 100 mg/m2 was administered every 3 weeks with 5 days of dexamethasone prophylaxis to avoid hypersensitivity reactions and edema formation . Transcapillary forces , ie , colloid osmotic pressure of plasma ( COPpl ) and interstitial fluid ( COPint ) and interstitial hydrostatic pressure ( Pint ) , were measured before the start of treatment and after total docetaxel doses of 200 and 500 mg/m2 by means of the well-documented wick and wick-in-needle methods . Body weight , degree of edema , blood pressure , and heart rate and hemoglobin , hematocrit , albumin , and total protein values were registered in parallel . RESULTS After a total docetaxel dose of 200 mg/m2 , COPpl , COPint , and hemoglobin , hematocrit , albumin , and total protein values had decreased significantly ; Pint and body weight were unchanged ; and only mild edema was observed . These findings suggest a plasma volume increase followed by enhanced fluid filtration to the interstitium . After a cumulative docetaxel dose of 500 mg/m2 , the COPpl continued to decrease significantly , but COPint remained unchanged despite a significant increase in mean body weight and edema formation . These observations support the theory of a capillary protein leakage . CONCLUSION Docetaxel appears to induce an initial enhancement of fluid filtration followed by a capillary protein leakage that leads to edema formation PURPOSE The combination of doxorubicin and cyclophosphamide ( AC ) is a st and ard adjuvant chemotherapy regimen . Studies of docetaxel and cyclophosphamide ( TC ) in metastatic breast cancer ( MBC ) showed promise in MBC . In 1997 , we 
    Output:
    
The trial of weakest method ological quality reported the highest incidence of oedema .
The results moderately suggest that adjuvant chemotherapy containing docetaxel is related to a significantly increased risk of developing oedema , compared with docetaxel-free chemotherapy