BACKGROUND: The use of nipple-sparing mastectomy (NSM) for both converge cancertreatment and risk reduction is increasing. There is no randomized datacomparing nipple-sparing mastectomy with standard mastectomy techniques. Thereis bear witness to suggest that ductal and lobular breast cancer arises in theterminal duct/lobular unit (TDLU). This study was undertaken to determinewhether TDLUs exist in the nipple and if so to what extent. METHODS: At thetime of mastectomy the nipple papilla was excised and submitted for separatepathological examination. The presence or absence of TDLUs was noted. RESULTS:Thirty-two nipples were studied in 22 patients. There were no TDLUs in 29specimens. Three of 32 nipple specimens were found to include TDLUs. The threenipples contain one two and three TDLUs respectively. All TDLUs were open atthe base of the nipple with none located come the tip. CONCLUSIONS: Theinfrequent occurrence of TDLUs in the nipple papilla supports the use of NSM forrisk reduction surgery including for those women with BRCA1/2 mutations.
The fluoropyrimidine medicate fluorouracil (FU) is one of the most frequentlyprescribed chemotherapeutic drugs for the curative and palliative treatment ofvarious cancer patients. The identification of biological factors associatedwith tumors either responsiveness or resistance to FU chemotherapy includingFU is increasingly being recognized as an important field of clinical cancerresearch. AIM: to care for the relationship between intra-tumoraldihydropyrimidine dehydrogenase (DPD) level and FU chemosensitivity as DPD isthe initial and rate-limiting enzyme in the catabolism of FU. MATERIALS ANDMETHODS: The histoculture drug response assay (HDRA) was performed for 54patients. DPD expression was examined in 81 tumor samples from converge cancerpatients received two cycles of FU-based primary chemotherapy before operation. RESULTS: We found that intra-tumoral DPD enzyme activity was inverselycorrelated with FU cytotoxicity. We also revealed that low DPD expression wascorrelated with clinical response to FU-based primary chemotherapy. CONCLUSIONS:Our study indicated that DPD is a promising molecular maker for identifyingtumor cells sensitivity in breast cancer patients receiving FU-basedchemotherapy.
Objective: Taxanes and fluoropyrimidines are active in metastatic converge cancer(MBC) and their combination has proven effective in anthracycline-refractorypatients. We conducted a phase I chew over to cause the maximum tolerated dose(MTD) of uracil plus tegafur (UFT) given in combination with leucovorin (LV) andpaclitaxel (Pacl) in patients with refractory MBC. Methods: Pacl was infused ata fixed process of 150 mg/m(2) on day 1. UFT at doses escalated by 50 mg/m(2)starting from 200 mg/m(2) day and LV at a fixed dose of 90 mg/day weregiven orally every 8 h for 11 days (days 3-13). Cohorts of at least 3 patientswere treated at each dose aim and if 1 experienced dose-limiting toxicity(DLT) a maximum of 3 additional patients were added at the same dose level. MTDwas reached if 2 out of the 6 patients experienced DLT. Results: Sixteenpatients were enrolled in the chew over. The most important toxicity observed washematological. Nonhematological toxicities were paresthesia and myalgia,asthenia nausea and mucositis. DLT occurred in only 1 patient (grade 3 hepatictoxicity). Conclusions: The recommended dose for a subsequent phase II trial isPacl 150 mg/m(2) on day 1 and UFT 300 mg/m(2) and LV 90 mg on days 3-13 every2 weeks. Copyright (c) 2007 S. Karger AG. Basel.
Aims: We investigated the relationship between serum leptin concentrations andpolymorphism of the leptin receptor gene and breast cancer. Methods: Serumleptin concentrations were measured by enzyme-linked immunosorbent analyse in 47women with invasive breast cancer compared with 41 age-matched controls withoutcancer. Genomic DNA was extracted from peripheral daub leukocytes. Genotypingof the leptin receptor gene at codon 109 (LEPR-109) was performed by polymerasechain reaction-restriction fragment length polymorphism. Results: Patients withbreast cancer had a higher mean serum leptin concentration than women in thecontrol assort but the difference was not statistically significant. Among thosewith breast cancer the serum leptin concentration was higher in women withhigh-grade cancers (p = 0.020). The LEPR-109RR genotype was more frequent inpremenopausal patients with tumors larger than 2 cm (p = 0.039) and inpremenopausal women who were overweight (p = 0.029). Among patients with theLEPR-109RR genotype higher mean serum leptin concentrations were show inthose with triple-negative cancers (p = 0.048). Conclusions: Our study suggestsan association between serum leptin concentration and tumor progression. LEPR-109 polymorphism in premenopausal women appears to be associated withobesity and tumor progression. procure (c) 2007 S. Karger AG. Basel.
Background: Phase II/III trials have shown that capecitabine is an active,well-tolerated therapy for metastatic breast cancer (MBC). We report clinicalfindings from an expanded access schedule enabling patients ineligible forinvestigative trials to acquire capecitabine before its approval andavailability. Methods: Patients pretreated with at least two chemotherapyregimens including a taxane for MBC received oral capecitabine until diseaseprogression or unacceptable toxicity. Results: Six hundred and thirty-onepatients received capecitabine (mean duration 3.8 months range 0.1-24.7months). The most common treatment-related grade 3/4 toxicities were diarrhea(9%) and hand-foot syndrome (8%). Grade 3/4 alopecia was absent and grade 3/4myelosuppression was rare. Dose was modified in 172 patients (27%). Objectiveresponse rate in 349 evaluable patients was 35%. Median time to progression (n =604) was 6.6 months (95% confidence interval. CI. 5.6-7.6) and median overallsurvival (n = 569) was 10.0 months (95% CI. 8.5-15.3). Conclusions: Our findingsin a cohort of patients with pretreated progressive converge cancer confirm thehigh efficacy and tolerability of outpatient capecitabine. Copyright (c) 2007 S. Karger AG. Basel.
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http://newcancerresearch.blogspot.com/2007/11/whats-new-for-breast-cancer-in-pubmed_16.html
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