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    The effect of combination of Tamoxifen with interval and continue training on tumor mass in Mice with breast cancer tumor
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    Abstract:
    Background: Beast cancer is considered as the most common malignancy among females in the world .in Iran, this cancer is also the most prevalent malignancy among women. The aim of this study is to compare the effects of Tamoxifen and interval and continues training on tumor mass Balb/c mice suffering from breast cancer Methods: for this reason 30 female balb/c mice were utilized and after transplant carcinoma tumor to mice randomly divided in 4 groups 6 groups as follow : 1:tumor-control 2:tumor-continue training 3:tumor –continue training-Tamoxifen 4:tumor-interval training 5: tumor-interval training-Tamoxifen 6:tumor-tamoxifen. Continues training protocol was done for 6 weeks at 25% to 75% vo2max and interval training protocol was done for 6 weeks at 20% to 55%vot2 max between 1 until 10 interval rep *1 min . The drug was injected every day during research program. Blood samples were collected after protocol. The levels of Heat shock protein 70-kDa (Hsp70), interleukin 4 (IL-4), and interferon gamma (IFN γ) were measured with ELISA method, and the resulting data was analyzed with SPSS 10 statistical software Result: Data analysis showed that the Hsp70 levels in both groups of interval and interval plus Tamoxifen were decreased (P=0.459). Also in continues group was increased (p>0/05).The IL-4 level in both groups of interval and interval plus Tamoxifen showed no significant differences compared to tumor control (P=0.112). The IFN γ level in both groups of interval and interval plus Tamoxifen showed an increase, but was not significant compared to control group(P=0.784). Conclusion: tumor mass in interval training only, interval training and Tamoxifen treated showed a significant decrease in the tumor growth in comparison with control group. But tumor mass in continues group was increased in comparison control group.
    Keywords:
    Interval training
    Breast carcinoma
    The aim of the present investigation was to determine whether the administration of a third year of tamoxifen, following 2 years of L-phenylalanine mustard, 5-fluorouracil and tamoxifen, would benefit women with primary breast cancer. The data at 5 years indicate that in patients receiving a third year of tamoxifen treatment, a significant prolongation in disease-free survival occurs, when compared to patients who receive only 2 years of tamoxifen. This benefit is limited to patients older than 49 years of age, and is not apparent in women younger than 50. It is concluded that an additional year of tamoxifen therapy, following the completion of chemotherapy prolongs both disease-free survival and actual survival in node-positive, 'tamoxifen-responsive' patients.
    Adjuvant Therapy
    Citations (3)
    Aim The estrogen receptor coactivator Amplified in Breast Cancer 1 (AIB1) has been associated with an improved response to adjuvant tamoxifen in breast cancer, but also with endocrine treatment resistance. We hereby use metachronous contralateral breast cancer (CBC) developed despite prior adjuvant tamoxifen for the first tumor as an “in vivo”-model for tamoxifen resistance. AIB1-expression in the presumable resistant (CBC after prior tamoxifen) and naïve setting (CBC without prior tamoxifen) is compared and correlated to prognosis after CBC. Methods From a well-defined population-based cohort of CBC-patients we have constructed a unique tissue-microarray including >700 patients. Results CBC developed after adjuvant tamoxifen more often had a HER2-positive/triple negative-subtype and a high AIB1-expression (37% vs. 23%, p = 0.009), than if no prior endocrine treatment had been administered. In patients with an estrogen receptor (ER) positive CBC, a high AIB1-expression correlated to an inferior prognosis. However, these patients seemed to respond to tamoxifen, but only if endocrine therapy had not been administered for BC1. Conclusions Metachronous CBC developed after prior endocrine treatment has a decreased ER-expression and an increased HER2-expression. This is consistent with endocrine treatment escape mechanisms previously suggested, and indicates metachronous CBC to be a putative model for studies of treatment resistance “in vivo”. The increased AIB1-expression in CBC developed after prior tamoxifen suggests a role of AIB1 in endocrine treatment resistance. In addition, we found indications that the response to tamoxifen in CBC with a high AIB1-expression seem to differ depending on previous exposure to this drug. A different function for AIB1 in the tamoxifen treatment naïve vs. resistant setting is suggested, and may explain previously conflicting results where a high AIB1-expression has been correlated to both a good response to adjuvant tamoxifen and tamoxifen resistance.
    Abstract The study of changes in proliferation as a marker of treatment benefit during presurgical endocrine treatment of breast cancer has become increasingly popular, particularly using the nuclear marker Ki67, and holds the potential for prioritizing new treatments for full clinical development. There are weakly significant relationships between Ki67 change and clinical response that differ according to data handling. In the neoadjuvant Immediate Preoperative Anastrozole, Tamoxifen, or Combined with Tamoxifen trial, suppression of Ki67 at both 2 and 12 weeks was greater with the aromatase inhibitor anastrozole than with either tamoxifen or the combination of anastrozole and tamoxifen. We report here that absolute values of Ki67 after 2 weeks were also significantly lower with anastrozole than with tamoxifen and the combination. This indicates that it may be possible to make such comparisons using surgical samples only. We argue that these changes in proliferation and concurrent changes in apoptosis may be expected to be more predictive of adjuvant benefit from endocrine therapy than clinical response.
    Anastrozole
    Aromatase inhibitor
    Neoadjuvant Therapy
    Adjuvant Therapy
    137 Background: The purpose of this study was to compare treatment outcomes between gonadotropin-releasing hormone (GnRH) agonist plus tamoxifen and adriamycin and cyclophosphamide (AC)-containing chemotherapy plus tamoxifen in hormone-responsive, premenopausal, node-negative, breast cancer patients. Methods: Among 7278 breast cancer patients who were diagnosed as breast cancer at Asan medical center, Seoul, Korea, 994 premenopausal women with node-negative, hormone receptor-positive, HER2-negative, T1-2 breast cancers were included in this retrospective cohort study: A median follow-up was 7.4 years (range, 0.5-11.4 years). 608 patients (61.2%) were treated with GnRH agonist together with tamoxifen, and 386 patients (38.8%) were treated with AC-containing chemotherapy with tamoxifen. The propensity score matching and inverse probability weighting was applied to original cohort based on patients’ age, operation method, nuclear and histologic grade, estrogen receptor and progesterone receptor positivity, T stage, Her2 positivity, and p53 positivity. In final analysis, 260 patients for each treatment arm were included. Results: In propensity matched cohorts (n = 520), a total of 34 patients had recurrence. There were 5 cancer-specific deaths and 12 overall deaths among total 520 patients. There were no survival differences for recurrence-free survival (p= 0.306), cancer-specific survival (p= 0.212), and overall survival (p= 0.102) between the two treatment groups. After applying inverse probability weighting, there were no survival differences for recurrence-free survival (p = 0.522), cancer-specific survival (p= 0.154). However, GnRH agonist with tamoxifen arm showed better overall survival than AC chemotherapy with tamoxifen arm (p= 0.021). Conclusions: Adding GnRH agonist to tamoxifen is a reasonable alternative to adding AC chemotherapy to tamoxifen in premenopausal, hormone-responsive, HER2-negative, lymph node-negative, T1-2, breast cancer patients.
    Antiestrogen
    Sixty-nine postmenopausal women with disseminated breast cancer previously treated with endocrine and cytotoxic therapy were treated with tamoxifen (20 mg/day). Complete plus partial response (CR+PR) was observed in 29 % (CR 16 %) and stable disease in 28 %. The objective response was higher in soft tissue sites (52 %) compared to osseous (12 %) and visceral (13 %) disease. No regression or disease stabilization was observed in the presence of liver involvement. Free-interval, length and type of menopause, and estrogen receptor status (carried out only 26 patients) did not statistically influence the percent of objective response. Only 1 of 16 patients (6 %) who did not respond to previous endocrine therapy responded to tamoxifen, while 3 of 9 previous hormonal responders (33 %) achieved objective regression with antiestrogen therapy. On the contrary, the response to previous chemotherapy failed to influence the subsequent response to tamoxifen. The median duration of the response was more than 12 months and the median survival more than 18 months. Treatment was generally very well tolerated and in only one patient was temporarily discontinued because of thrombocytopenia.