scholarly journals TGF-beta1 in breast cancer-estrogen regulation

2002 ◽  
Vol 10 (3) ◽  
pp. 164-165
Author(s):  
Natasa Todorovic-Rakovic ◽  
Vesna Ivanovic ◽  
Miroslav Demajo ◽  
Borka Neskovic ◽  
Zora Neskovic-Konstantinovic ◽  
...  

TGF-beta1 is a pluripotent cytokine with diverse effects in the normal development of mammary glands, and in the development of malignant tumors of the breast. The aim of the study was to determine the levels of TGF-beta1 in the group of advanced breast cancer, in which increased TGF-beta1 levels were most likely to be expected. TGF-beta1 levels were also compared with estradiol levels. Our results suggested that TGF-beta1 synthesis may be regulated by estrogen or anti-estrogen through ER. Finding of increased TGF-beta1 levels, due to its possible role in predicting invasive phenotype in later phases of tumor progression, may indicate the tendency of tumor tissue towards autonomy.

1996 ◽  
Vol 82 (1) ◽  
pp. 45-47
Author(s):  
Jacqueline Dalski ◽  
Max Görlich

Antiestrogens, particularly tamoxifen, are effective in the treatment of pre- and postmenopausal women suffering from all stages of breast cancer. Unfortunately, many patients become resistant to tamoxifen during therapy, which allows the tumor to progress. Thus, a preclinical recognition of tumor progression, i.e. by monitoring serum hormone levels, could be worthwhile. The serum levels of dehydroepiandrosterone sulfate and estradiol of postmenopausal women with advanced breast cancer treated by the new antiestrogen droloxifene were therefore checked. However, only non-significant changes in the hormone levels during droloxifene therapy were observed, and no relation was found between hormone levels and the course of the disease, success or exhaustion of droloxifene application, or development of tumor progression. Our data do not confirm earlier findings reported in the literature that measurement of hormones seems to be suitable for an early indication of tumor progression during an antiestrogen therapy before its clinical manifestation.


2021 ◽  
Vol 39 (15_suppl) ◽  
pp. e12510-e12510
Author(s):  
Ignazio Ugo Carreca ◽  
Viviana Bazan ◽  
Antonio Galvano ◽  
Anna Paola Carreca ◽  
Stefania Cusenza ◽  
...  

e12510 Background: Due to current lengthening of average lifespan and progressive increase of malignant tumors in mankind, more new strategies must be constantly sought especially for thirdage neoplasms. Nevertheless because severe toxicity developed in the majority of frail patients, administration of therapy may cause high risk of life-threatening AIM: We have considered in this paper ABC in frail patients like OW. Purpose of the study is preliminary detection of the overall toxicity (OTox) through the possible use of specifics tests adopted specially in frail patients such as OW, to ensure greater control in drugs administration with good effectiveness. AIM: We have considered in this paper ABC in frail patients like OW. Methods: Sixty-two patients with advanced breast cancer at presentation ABC-p were enrolled between January 2018 and December 2019. Eligibility criteria: • women aging eighty or older; • acquired written consensus; • confirmed diagnosis of ABC; • one or two measurable lesions (bone or visceral or both); • no brain secondarisms; • Charlson’s Comorbidity Scale 1-3 score points; CGA Evaluation permissive for treatment. CARG-TS (Cancer and Aging Research Group-Test Score) and CRASH-TS (Chemotherapy Risk Assessment Scale for High-Age Patients Test S) are rated for predictive assessment of the risk of severe chemotox in all patients. Further Evaluations tools: Clinical Benefit according to ESMO CB scale v2a; Tox Profile CTCAE v3.0 Criteria; QoL by EORTC QLQ-C20 Results: CARG-TS predicts severe OTox; CRASH-TS predicts hematologic non-hematologic toxicity. Using a combination of CGA-ES+CARG-TS+CRASH-TS, we were able to divide patients into three categories: • LR -Low risk (score0-5); • MR-Medium risk (score 5-10); • HR High risk (score over 10). On this basis HR people was directed to receive endocrine therapy (if ER+PGR+) or RT alone. The MR group experienced a reduced schedule of eribulin (0.90mg/sqm d1,d28 until P-progression or INT-intolerable toxicity). Finally LR group received a schedule with eribulin alone(E 0.96-1.1 mg/sqm IV on d1, d21 dosage depending on creatinine clearance value according to the Kintzel-Dorr’s method and until P or INT-toxicity). Conclusions: With contemporary use of CGA-ES, CARG-TS, CRASH-TS we obtained two diagrams: the first “predicted risk” ; the second “observed risk” for each patient. The first curve was almost perfectly in line (p<0.001) with that of the “observed risk”. This allowed to have extremely personalized treatments, negligible OTox, and very good values for both CB and QoL.


2016 ◽  
Vol 62 (4) ◽  
pp. 411-417
Author(s):  
G.S. Zamay ◽  
I.V. Belayanina ◽  
A.S. Zamay ◽  
M.A. Komarova ◽  
A.V. Krat ◽  
...  

A method of selection of DNA aptamers to breast tumor tissue based on the use of postoperative material has been developed. Breast cancer tissues were used as the positive target; the negative targets included benign tumor tissue, adjacent healthy tissues, breast tissues from mastopathy patients, and also tissues of other types of malignant tumors. During selection a pool of DNA aptamers demonstrating selective binding to breast cancer cells and tissues and insignificant binding to breast benign tissues has been obtained. These DNA aptamers can be used for identification of protein markers, breast cancer diagnostics, and targeted delivery of anticancer drugs.


2007 ◽  
Vol 25 (18_suppl) ◽  
pp. 1078-1078
Author(s):  
J. Zidan ◽  
A. Abzah ◽  
L. Chetver ◽  
W. Basher ◽  
J. Shneider ◽  
...  

1078 Background: The aromatase inhibitor (AI) letrozole and other members of this treatment group are very effective in the treatment of postmenopausal women with breast cancer. AIs markedly reduce estrogen levels in postmenopausal women by inhibiting aromatase. At menopause estradiol levels are about 25 pmol/l. Estradiol levels are higher in plasma of women with breast cancer as compared with women with no breast cancer. The purpose of this prospective study is to evaluate estradiol levels before and during letrozole treatment and the effect of primary estradiol levels and their decrease on response rate. Methods: Letrozole 2.5 mg/day orally was given to 50 patients (pts) with metastatic and locally advanced breast cancer (MBC). All pts had measurable disease. Overnight fasting clotted blood samples used for assessment of serum levels of estradiol at baseline and after 3, 6 and 12 months. Estradiol levels were compared to clinical response in this single stage study. Results: Mean age was 56 years (range 46–89 y). Mean years from menopause to starting letrozole was 9 years.12% of pts received previous hormonotherapy and and 30% received chemotherapy for their metastatic disease. Estradiol levels decreased from a mean of 40 pmol/l before letrozole to 40 pmol/l and <40 pmol/l in 19 pts (38%). No difference in estradiol depression rate was found between the 2 groups. In the first group (estradiol >40 pmol/l) objective response rate was 48%: 4 complete responses (CR) and 11 partial responses (PR) out of 31 pts, 12 pts had stabilization of the disease (SD). In the second group 3 pts had CR, 5 had PR: objective response rate of 42% (8/19), and 42% SD. There is a trend (not significant) for higher response rate in pts with higher estradiol levels at the beginning of treatment. Conclusions: Letrozole was found to cause very high estradiol suppression and high response rates in postmenopausal women with advanced breast cancer. A trend was found for higher response rates in pts with higher estradiol levels at baseline although difference was not significant. This is the first study to address this issue. No significant financial relationships to disclose.


2005 ◽  
Vol 12 (4) ◽  
pp. 749-760 ◽  
Author(s):  
R Serra ◽  
M R Crowley

It is now recognized that transforming growth factor β (TGF-β) is an important factor that regulates normal breast development as well as breast cancer. Genetically engineered mouse models have been used to determine the role and mechanism of TGF-β action in normal development and diseases of the breast. Using these models, it has been determined that TGF-β regulates many steps of normal mammary gland development including branching morphogenesis, functional differentiation, cell-lineage decisions, and involution. Effects of TGF-β on normal development are mediated through signaling in both the epithelial and stromal compartments. In cancer, mouse models have indicated that TGF-β has biphasic effects on tumor progression, acting as a tumor suppressor in early stages of cancer and promoting invasion and metastasis at later stages. In addition, TGF-β may play a role in tumor progression through effects on the microenvironment. Recently, experiments in several mouse models have suggested that antagonism of TGF-β signaling may provide a therapeutic target for late-stage breast cancer, blocking metastasis without detrimental side effects. In the future, genetically altered mice will be used to establish models of human breast disease providing opportunities to test strategies for disease prevention and treatment.


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