A proposed mechanism of tamoxifen in breast cancer prevention

Yu, Fu‐Li; Bender, Wanda

doi:10.1016/s0361-090x(02)00124-1

Cited by 20 publications

(5 citation statements)

References 30 publications

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“…It can be roughly grouped as luminal (luminal A and B), HER2 positive, and triple negative breast cancers (TNBC) according to the presence or expression of estrogen receptor (ER), progesterone receptor (PR), and epidermal growth factor receptor 2 (HER2). Successes on targeted therapies have been reported on luminal tumors such as Tamoxifen (8), and HER2 positive cancer such as Herceptin (9). TNBCs are characterized by a poor prognosis and lack of effective targeted therapies due to the absence of the three primary surface receptors (10–13).…”

Section: Introductionmentioning

confidence: 99%

FA2H Exhibits Tumor Suppressive Roles on Breast Cancers via Cancer Stemness Control

et al. 2019

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Background: Triple negative breast cancers are aggressive, enriched with cancer stem cells, and lack effective targeted therapies with little side effects.Methods: We isolated cancer stem cells from two triple negative breast cancer cell lines via cell sorting following transcriptome sequencing, bioinformatics analysis, experimental and clinical validations, as well as functional investigations to explore genes capturing triple negative breast cancer features for improved diagnosis and therapeutics in clinics.Results: We found that FA2H is under-expressed in triple negative breast cancers both in vitro and in clinics, and FA2H suppresses cancer stemness via inhibiting the STAT3/IL6 axis and NFkB signaling.Conclusions: This study reports the tumor suppressive roles of FA2H on breast cancer cells through cancer stemness control. FA2H and other candidates unveiled in this study that capture the features of cancer stem cells may contribute as diagnostic marker and/or effective therapeutic targets for improved triple negative breast cancer management.

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Section: Introductionmentioning

confidence: 99%

FA2H Exhibits Tumor Suppressive Roles on Breast Cancers via Cancer Stemness Control

et al. 2019

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“…Canonically, breast carcinomas are grouped as luminal (luminal A and B), HER2 positive, and triple negative subtypes based on the status of estrogen receptor (ER), progesterone receptor (PR) and epidermal growth factor receptor 2 (HER2). While luminal tumors respond well to the hormonal therapy Tamoxifen 8 , and HER2 positive cancers could be properly treated with Herceptin 9 , triple negative breast cancers do not actively react to any available targeted modalities without severe adverse effects due to, primarily, lack of the three primary surface receptors 10–13 .…”

Section: Introductionmentioning

confidence: 99%

Integrated diagnostic network construction reveals a 4-gene panel and 5 cancer hallmarks driving breast cancer heterogeneity

Dai

Hua

Hong

2017

Sci Rep

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Breast cancer encompasses a group of heterogeneous diseases, each associated with distinct clinical implications. Dozens of molecular biomarkers capable of categorizing tumors into clinically relevant subgroups have been proposed which, though considerably contribute in precision medicine, complicate our understandings toward breast cancer subtyping and its clinical translation. To decipher the networking of markers with diagnostic roles on breast carcinomas, we constructed the diagnostic networks by incorporating 6 publically available gene expression datasets with protein interaction data retrieved from BioGRID on previously identified 1015 genes with breast cancer subtyping roles. The Greedy algorithm and mutual information were used to construct the integrated diagnostic network, resulting in 37 genes enclosing 43 interactions. Four genes, FAM134B, KIF2C, ALCAM, KIF1A, were identified having comparable subtyping efficacies with the initial 1015 genes evaluated by hierarchical clustering and cross validations that deploy support vector machine and k nearest neighbor algorithms. Pathway, Gene Ontology, and proliferation marker enrichment analyses collectively suggest 5 primary cancer hallmarks driving breast cancer differentiation, with those contributing to uncontrolled proliferation being the most prominent. Our results propose a 37-gene integrated diagnostic network implicating 5 cancer hallmarks that drives breast cancer heterogeneity and, in particular, a 4-gene panel with clinical diagnostic translation potential.

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“…This effect is mediated by the inhibition of the action of both 17 β estradiol and esterone (Yu and Bender, 2002;Stefano et al, 2003) and competition with estrogen for binding to its receptor (Ali and Coombes, 2002). Also, tamoxifen is able dramatically to inhibit the formation of 17 β estradiol and esterone epoxides as measured by both the loss of their ability to inhibit DNA-dependent RNA synthesis and to bind to nuclear DNA (Yu and Bender, 2002).…”

Section: Introductionmentioning

confidence: 99%

The Effect of Dimethyl Dimethoxy Biphenyl Dicarboxylate (DDB) against Tamoxifen-induced Liver Injury in Rats: DDB Use Is Curative or Protective

El-Beshbishy¹

2005

BMB Reports

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Tamoxifen citrate is an anti-estrogenic drug used for the treatment of breast cancer. It showed a degree of hepatic carcinogenesis, when it used for long term as it can decrease the hexose monophosphate shunt and thereby increasing the incidence of oxidative stress in liver rat cells leading to liver injury. In this study, a model of liver injury in female rats was done by intraperitoneal injection of tamoxifen in a dose of 45 mg/kg body weight for 7 successive days. This model produced a state of oxidative stress accompanied with liver injury as noticed by significant declines in the antioxidant enzymes (glutathione-S-transferase, glutathione peroxidase and catalase) and reduced glutathione concomitant with significant elevations in TBARS (thiobarbituric acid reactive substance) and liver transaminases; sGPT (serum glutamate pyruvate transaminase) and sGOT (serum glutamate oxaloacetate transaminase) levels. The oral administration of dimethyl dimethoxy biphenyl dicarboxylate (DDB) in a dose of 200 mg/kg body weight daily for 10 successive days, resulted in alleviation of the oxidative stress status of tamoxifen-intoxicated liver injury in rats as observed by significant increments in the antioxidant enzymes (glutathione-S-transferase, glutathione peroxidase and catalase) and reduced glutathione concomitant with significant decrements in TBARS and liver transaminases; sGPT and sGOT levels. The administration of DDB before tamoxifen intoxication (as protection) is more little effective than its curative effect against tamoxifen-induced liver injury. The data obtained from this study speculated that DDB can mediate its biochemical effects through the enhancement of the antioxidant enzyme activities and reduced glutathione level as well as decreasing lipid peroxides.

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A proposed mechanism of tamoxifen in breast cancer prevention

Cited by 20 publications

References 30 publications

FA2H Exhibits Tumor Suppressive Roles on Breast Cancers via Cancer Stemness Control

FA2H Exhibits Tumor Suppressive Roles on Breast Cancers via Cancer Stemness Control

Integrated diagnostic network construction reveals a 4-gene panel and 5 cancer hallmarks driving breast cancer heterogeneity

The Effect of Dimethyl Dimethoxy Biphenyl Dicarboxylate (DDB) against Tamoxifen-induced Liver Injury in Rats: DDB Use Is Curative or Protective

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