Dataset Information

Genetic Influences in Breast Cancer Drug Resistance.

ABSTRACT: Breast cancer is the most common cancer in adult women aged 20 to 50 years. The therapeutic regimens that are commonly recommended to treat breast cancer are human epidermal growth factor receptor 2 (HER2) targeted therapy, endocrine therapy, and systemic chemotherapy. The selection of pharmacotherapy is based on the characteristics of the tumor and its hormone receptor status, specifically, the presence of HER2, progesterone receptors, and estrogen receptors. Breast cancer pharmacotherapy often gives different results in various populations, which may cause therapeutic failure. Different types of congenital drug resistance in individuals can cause this. Genetic polymorphism is a factor in the occurrence of congenital drug resistance. This review explores the relationship between genetic polymorphisms and resistance to breast cancer therapy. It considers studies published from 2010 to 2020 concerning the relationship of genetic polymorphisms and breast cancer therapy. Several gene polymorphisms are found to be related to longer overall survival, worse relapse-free survival, higher pathological complete response, and increased disease-free survival in breast cancer patients. The presence of these gene polymorphisms can be considered in the treatment of breast cancer in order to shape personalized therapy to yield better results.

SUBMITTER: Daniyal A

PROVIDER: S-EPMC7882715 | biostudies-literature | 2021

REPOSITORIES: biostudies-literature

ACCESS DATA

Publications

Genetic Influences in Breast Cancer Drug Resistance.

Daniyal Adhitiya A Santoso Ivana I Gunawan Nadira Hasna Putri NHP Barliana Melisa Intan MI Abdulah Rizky R

Breast cancer (Dove Medical Press) 20210209

Breast cancer is the most common cancer in adult women aged 20 to 50 years. The therapeutic regimens that are commonly recommended to treat breast cancer are human epidermal growth factor receptor 2 (HER2) targeted therapy, endocrine therapy, and systemic chemotherapy. The selection of pharmacotherapy is based on the characteristics of the tumor and its hormone receptor status, specifically, the presence of HER2, progesterone receptors, and estrogen receptors. Breast cancer pharmacotherapy often ...[more]

PMID: 33603458

Similar Datasets

Project description:BackgroundDrug resistance is a major challenge in cancer therapeutics. Abundant evidence indicates that DNA repair systems are enhanced after repetitive chemotherapeutic treatments, rendering cancers cells drug-resistant. Flap endonuclease 1 (FEN1) plays critical roles in DNA replication and repair and in counteracting replication stress, which is a key mechanism for many chemotherapeutic drugs to kill cancer cells. FEN1 was previously shown to be upregulated in response to DNA damaging agents. However, it is unclear about the transcription factors that regulate FEN1 expression in human cancer. More importantly, it is unknown whether up-regulation of FEN1 has an adverse impact on the prognosis of chemotherapeutic treatments of human cancers.MethodsTo reveal regulation mechanism of FEN1 expression, we search and identify FEN1 transcription factors or repressors and investigate their function on FEN1 expression by using a combination of biochemical, molecular, and cellular approaches. Furthermore, to gain insights into the impact of FEN1 levels on the response of human cancer to therapeutic treatments, we determine FEN1 levels in human breast cancer specimens and correlate them to the response to treatments and the survivorship of corresponding breast cancer patients.ResultsWe observe that FEN1 is significantly up-regulated upon treatment of chemotherapeutic drugs such as mitomycin C (MMC) and Taxol in breast cancer cells. We identify that the transcription factor/repressor YY1 binds to the FEN1 promoter and suppresses the expression of FEN1 gene. In response to the drug treatments, YY1 is dissociated from the FEN1 promoter region leading over-expression of FEN1. Overexpression of YY1 in the cells results in down-regulation of FEN1 and sensitization of the cancer cells to MMC or taxol. Furthermore, we observe that the level of FEN1 is inversely correlated with cancer drug and radiation resistance and with survivorship in breast cancer patients.ConclusionAltogether, our current data indicate that YY1 is a transcription repressor of FEN1 regulating FEN1 levels in response to DNA damaging agents. FEN1 is up-regulated in human breast cancer and its levels inversely correlated with cancer drug and radiation resistance and with survivorship in breast cancer patients.

Dataset Information

Genetic Influences in Breast Cancer Drug Resistance.

Publications

Genetic Influences in Breast Cancer Drug Resistance.

Similar Datasets

OmicsDI is part of the ELIXIR infrastructure

Tweets