Chemotherapy is still the leader option for cancer treatment. Nevertheless some patients develop chemotherapy resistance. One major research goal is to identify the critical genes involved in chemotherapy response to predict the best therapy option for patients. Germline mutations in the BReast Cancer susceptibility gene (BRCA1) are associated to increased risk of developing breast, ovarian and other types of cancers. However, due to harmful BRCA1 gene mutations are relatively rare in the general population, nowadays most researchers focused on BRCA1 expression downregulation and/or epigenetic inactivation in sporadic tumors as a prognosis tool for chemotherapy response in patients. Chemotherapy response can be dramatically different depending on BRCA1 expression status, tumor type and drug. Hence, the chemotherapy response could be dissimilar in breast, ovarian, uterine, prostate, esophageal, gastric and lung cancers. Additionally, differential BRCA1 expression in sporadic tumors shows different response to DNA-damaging agents, mitotic inhibitors or PARP inhibitors. In this review we will examine the response to different chemotherapy agents in several cancer types depending on BRCA1 expression status.
Download full-text PDF |
Source |
---|---|
http://dx.doi.org/10.2741/E752 | DOI Listing |
J Cell Mol Med
January 2025
Cancer Biology Research Center, Cancer Institute, Tehran University of Medical Sciences, Tehran, Iran.
This study identifies microRNAs (miRNAs) with significant discriminatory power in distinguishing melanoma from nevus, notably hsa-miR-26a and hsa-miR-211, which have exhibited diagnostic potential with accuracy of 81% and 78% respectively. To enhance diagnostic accuracy, we integrated miRNAs into various machine-learning (ML) models. Incorporating miRNAs with AUC scores above 0.
View Article and Find Full Text PDFAm J Transl Res
December 2024
Department of Pharmacy, Shanghai Fifth People's Hospital, Fudan University 801 Heqing Road, Shanghai 200240, China.
Objective: This study investigates the mechanism underlying sorafenib resistance in hepatocellular carcinoma cells (HCC), focusing on DNA damage repair (DDR) pathways to develop targeted therapeutic strategies.
Methods: Bioinformatics analysis was used to screen genes associated with sorafenib resistance, which was further demonstrated by western blotting. Cell proliferation was determined using the EdU assay.
Objectives: To explore the landscape of BRCA1/2 mutations in gastric cancer patients.
Methods: Next-generation sequencing (NGS), Sanger sequencing, reverse transcription quantitative polymerase chain reaction (RT-qPCR), Immunohistochemistry, The Cancer Genome Atlas (TCGA), gnomAD, and DAVID.
Results: With 95% of bases boasting a phred score surpassing 30 and a minimum coverage depth of 500X, our NGS approach ensures high-quality data acquisition.
Adv Exp Med Biol
January 2025
Cancer Biology and Stem Cells Division, The Walter and Eliza Hall Institute of Medical Research, Parkville, VIC, Wurundjeri Country, Melbourne, Australia.
Both intrinsic and extrinsic mechanisms underpin the profound intertumoral heterogeneity in breast cancer. Increasing evidence suggests that the intrinsic characteristics of breast epithelial precursor cells may influence tumour phenotype. These "cells-of-origin" of cancer preside in normal breast tissue and are uniquely susceptible to mutagenesis upon exposure to distinct oncogenic stimuli.
View Article and Find Full Text PDFJ Clin Invest
January 2025
Department of Biochemistry and Molecular Genetics and.
Mutations or homozygous deletions of MHC class II (MHC-II) genes are commonly found in B cell lymphomas that develop in immune-privileged sites and have been associated with patient survival. However, the mechanisms regulating MHC-II expression, particularly through genetic and epigenetic factors, are not yet fully understood. In this study, we identified a key signaling pathway involving the histone H2AK119 deubiquitinase BRCA1 associated protein 1 (BAP1), the interferon regulatory factor interferon regulatory factor 1 (IRF1), and the MHC-II transactivator class II transactivator (CIITA), which directly activates MHC-II gene expression.
View Article and Find Full Text PDFEnter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!