It has been suggested that gene-environment interaction is related to the risk of cancer. To evaluate departure from multiplicative effects between BRCA mutations and diet diversity in breast cancer (BC), a case-only study was carried out in a French-Canadian population including 738 patients with incident primary BC comprising 38 BRCA mutation carriers. Diet diversity was assessed using a validated food frequency questionnaire. Unconditional logistic regression analysis was performed to assess case-only odds ratio (COR) and 95% confidence interval (CI) while adjusting for age, body mass index, smoking, hormonal replacement therapy, and total energy intake. Ours results reveal a strong and significant interaction between BRCA mutations and vegetable and fruit diversity (COR = 0.27; 95%CI = 0.10-0.80; P = 0.03) when comparing the upper to the lower quartiles. The estimates for departure from multiplicative effects between BRCA mutations and total or other food groups' diversity were not supportive of the idea of a gene-environment interaction. The results of this study suggest that the combination of BRCA mutations and vegetable and fruit diversity may be associated with a reduced risk of BC.
Download full-text PDF |
Source |
---|---|
http://dx.doi.org/10.1007/s10549-008-0292-y | DOI Listing |
Asia Pac J Clin Oncol
January 2025
LifeStrands Genomics Australia, Mount Waverley, Victoria, Australia.
Some patients with metastatic castration-resistant prostate cancer (mCRPC) possess germline or acquired defects in the DNA damage repair (DDR) genes BRCA1 and BRCA2. Tumors with BRCA mutations exhibit sensitivity to poly-ADP ribose polymerase inhibitors (PARPi) such as olaparib and rucaparib. As a result, molecular diagnostic testing to identify patients with BRCA mutations eligible for the PARPi therapy has become an integral component of managing patients with mCRPC.
View Article and Find Full Text PDFObjectives: 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.
Breast Cancer Res
January 2025
Department of Medicine (Hematology/Oncology), School of Medicine, University of California San Francisco, 1450 Third St, San Francisco, CA, 94158, USA.
Background: Poly (ADP-Ribose) polymerase inhibitors are approved for treatment of tumors with BRCA1/2 and other homologous recombination repair (HRR) mutations. However, clinical responses are often not durable and treatment may be detrimental in advanced cancer due to excessive toxicities. Thus we are seeking alternative therapeutics to enhance PARP-directed outcomes.
View Article and Find Full Text PDFFuture Oncol
January 2025
Division of Gynecologic Oncology, The Ohio State University Wexner Medical Center and James Hospital Comprehensive Cancer Center, Columbus, OH, USA.
Aims: To assess real-world progression-free survival (rwPFS) and time to next treatment (rwTTNT) among patients with epithelial ovarian cancer (EOC) who received first-line maintenance (1LM) niraparib monotherapy.
Patients & Methods: In this US-nationwide, electronic health record-derived, deidentified database study, eligible patients with EOC initiated 1LM niraparib monotherapy (1 January 2017-1 December 2022) following first-line platinum-based chemotherapy. Median rwPFS and rwTTNT were estimated with Kaplan-Meier methodology overall and in a homologous recombination-deficient (HRd) subgroup (further stratified as wild-type [wt] or -mutated [m]).
J Med Chem
January 2025
Department of Biochemistry, Albert Einstein College of Medicine, Bronx, New York 10461, United States.
DNPH1 is responsible for eliminating the epigenetically modified nucleotide, 5-hydroxymethyl-2'-deoxyuridine 5'-monophosphate (hmdUMP), preventing formation of hmdUTP, a mutation-inducing nucleotide. Loss of DNPH1 activity sensitizes PARP inhibition-resistant BRCA-deficient cancers by causing incorporation of hmdUTP into DNA. Hydrolysis of hmdUMP by DNPH1 proceeds through a covalent intermediate between Glu104 and 2-deoxyribose 5-phosphate, followed by hydrolysis, a reaction cycle with two transition states.
View Article and Find Full Text PDFEnter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!