China 
Africa 
Explore chapters and articles related to this topic
Overview of Traditional Methods of Diagnosis and Treatment for Women-Associated Cancers
Published in Shazia Rashid, Ankur Saxena, Sabia Rashid, Latest Advances in Diagnosis and Treatment of Women-Associated Cancers, 2022
Malika Ranjan, Namyaa Kumar, Safiya Arfi, Shazia Rashid
Ovarian cancer refers to any cancerous growth that originates in the ovaries, or in related areas of the fallopian tube and the peritoneum. The cause of ovarian cancer is multifactorial which mainly include genetic, immunologic, and environmental factors. Some most common causes of ovarian cancer are inherited gene changes (including BRCA1, BRCA2, BRIP1, RAD51C, RAD51D and genes associated with Lynch syndrome), postmenopausal hormone replacement therapy and endometriosis [16]. The use of oral contraceptives, like birth control pills, has been shown to dramatically reduce the risk of ovarian cancer and endometrial cancer [17].
Molecular Mediator of Prostate Cancer Progression and Its Implication in Therapy
Published in Surinder K. Batra, Moorthy P. Ponnusamy, Gene Regulation and Therapeutics for Cancer, 2021
Samikshan Dutta, Navatha Shree Sharma, Ridwan Islam, Kaustubh Datta
TCGA database suggested mutations in many DNA repair genes like BRCA1, BRCA2, FANCD2, CKD12 and ATM in primary prostate cancer, although it is to be noted that the frequency of DNA repair mutations in localized prostate cancer is low [108, 178, 179]. Interestingly, mutations in DNA repair enzymes (BRCA2, ATM, BRCA1, FANCA, RAD51B, RAD51C, MLH1, and MSH2) are the major disease-specific mutations in mCRPC [180, 181]. The understanding that a quarter of men with mCRPC have mutations in DNA repair pathway genes such as BRCA genes has led to clinical trials with poly ADP ribose polymerase (PARP) inhibitors. PARPs are required to repair the DNA single-strand breaks through base-excision repair. It has been shown that cancer cells with BRCA gene mutations become significantly more sensitive to PARP inhibitors as a therapeutic approach popularly known as synthetic lethal strategy [180, 181]. It is further noted that mutations of other DNA repair pathway genes can be sensitive to PARP inhibitors. These genes are ATM, BRIP1, BARD1, CDK12, CHEK2, FANCA, NBN, PALB2, and RAD51 [182, 183].
Ovarian, Fallopian Tube, and Primary Peritoneal Cancer
Published in Pat Price, Karol Sikora, Treatment of Cancer, 2020
Robert D. Morgan, Andrew R. Clamp, Gordon C. Jayson
Other genes associated with hereditary ovarian cancer, which also have a functional role in HR repair, include RAD51C, RAD51D, and BRIP1,21–23 although variants in these genes are much less frequently detected (<1% of all cases).
Recommendations for pregnancy in Fanconi anemia
Published in Expert Opinion on Biological Therapy, 2021
Charbel F. Matar, Rayan Bou-Fakhredin, Roberta Russo, Immacolata Andolfo, Achille Iolascon, Ali T. Taher
Patients of childbearing age should be informed with evidence-based data detailing maternal and neonatal morbidity and mortality possibly at preconception or during a regular follow-up visit with a maternal-fetal medicine specialist or hematologist. Genetic counseling should be offered to all couples affected with FA. The possibility of having affected child should be addressed and discussed between the couples and the genetic team. Moreover, the possibility of the parents having different alleles or being heterozygous FA should be addressed along with the risks of having affected newborn. Genetic counseling should also assess the cancer risk for heterozygous child generated by a mother with FA. Indeed, most carriers of mutations in the FA-related genes are not at increased risk of developing cancer. Nevertheless, several specific genes or mutations have been associated with an increased cancer risk in carriers, such as pathogenic variants in FANCD1 (BRCA2), FANCN (PALB2), or FANCJ (BRIP1) [34]. The optimal time of counseling including discussion of potential risks to offspring and availability of prenatal testing is before pregnancy. Pregnant FA-affected patients will require close monitoring and follow-up at least once monthly by an expert gynecologist due to complicated obstetric management. Fetal growth monitoring using ultrasound is mandatory for better assessment of fetal wellbeing [12]. Patients who are under androgens therapy and become pregnant should discontinue the use of hormones to decrease the risk of affecting a female fetus into virilization [35].
Aberrations of DNA repair pathways in prostate cancer: a cornerstone of precision oncology
Published in Expert Opinion on Therapeutic Targets, 2021
Stergios Boussios, Elie Rassy, Sidrah Shah, Evangelia Ioannidou, Matin Sheriff, Nicholas Pavlidis
PARP inhibitor monotherapy induces an objective antitumor activity in patients with PALB2, BRIP1, or FANCA aberrations. In contrast, those with ATM and CDK12 alterations do not seem to benefit. The data from TOPARP-B indicate that olaparib may be therapeutically effective in ATM-altered mCRPC. However, detection of ATM alterations alone might be insufficient to identify this subset of patients and further studies are required to elucidate the potentially additional genomic alterations, essential to sensitize to PARP inhibition. The fact that a fraction of biomarker-negative patients respond to PARP inhibitors is indicative of undetected DDR mutations that may exist in genomic regions less effectively covered by NGS. Olaparib has been approved by the FDA for mCRPC with genomic alterations in 14 different DNA repair genes, whilst only for BRCA-mutant cancers by the European Medicines Agency (EMA). This discordance in approvals underlines that it is crucial to further study biomarkers that predict clinical benefit from PARP inhibition. Rucaparib has been approved by the FDA for the treatment of mCRPC patients with somatic and/or germline DDR alterations who have progressed through enzalutamide or abiraterone treatment [17]. Different trials are using different panels of DDR genes and yielded variable results and inconsistent outcomes in terms of specific gene alterations. This may be partly due to the differences in the PARP inhibitors themselves.
Curcumin induces DNA damage by mediating homologous recombination mechanism in triple negative breast cancer
Published in Nutrition and Cancer, 2020
Gamze Guney Eskiler, Elvan Sahin, Asuman Deveci Ozkan, Ozlem Tugce Cilingir Kaya, Suleyman Kaleli
DNA damage response is regulated by different pathways including base excision repair (BER), mismatch repair (MMR), non-homologous end joining (NHEJ) and homologous recombination (HR)-associated genes such as BRCA1/2, RAD50/51, PALB2, CHEK2, BARD1, BRIP1 etc. The BRCA1 gene plays a crucial role in HR mechanism in response to DNA double-strand breaks (dsDNA). BRCA1 interacts with RAD51 to repair dsDNA breaks and maintain genomic stability and thus, BRCA1 and RAD51 are the main mediator of HR mechanism (9–12). Furthermore, phosphorylation of H2AX (γH2AX) is an important step in recruitment of DNA repair proteins and thus, BRCA1, RAD50, and NBS1 localize with γ-H2AX at sites of DNA damage (13,14). Additionally, DNA breaks are also recognized by poly (ADP-ribose) polymerase 1 (PARP1) and thus PARP1 mediates both DNA repair and cell death (15,16). Therefore, the association H2AX, PARP1, BRCA1, and RAD51 with DNA repair and DNA-damage-induced cell death should be further elucidated.