In this task, you are given a passage which has a question and the context. You have to generate an answer to the question based on the information present in the context.

Context: L-Carnosine inhibits senescence of somatic cells and displays anticancer activity. Here we analyzed if L-carnosine (20 mM) retards senescence of human peritoneal mesothelial cells (HPMCs) and inhibits progression of ovarian cancer cells.', 'Experiments were performed with primary HPMCs established from patients undergoing abdominal surgery and with three ovarian cancer cell lines: A2780, OVCAR-3 and SKOV-3.', 'L-Carnosine retards senescence of HPMCs plausibly via inhibition of mitochondria-related oxidative stress. Prolonged exposure of HPMCs to L-carnosine prevented senescent HPMC-dependent exacerbation of cancer cell adhesion, migration, invasion and proliferation, which may be linked with decreased secretion of various pro-cancerogenic agents by HPMCs. Cancer cells exposed directly to L-carnosine displayed reduced viability, increased frequency of apoptosis and unaltered proliferation.\Question: Does l-Carnosine prevent the Pro-cancerogenic Activity of Senescent Peritoneal Mesothelium Towards Ovarian Cancer Cells?
L-carnosine may be a valuable anticancer drug, especially in the context of prevention and therapy of intraperitoneal ovarian cancer metastasis.

Context: No formal assessment of life expectancy in women with BRCA1 and BRCA2 mutations in these genes has been reported previously. We have evaluated life expectancy using actuarial analysis and assessed the effect of breast and ovarian cancers on premature death in >1,000 BRCA1/2 carriers.', 'Families with pathogenic mutations in BRCA1 and BRCA2 have been ascertained in a 10-million population region of United Kingdom since 1996. Mutation carriers and their first-degree relatives were used in an analysis of breast and ovarian cancer incidence and mortality as well as to derive and compare an actuarial assessment of life expectancy.', 'Six hundred twelve BRCA1 and 482 BRCA2 female mutation carriers were identified from 482 families. Life expectancy was significantly reduced for BRCA1 carriers compared with BRCA2 (P = 0.0002). This effect was attributable to an increased death rate from ovarian cancer (P = 0.04). Kaplan-Meier analysis revealed a better long-term survival from early-stage ovarian cancer in BRCA2 carriers but no significant differences in deaths from breast cancer or from women presenting with late-stage ovarian cancer. There was no other major contributing cause to death other than breast/ovarian cancer in BRCA1/2 female carriers.\Question: Is better life expectancy in women with BRCA2 compared with BRCA1 mutations attributable to lower frequency and later onset of ovarian cancer?
Interventions to reduce ovarian cancer incidence are likely to have a greater effect on life expectancy in BRCA1 compared with BRCA2 carriers.

Context: Human de novo single-nucleotide variation (SNV) rate is estimated to range between 0.82-1.70×10(-8) mutations per base per generation. However, contribution of early postzygotic mutations to the overall human de novo SNV rate is unknown.', 'We performed deep whole-genome sequencing (more than 30-fold coverage per individual) of the whole-blood-derived DNA samples of a healthy monozygotic twin pair and their parents. We examined the genotypes of each individual simultaneously for each of the SNVs and discovered de novo SNVs regarding the timing of mutagenesis. Putative de novo SNVs were validated using Sanger-based capillary sequencing.', 'We conservatively characterised 23 de novo SNVs shared by the twin pair, 8 de novo SNVs specific to twin I and 1 de novo SNV specific to twin II. Based on the number of de novo SNVs validated by Sanger sequencing and the number of callable bases of each twin, we calculated the overall de novo SNV rate of 1.31×10(-8) and 1.01×10(-8) for twin I and twin II, respectively. Of these, rates of the early postzygotic de novo SNVs were estimated to be 0.34×10(-8) for twin I and 0.04×10(-8) for twin II.\Question: Do early postzygotic mutations contribute to de novo variation in a healthy monozygotic twin pair?

Early postzygotic mutations constitute a substantial proportion of de novo mutations in humans. Therefore, genome mosaicism resulting from early mitotic events during embryogenesis is common and could substantially contribute to the development of diseases.