AI Article Synopsis

  • - Ovarian cancer often goes undetected until advanced stages due to vague symptoms and is linked to genetic mutations, particularly in BRCA1 and BRCA2 genes associated with family history.
  • - A study on 30 women with confirmed ovarian cancer found multiple genetic variants, including some novel ones, but did not identify the known BRCA founder mutations in the participants.
  • - While BRCA mutations account for a significant portion of familial ovarian cancer cases, they only explain a fraction of the overall genetic risk, suggesting the involvement of other genetic factors like single nucleotide polymorphisms (SNPs).

Article Abstract

Ovarian cancer is a silent killer as most patients have non-specific symptoms and usually present in advanced stage of the disease. It occurs due to certain genetic alterations and mutations namely founder mutations, 187delAG and 5385insC in BRCA1 and 6174delT in BRCA2 which are associated with specific family histories. These highly penetrant susceptibility genes responsible for approximately half of families containing 2 or more ovarian cancer cases account for less than 40% of the familial excess malignancy risk. The remaining risk may be due to single nucleotide polymorphisms (SNPs) which are single base change in a DNA sequence with usual alternatives of two possible nucleotides at a given position. Preliminary study involving 30 women with histologically proven epithelial ovarian cancer was conducted and their detailed genetic analysis was carried out. Regions of founder mutations on BRCA1 and BRCA2 were amplified and sequenced using primers designed based on 200 bp upstream and downstream regions of the mutation sites. Five sequence variants in BRCA1 were identified of which three novel sequence variants were found in 23 patients while in BRCA2, one novel sequence variant was found. The three founder mutations 187delAG, 5385insC in BRCA1 and 6174delT in BRCA2 were not seen in any of the subjects.

Download full-text PDF

Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4058959PMC

Publication Analysis

Top Keywords

ovarian cancer
16
founder mutations
12
brca1 brca2
8
epithelial ovarian
8
mutations 187delag
8
187delag 5385insc
8
5385insc brca1
8
brca1 6174delt
8
6174delt brca2
8
sequence variants
8

Similar Publications

Despite recent advances, improvements to long-term survival in metastatic carcinomas, such as pancreatic or ovarian cancer, remain limited. Current therapies suppress growth-promoting biochemical signals, ablate cells expressing tumor-associated antigens, or promote adaptive immunity to tumor neoantigens. However, these approaches are limited by toxicity to normal cells using the same signaling pathways or expressing the same antigens, or by the low frequency of neoantigens in most carcinomas.

View Article and Find Full Text PDF

Ovarian cancer is one of the deadliest gynecologic cancers affecting the female reproductive tract. This is largely attributed to frequent recurrence and development of resistance to the platinum-based drugs cisplatin and carboplatin. One of the major contributing factors to increased cancer progression and resistance to chemotherapy is the tumor microenvironment (TME).

View Article and Find Full Text PDF

Background: Ovarian cancer is difficult to detect in its early stages, and it has a high potential for invasion and metastasis, along with a high rate of recurrence. These factors contribute to the poor prognosis and reduced survival times for patients with this disease. The effectiveness of conventional chemoradiotherapy remains limited.

View Article and Find Full Text PDF

Objectives: , which is primarily recognized for determining blood types, shows variable expression patterns in different tissues and cancer types. This study investigated the relationship between gene expression and cancer, and assessed its potential impact on patient survival.

Methods: Utilizing the GEPIA database, we analyzed expression in normal and tumor tissues across various cancer types using online tools for comprehensive evaluation.

View Article and Find Full Text PDF

Drug repurposing has potential to improve outcomes for high-grade serous ovarian cancer (HGSOC). Repurposing drugs with PARP family binding activity may produce cytotoxic effects through the multiple mechanisms of PARP including DNA repair, cell-cycle regulation, and apoptosis. The aim of this study was to determine existing drugs that have PARP family binding activity and can be repurposed for treatment of HGSOC.

View Article and Find Full Text PDF

Want AI Summaries of new PubMed Abstracts delivered to your In-box?

Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!