scholarly journals Utility of Serum miR-125b as a Diagnostic and Prognostic Indicator and Its Alliance with a Panel of Tumor Suppressor Genes in Epithelial Ovarian Cancer

PLoS ONE ◽  
2016 ◽  
Vol 11 (4) ◽  
pp. e0153902 ◽  
Author(s):  
Mariyam Zuberi ◽  
Imran Khan ◽  
Rashid Mir ◽  
Gauri Gandhi ◽  
Prakash Chandra Ray ◽  
...  
Gene ◽  
2018 ◽  
Vol 672 ◽  
pp. 34-44 ◽  
Author(s):  
Rawiah Alsiary ◽  
Samantha C. Brownhill ◽  
Anke Brüning-Richardson ◽  
Richard Hutson ◽  
Nicholas Griffin ◽  
...  

1993 ◽  
Vol 39 (11) ◽  
pp. 2444-2451 ◽  
Author(s):  
R C Bast

Abstract More fundamental understanding of cell growth regulation will provide novel approaches for detecting, preventing, and treating different cancers. Activation of protooncogenes or loss of tumor-suppressor genes can have both prognostic and therapeutic importance. In epithelial ovarian cancer, poor prognosis is associated with continued expression or overexpression of tyrosine kinase growth factor receptors p170EGFR, p165fms, and p185erbB-2. Over-expression of erbB-2 (HER-2/neu) by breast and ovarian cancers already permits effective targeting of antibodies and immunotoxins. Ultimately, molecular analysis of individual cancers will guide the application of specific therapies to inhibit activated oncogenes or restore the function of tumor-suppressor genes. Circulating growth factors, oncogene products, and tumor-associated antigens may provide markers for earlier detection of some cancers. In epithelial ovarian cancer, concentrations of CA 125 can be increased 1-5 years before clinical diagnosis, and approximately 50% of patients with stage I disease have had an abnormal CA 125 concentration. Combining CA 125 with two novel markers--OVX1 and M-CSF--has retrospectively detected > 98% of stage I ovarian cancers. Although the specificity of the three markers is insufficient for cost-effective screening, serum tests for them could prompt the performance of transvaginal sonography, substantially decreasing the number of sonograms required. Genetic markers in the germ line of patients at increased risk for certain cancers will almost certainly influence strategies for prevention or detection. In familial breast, and ovarian cancer, a locus on chromosome 17q tracks risk of cancer in a fraction of kindreds. How often germline abnormalities will be detected in patients with apparently sporadic cancer remains to be determined.


2013 ◽  
Vol 35 (3) ◽  
pp. 546-553 ◽  
Author(s):  
Pradeep S. Tanwar ◽  
Gayatry Mohapatra ◽  
Sarah Chiang ◽  
David A. Engler ◽  
LiHua Zhang ◽  
...  

Biomedicines ◽  
2021 ◽  
Vol 9 (2) ◽  
pp. 207
Author(s):  
Amreen Salwa ◽  
Alessandra Ferraresi ◽  
Menaka Chinthakindi ◽  
Letizia Vallino ◽  
Chiara Vidoni ◽  
...  

Background: BRCA1, BECN1 and TP53 are three tumor suppressor genes located on chromosome 17 and frequently found deleted, silenced, or mutated in many cancers. These genes are involved in autophagy, apoptosis, and drug resistance in ovarian cancer. Haploinsufficiency or loss-of-function of either TP53, BRCA1 or BECN1 correlates with enhanced predisposition to cancer development and progression, and chemoresistance. Expectedly, the combined altered expression of these three tumor suppressor genes worsens the prognosis of ovarian cancer patients. However, whether such a genotypic pattern indeed affects the chemo-responsiveness to standard chemotherapy thus worsening patients’ survival has not been validated in a large cohort of ovarian cancer patients. Aim: We interrogated datasets from the TCGA database to analyze how the expression of these three tumor suppressor genes impacts on the clinical response to platinum-based chemotherapy thus affecting the survival of ovarian cancer patients. Results and conclusion: Compared to EOC with homozygous expression of BECN1 and BRCA1, tumors expressing low mRNA expression of these two tumor suppressor genes (either because of shallow (monoallelic) co-deletion or of promoter hypermethylation), showed higher sensitivity to platinum-based therapies and were associated with a better prognosis of ovarian cancer-bearing patients. This outcome was independent of TP53 status, though it was statistically more significant in the cohort of patients with mutated TP53. Thus, sensitivity to platinum therapy (and probably to other chemotherapeutics) correlates with low expression of a combination of critical tumor suppressor genes. Our study highlights the importance of thoroughly assessing the genetic lesions of the most frequently mutated genes to stratify the patients in view of a personalized therapy. More importantly, the present findings suggest that targeting the function of both BECN1 and BRCA1 could be a strategy to restore chemosensitivity in refractory tumors.


Sign in / Sign up

Export Citation Format

Share Document