Published online Sep 28, 2021. doi: 10.3748/wjg.v27.i36.6093
Peer-review started: April 7, 2021
First decision: May 27, 2021
Revised: June 10, 2021
Accepted: July 13, 2021
Article in press: July 13, 2021
Published online: September 28, 2021
Processing time: 168 Days and 14.7 Hours
Pancreatic cancer (PC) is one of the deadliest malignancies with an alarming mortality rate. Despite significant advancement in diagnostics and therapeutics, early diagnosis remains elusive causing poor prognosis, marred by mutations and epigenetic modifications in key genes which contribute to disease progression.
To explore the various biological tumor markers collectively and mutational analysis of key regulatory genes for early diagnosis and prognosis of PC.
To evaluate various biological tumor markers collectively in PC and their association with genetic mutation and epigenetic modification of key regulatory genes that could act as early diagnostic and prognostic biomarkers and will help in future therapeutics of PC in Kashmir valley.
The current study includes 50 confirmed PC cases to evaluate the levels of carbohydrate antigen 19-9 (CA 19-9), tissue polypeptide specific antigen (TPS), carcinoembryonic antigen (CEA), vascular endothelial growth factor-A (VEGF-A), and epidermal growth factor receptor (EGFR) by enzyme-linked immunosorbent assay (ELISA) method. Mutational analysis of key genes Kirsten rat sarcoma (KRAS), Breast cancer type 2 (BRCA-2), and deleted in pancreatic cancer-4 (DPC-4) genes was performed to evaluate the mutations at hotspot regions. Furthermore, epigenetic modifications were performed in the promoter regions of cyclin-dependent kinase inhibitor 2A (p16; CDKN2A), MutL homolog 1 (hMLH1), and Ras association domain-containing protein 1 (RASSF1A) genes.
Besides significant elevation in levels of tumor markers CA 19-9 (P ≤ 0.05), TPS (P ≤ 0.05), CEA (P ≤ 0.001), and VEGF (P ≤ 0.001), our mutational analysis observed that KRAS gene mutation is predominant in codon 12 (16 subjects, P ≤ 0.05), and 13 (12 subjects, P ≤ 0.05). Additionally, epigenetic modification analysis suggests that CpG methylation was observed in 21 (P ≤ 0.05) and 4 subjects in the promoter regions of the p16 and hMLH1 gene, respectively.
The study revealed the significant elevation of serum biological markers in PC patients and the causal association of hotspot mutations and epigenetic modification of key with PC pathogenesis thus indicates the potential of biological markers, mutational status, and epigenetic modifications of key genes collectively for predisposition, susceptibility as well as diagnostics and prognostics of PC.
The study strongly suggests that the elevated levels of serum CA 19-9, TPS, CEA, and VEGF-A can be used as predictive biomarkers in PC subjects. Additionally, mutational analysis epigenetic modifications in the promoter region of key genes may act as prognostic biomarkers to benefit the patients who are on a different regimen of chemotherapeutic interventions. Further to validate these results, future studies need comprehensive, cohort, and explicative studies with large sample sizes.