Novel genetic risk markers identified in pancreatic cancer

Pancreatic cancer is one of the most causes of cancer-related death in the United States. While there has been minimal progress regarding cancer-specific outcomes in recent decades, effective biomarkers are a promising tool that will undoubtedly have an important role in the management of patients with pancreatic cancer.

As reported, a large DNA analysis of people with and without pancreatic cancer has identified several novel genetic markers that reflect increased risk of suffering the highly lethal disease. The discovery of these markers is important in identifying people at risk and in interpreting susceptibility to pancreatic cancer.

Explore disease-causing gene mutations

Investigators used sequencing technology to examine more than 700,000 sites of the genome known to have single nucleotide polymorphisms (SNPs). They then looked for variants that are likely to be associated with the alteration of gene expression, and found 5 new risk markers, along with 4 risk-associated SNPs identified previously.

Previously approved by the Food and Drug Administration, serum Ca-19-9 (carbohydrate antigen 19-9) is utilized for pancreatic cancer as a prognostic marker and as a marker of disease recurrence.

The risks linked to each SNP or marker were largely independent and additive, so that they may have utility in future attempts to identify individuals in the general population at higher risk for pancreatic cancer. The average lifetime risk of pancreatic cancer is 1.5 %.

The long-term goal is to create a "risk stratification tool" that could be used in primary care practice to identify individuals who should undergo screening for pancreatic cancer with tests such as ultrasound or MRI.

Cancer research over the last quarter century has focused almost exclusively on identifying the molecular features of cancer cells based on the idea that genomic changes are in and of themselves the drivers of cancer. Thus, in their original review, Hanahan and Weinberg attributed the six hallmarks of cancer to genetic alterations within the cancer cell. Similarly, experimental rodent models of cancer focused predominantly on "targets," that is, the genome of the cell that underwent neoplastic transformation, which afforded a great deal of insight into pathways that are deregulated by genetic aberrations and paved the way for targeted therapeutics.

This focus on the cancer cell genome overshadowed the essential contribution of the tumor microenvironment. The genetic changes occurring in cancer cells were known to affect the microenvironment, but their acquisition was considered to be stochastic. A notable exception was Folkman's early recognition that vascularity could be the Achilles heel of tumors. Even so, antiangiogenic targets are often conceived of as a means of depriving the autonomous cancer cell of nutrients rather than modifying a necessary cellular partner in neoplastic growth.

Numerologist Warda is hooked on OG-L002 fishing, collecting. And lastly her encouragement comes from socializing along with her companions.