Pharma Strategy Blog

Commentary on Pharma & Biotech Oncology / Hematology New Product Development

Pancreatic cancer is particularly nasty, mainly because there is no easy way to detect it by screening or biomarkers in the general population, symptoms are often insidious and thus the cancer is sadly not picked up until the advanced stages.  Less than 20% of people present with early stage disease, meaning they are small, resectable and therefore treatable.

It is clear that more progress beyond incremental improvements will come as we learn more about the biology of the disease and develop accurate tests for early diagnosis.  The big question, though, is what subtle, and not so subtle, changes are happening with tumorigenesis and pathogenesis?  If we can understand the process we might be able to figure out some appropriate markers and develop a diagnostic test, since many people will not have the classic risk factors, making screening in the general population difficult.

With all this background in mind, I noticed an interesting paper recently from Cancer Research:

“… there is a need for sensitive, specific, and accurate tests that would facilitate the rapid diagnosis of pancreatic cancer and its precursors.  New candidate markers have been described in recent years that have been evaluated in serum and in pancreatic secretions and ductal brushings to detect local pancreatic neoplasia, but more accurate markers are needed.”

What’s also interesting is that following some recent posts on microRNA (see lung cancer and general information on miRNA for examples), it seems that almost every other article is about miRNA in some shape or form when I check out journals.  Maybe it was there before but I’m only just seeing it after writing about it.

As Li et al., pointed out in their paper, we know that DNA methylation and miRNA expression are important in pancreatic cancer pathogenesis, but what precisely is happening?  In their experiments, they found that:

“We identified two members of miR-200 family, miR-200a and miR-200b, that were hypomethylated and overexpressed in pancreatic cancer.”

Downstream, other changes were also taking place:

“We also identified prevalent hypermethylation and silencing of one of their downstream targets, SIP1 (ZFHX1B, ZEB2), whose protein product suppresses E-cadherin expression and contributes to epithelial mesenchymal transition.”

What does this mean in short?

“The elevated serum levels of miR-200a and miR-200b in most patients with pancreatic cancer could have diagnostic utility.”

It will be interesting to see where these ideas go, particularly in high risk populations.

ResearchBlogging.org Li, A., Omura, N., Hong, S., Vincent, A., Walter, K., Griffith, M., Borges, M., & Goggins, M. (2010). Pancreatic Cancers Epigenetically Silence SIP1 and Hypomethylate and Overexpress miR-200a/200b in Association with Elevated Circulating miR-200a and miR-200b Levels Cancer Research, 70 (13), 5226-5237 DOI: 10.1158/0008-5472.CAN-09-4227

One Response to “DNA methylation and microRNA expression in pancreatic cancer”

  1. DNA Methylation

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