Format

Send to

Choose Destination
See comment in PubMed Commons below
Expert Opin Investig Drugs. 2014 Nov;23(11):1499-515. doi: 10.1517/13543784.2014.933206. Epub 2014 Jul 31.

Challenges and future directions in therapeutics for pancreatic ductal adenocarcinoma.

Author information

  • 1Department of Physiology, College of Medicine and Health Sciences, United Arab Emirates University , PO Box 17666, Al Ain , UAE.

Abstract

INTRODUCTION:

Pancreatic ductal adenocarcinoma (PDAC) is the fourth leading cause of cancer death in the USA. The 5-year survival of < 5% has not changed in decades. In contrast to other major cancers, the incidence of PDAC is increasing.

AREAS COVERED:

The aims of this paper are first to analyze why PDAC is so difficult to treat and, second, to suggest future directions for PDAC therapeutics. The authors provide an article that is based on a comprehensive search through MEDLINE and the clinicalTrials.gov website.

EXPERT OPINION:

Progress has been made recently. Notably, FOLFIRINOX or nab-paclitaxel plus gemcitabine provide survival benefit over gemcitabine alone, which was previously the mainstay of therapy for PDAC. Most of the current trials are testing combinations of repurposed drugs rather than addressing key targets in the PDAC pathogenesis. It is clear that to really make an impact on this disease, it will be necessary to address three different problems with targeted therapeutics. First, it is important to eradicate PDAC stem cells that result in recurrence. Second, it is important to reduce the peritumoral stroma that provides the tumors with growth support and provides a barrier to access of therapeutic agents. Finally, it is important to address the marked cachexia and metabolic derangement that contribute to morbidity and mortality and further complicate therapeutic intervention.

KEYWORDS:

cachexia; cancer stem cells; pancreatic cancer; pancreatic ductal adenocarcinoma; therapy; tumor microenvironment

PMID:
25078674
DOI:
10.1517/13543784.2014.933206
[PubMed - indexed for MEDLINE]
PubMed Commons home

PubMed Commons

0 comments
How to join PubMed Commons

    Supplemental Content

    Full text links

    Icon for Taylor & Francis
    Loading ...
    Support Center