Abstract
We have collectively been spoiled by the astounding clinical benefit of antimicrobials. Much like the discovery and use of penicillin to eradicate once deadly infections, we continue to desperately search for the next “magic bullet” to kill cancer while sparing the non‐transformed cells. Greater appreciation for the molecular intricacies of malignancy has resulted in dedicated pursuit of cancer genomics and large‐scale informatics to identify “drugable” targets within the cancer cell itself. However, studies at the bench elucidating a dynamic relationship between tumor and microenvironment have become more common and demonstrate promise for novel therapeutic intervention.
Highlights
We have collectively been spoiled by the astounding clinical benefit of antimicrobials
Should we focus on the pharmacologic promotion of desmoplasia or can more specific targeting of stromal depletion be achieved, enhancing drug delivery while preventing increased aggressiveness? A more precise modulation of desmoplasia as opposed to global stromal depletion clearly deserves further investigation
Despite this relatively diminished vascularity compared to other tumor types, elevated pro-angiogenic vascular endothelial growth factor A (VEGF-A) levels in patients have been found to correlate with increased vascular density of pancreatic ductal adenocarcinoma (PDAC) and greater disease progression
Summary
Depletion of the tumor–stroma is currently a controversial strategy for PDAC treatment. Olive et al (2009) first demonstrated the potential benefit of Sonic hedgehog (Shh) inhibition in disrupting desmoplasia. Depletion of the tumor–stroma is currently a controversial strategy for PDAC treatment. Olive et al (2009) first demonstrated the potential benefit of Sonic hedgehog (Shh) inhibition in disrupting desmoplasia. Based on data from a genetically engineered mouse model (GEMM), Shh pathway inhibitor (IPI-926) treatment yielded reduced
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