Epidermal growth factor receptor-activating mutation(E746_T751&gt;VP) in pancreatic ductal adenocarcinoma responds to erlotinib, followed by epidermal growth factor receptor resistance-mediating mutation (A647T): A case report and literature review

Patel, Girijesh Kumar; Perry, Josiah; Abdul-Rahim, Osama; Frankel, Arthur E.; Cameron, Daniel; Taylor, William R.; Rocconi, Rodney P.; Abushahin, Laith; Nelson, Cindy; Singh, Ajay P.; Khushman, Moh’d

doi:10.4103/jcrt.jcrt_729_18

Cited by 8 publications

(1 citation statement)

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“…Cancer cells adopt a plethora of mechanisms to escape therapeutic regimen including epigenetic and genetic alterations (Table 1) leading to overexpression and amplification of oncogenes, drug expulsion transporters, and drug metabolizing enzymes [35,36,37,38,39,40,41,42,43,44,45,46,47]. In PCa, various modes of drug-resistance have been reported [48,49,50].…”

Section: Therapy Resistance In Prostate Cancermentioning

confidence: 99%

Neuroendocrine Differentiation of Prostate Cancer—An Intriguing Example of Tumor Evolution at Play

Patel

Chugh

Tripathi

2019

Cancers

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Our understanding of neuroendocrine prostate cancer (NEPC) has assumed a new perspective in light of the recent advances in research. Although classical NEPC is rarely seen in the clinic, focal neuroendocrine trans-differentiation of prostate adenocarcinoma occurs in about 30% of advanced prostate cancer (PCa) cases, and represents a therapeutic challenge. Even though our knowledge of the mechanisms that mediate neuroendocrine differentiation (NED) is still evolving, the role of androgen deprivation therapy (ADT) as a key driver of this phenomenon is increasingly becoming evident. In this review, we discuss the molecular, cellular, and therapeutic mediators of NED, and emphasize the role of the tumor microenvironment (TME) in orchestrating the phenotype. Understanding the role of the TME in mediating NED could provide us with valuable insights into the plasticity associated with the phenotype, and reveal potential therapeutic targets against this aggressive form of PCa.

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