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A comprehensive analysis of clinical trials in pancreatic cancer: what is coming down the pike?

ABSTRACT: OBJECTIVE:Pancreatic cancer is the most aggressive common cancer and is desperately in need of novel therapies. Unlike many other common cancers, there have been no new paradigm-changing therapies in the past 40 years beyond multi-agent chemotherapy. In this study, we perform the first comprehensive analysis of the current clinical trial landscape in pancreatic cancer to better understand the pipeline of new therapies. MATERIALS AND METHODS:We queried https://clinicaltrials.gov/ for registered pancreatic cancer clinical trials. Studies were curated and categorized according to phase of study, clinical stage of the study population, type of the intervention under investigation, and biologic mechanism targeted by the therapy under study. RESULTS:As of May 18, 2019, there were 430 total active therapeutic interventional trials testing 590 interventions. The vast minority of trials (n = 37, 8.6%) are in phase III testing. 189 (31%) interventions are immunotherapies, 69 (11%) target cell signaling pathways, 154 (26%) target cell cycle or DNA biology, and 35 (6%) target metabolic pathways. Of the late phase trials, only 14 are currently testing novel interventions. Rather, 23 phase III trials examine new ways to deliver existing FDA-approved drugs, procedures, or pain management. CONCLUSIONS:A large number of novel therapeutic strategies are currently under investigation. They include a broad range of therapies targeting diverse biologic processes. However, only a small number of novel therapies are in late-stage testing, suggesting that future progress is likely several years away, and dependent on the success of early-stage trials.

SUBMITTER: Katayama ES

PROVIDER: S-EPMC7517959 | biostudies-literature | 2020 Sep

REPOSITORIES: biostudies-literature

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A comprehensive analysis of clinical trials in pancreatic cancer: what is coming down the pike?

Katayama Erryk S ES Hue Jonathan J JJ Bajor David L DL Ocuin Lee M LM Ammori John B JB Hardacre Jeffrey M JM Winter Jordan M JM

Oncotarget 20200922 38

<h4>Objective</h4>Pancreatic cancer is the most aggressive common cancer and is desperately in need of novel therapies. Unlike many other common cancers, there have been no new paradigm-changing therapies in the past 40 years beyond multi-agent chemotherapy. In this study, we perform the first comprehensive analysis of the current clinical trial landscape in pancreatic cancer to better understand the pipeline of new therapies.<h4>Materials and methods</h4>We queried https://clinicaltrials.gov/ f ...[more]

PMID: 33014285

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Project description:BackgroundPancreatic ductal adenocarcinoma (PDAC) has the worst prognosis among common cancers. The genomic landscape of PDAC is defined by four mutational pathways: kirsten rat sarcoma virus (KRAS), cellular tumor antigen p53 (TP53), cyclin dependent kinase inhibitor 2A (CDKN2A), and SMAD family member 4 (SMAD4). However, there is a paucity of data on the molecular features associated with clinical outcomes after surgery or chemotherapy.MethodsWe performed comprehensive molecular characterization of tumor specimens from 83 patients with PDAC who received surgery, using whole-exome sequencing and ribonucleic acid sequencing on tumor and matched normal tissues derived from patients. We also systematically performed integrative analysis, combining genomic, transcriptomic, and clinical features to identify biomarkers and possible therapeutic targets.ResultsKRAS (75%), TP53 (67%), CDKN2A (12%), SMAD4 (20%), and ring finger protein 43 (RNF43) (13%) were identified as significantly mutated genes. The tumor-specific transcriptome was classified into two clusters (tumor S1 and tumor S2), which resembled the Moffitt tumor classification. Tumor S1 displayed two distinct subclusters (S1-1 and S1-2). The transcriptome of tumor S1-1 overlapped with the exocrine-like (Collisson)/ADEX (Bailey) subtype, while tumor S1-2 mostly consisted of the classical (Collisson)/progenitor (Bailey) subtype. In the analysis of combinatorial gene alterations, concomitant mutations of KRAS with low-density lipoprotein receptor related protein 1B (LRP1B) were associated with significantly worse disease-free survival after surgery (p = 0.034). One patient (1.2%) was an ultrahypermutant with microsatellite instability. We also identified high protein kinase C lota (PRKCI) expression as an overlapping, poor prognostic marker between our dataset and the TCGA dataset.ConclusionWe identified potential prognostic biomarkers and therapeutic targets of patients with PDAC. Understanding these molecular aberrations that determine patient outcomes after surgery and chemotherapy has the potential to improve the treatment outcomes of PDAC patients.

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A comprehensive analysis of clinical trials in pancreatic cancer: what is coming down the pike?

Publications

A comprehensive analysis of clinical trials in pancreatic cancer: what is coming down the pike?

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