ArticleScientific reports2018
The BET inhibitor I-BET762 inhibits pancreatic ductal adenocarcinoma cell proliferation and enhances the therapeutic effect of gemcitabine.
Article in Scientific reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 23 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
23 citing papers in PubMed, 33 citations in OpenAlex.
- KIF7 promotes the proliferation of clear cell renal cell carcinoma by activating the WNT/β-catenin signaling pathway.Clinical and experimental medicine · 2026Article
- A combinatorial screening protocol for identifying novel and highly potent dual-target inhibitor of BRD4 and STAT3 for kidney cancer therapy.Frontiers in pharmacology · 2025Article
- BRD9-SMAD2/3 Orchestrates Stemness and Tumorigenesis in Pancreatic Ductal Adenocarcinoma.Gastroenterology · 2024Article
- Article
- BET Bromodomain Inhibitors: Novel Design Strategies and Therapeutic Applications.Molecules (Basel, Switzerland) · 2023Review
- Molecular profiling and specific targeting of gemcitabine-resistant subclones in heterogeneous pancreatic cancer cell populations.Frontiers in oncology · 2023Article
- The Emerging Role of Super-enhancers as Therapeutic Targets in The Digestive System Tumors.International journal of biological sciences · 2023Review
- Target c-Myc to treat pancreatic cancer.Cancer biology & therapy · 2022Article
- Epigenetics in Pancreatic Ductal Adenocarcinoma: Impact on Biology and Utilization in Diagnostics and Treatment.Cancers · 2022Review
- Deregulated transcription factors in cancer cell metabolisms and reprogramming.Seminars in cancer biology · 2022Review
- The paradigm of drug resistance in cancer: an epigenetic perspective.Bioscience reports · 2022Review
- Article
- Mcl-1 inhibition overcomes BET inhibitor resistance induced by low FBW7 expression in breast cancer.Journal of cellular and molecular medicine · 2022Article
- XP-524 is a dual-BET/EP300 inhibitor that represses oncogenic KRAS and potentiates immune checkpoint inhibition in pancreatic cancer.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
- Bromodomain and extra-terminal inhibitors emerge as potential therapeutic avenues for gastrointestinal cancers.World journal of gastrointestinal oncology · 2022Review
- The role of protein acetylation in carcinogenesis and targeted drug discovery.Frontiers in endocrinology · 2022Review
- Epigenetic Small-Molecule Modulators Targeting Metabolic Pathways in Cancer.Sub-cellular biochemistry · 2022Article
- Mechanisms of Cancer Cell Death: Therapeutic Implications for Pancreatic Ductal Adenocarcinoma.Cancers · 2021Review
- Functional Roles of Bromodomain Proteins in Cancer.Cancers · 2021Review
- The BET Inhibitor JQ1 Augments the Antitumor Efficacy of Gemcitabine in Preclinical Models of Pancreatic Cancer.Cancers · 2021Article
Corrections and comments
- Retraction · 2023-11-28Concerns/Issues about Image · Euphemisms for Plagiarism · Investigation by Journal/Publisher · Investigation by Third Party · Original Data and/or Images not Provided and/or not Available · Paper Mill · Plagiarism of Data · Unreliable Results and/or Conclusions · · see also: https://pubpeer.com/publications/CCF29E8413A122BB9569E5FDAEF3CB
- Retracted
Authors and funding
8 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
As one of the most fatal malignancies, pancreatic ductal adenocarcinoma (PDAC) has significant resistance to the currently available treatment approaches. Gemcitabine, the standard chemotherapeutic agent for locally advanced and metastatic PDAC, has limited efficacy, which is attributed to innate/acquired resistance and the activation of prosurvival pathways. Here, we investigated the in vitro efficacy of I-BET762, an inhibitor of the bromodomain and extraterminal (BET) family of proteins, in treating PDAC cell lines alone and in combination with gemcitabine (GEM). The effect of these two agents was also examined in xenograft PDAC tumors in mice. We found that I-BET762 induced cell cycle arrest in the G0/G1 phase and cell death and suppressed cell proliferation and metastatic stem cell factors in PDAC cells. In addition, the BH3-only protein Bim, which is related to chemotherapy resistance, was upregulated by I-BET762, which increased the cell death triggered by GEM in PDAC cells. Moreover, GEM and I-BET762 exerted a synergistic effect on cytotoxicity both in vitro and in vivo. Furthermore, Bim is necessary for I-BET762 activity and modulates the synergistic effect of GEM and I-BET762 in PDAC. In conclusion, we investigated the effect of I-BET762 on PDAC and suggest an innovative strategy for PDAC treatment.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.