ArticleClinical cancer research : an official journal of the American Association for Cancer Research2012
Molecular determinants of retinoic acid sensitivity in pancreatic cancer.
Article in Clinical cancer research : an official journal of the American Association for Cancer Research, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers.
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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.
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Who cites it
44 citing papers in PubMed, 72 citations in OpenAlex.
- Phase I clinical trial repurposing all-trans retinoic acid as a stromal targeting agent for pancreatic cancer.Nature communications · 2020Trial
- Standard and novel imaging methods for multiple myeloma: correlates with prognostic laboratory variables including gene expression profiling data.Haematologica · 2013Trial
- Retinoic acid in health and disease.Signal transduction and targeted therapy · 2026Review
- Combination of cellular retinoic acid-binding protein 2 overexpression and all-trans retinoic acid synergistically inhibits oesophageal squamous cell carcinoma progression.Discover oncology · 2025Article
- ZEB1 and ALKBH5 coregulate CRABP2 and FABP5 and jointly determine the sensitivity of anaplastic thyroid cancers to gemcitabine and retinoic acid.NPJ precision oncology · 2025Article
- The Role of Intracellular Lipid-Binding Proteins in Digestive System Neoplasms.Current oncology (Toronto, Ont.) · 2025Review
- Review
- Blockage of retinoic acid signaling via RARγ suppressed the proliferation of pancreatic cancer cells by arresting the cell cycle progression of the G1-S phase.Cancer cell international · 2023Article
- Retinoic acid receptor β modulates mechanosensing and invasion in pancreatic cancer cells via myosin light chain 2.Oncogenesis · 2023Article
- Lycorine induces apoptosis of acute myeloid leukemia cells and inhibits triglyceride production via binding and targeting FABP5.Annals of hematology · 2023Article
- Epigenetics in Pancreatic Ductal Adenocarcinoma: Impact on Biology and Utilization in Diagnostics and Treatment.Cancers · 2022Review
- A Carabrane-Type Sesquiterpenolide Carabrone fromMolecules (Basel, Switzerland) · 2022Article
- Circular RNA hsa_circ_0011298 enhances Taxol resistance of non-small cell lung cancer by regulating miR-486-3p/CRABP2 axis.Journal of clinical laboratory analysis · 2022Article
- The MYCN inhibitor BGA002 restores the retinoic acid response leading to differentiation or apoptosis by the mTOR block in MYCN-amplified neuroblastoma.Journal of experimental & clinical cancer research : CR · 2022Article
- Oncogenic KRAS Requires Complete Loss of BAP1 Function for Development of Murine Intrahepatic Cholangiocarcinoma.Cancers · 2021Article
- Vav1 Sustains the In Vitro Differentiation of Normal and Tumor Precursors to Insulin Producing Cells Induced by all-Trans Retinoic Acid (ATRA).Stem cell reviews and reports · 2021Article
- Targeting and Reprograming Cancer-Associated Fibroblasts and the Tumor Microenvironment in Pancreatic Cancer.Cancers · 2021Review
- Epigenetic modulation of FBW7/Mcl-1 pathway for lung cancer therapy.Cancer biology & therapy · 2021Article
- Paradoxical Role of AT-rich Interactive Domain 1A in Restraining Pancreatic Carcinogenesis.Cancers · 2020Article
- Targeting PIN1 exerts potent antitumor activity in pancreatic ductal carcinoma via inhibiting tumor metastasis.Cancer science · 2019Article
Corrections and comments
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Authors and funding
11 authors at 2 institutions in 1 country.
Funding
Abstract
purposeTo identify a predictive molecular "signature" for sensitivity to retinoic acid in pancreatic cancer. EXPERIMENTAL
designFourteen patient-derived, low-passage pancreatic ductal adenocarcinoma (PDAC) lines with varied expression of fatty acid-binding protein 5 (FABP5) and cellular retinoic acid-binding protein 2 (CRABP2) were used to evaluate the response to all-trans retinoic acid (ATRA). Cell proliferation, apoptosis, and migration/invasion assays were used to measure the in vitro response. Tumor growth was monitored in subcutaneous xenografts in athymic nude mice for 4 weeks.
resultsResponse to ATRA was observed to be dependent upon differential expression of FABP5 versus CRABP2. Thus, elevated FABP5 expression was associated with minimal cytotoxicity and tumor growth inhibition and a paradoxical increase in migration and invasion. Conversely, CRABP2 expression in the absence of FABP5 was associated with significant tumor growth inhibition with ATRA, even in gemcitabine-resistant tumors. The ATRA-resistant phenotype of FABP5(high)CRABP2(null) cells could be circumvented by ectopic expression of CRABP2. Alternatively, reexpression of endogenous CRABP2 could be enabled in FABP5(high)CRABP2(null) PDAC lines by exposure to decitabine and trichostatin A, thereby relieving epigenetic silencing of the CRABP2 gene promoter. Immunohistochemical staining for FABP5 in archival human tissue microarrays identifies a subset of cases (13 of 63, ~20%) which are negative for FABP5 expression and might be candidates for ATRA therapy.
conclusionsThe widely used agent ATRA deserves a "second look" in PDAC, but needs to be targeted to patient subsets with biopsy-proven FABP5-negative tumors, or be combined with a chromatin-modifying agent to reexpress endogenous CRABP2.
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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.