ArticleOncotarget2015
Deciphering the cellular source of tumor relapse identifies CD44 as a major therapeutic target in pancreatic adenocarcinoma.
Article in Oncotarget, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 30 citations in OpenAlex.
- The multiple myeloma microenvironment is defined by an inflammatory stromal cell landscape.Nature immunology · 2021Trial
- CD44 Marks Dormant Tumor Cells After HER2 Inhibition in Breast Cancer Cells.International journal of molecular sciences · 2025Article
- An IL-1β-driven neutrophil-stromal cell axis fosters a BAFF-rich protumor microenvironment in individuals with multiple myeloma.Nature immunology · 2024Article
- Review
- Oncostatin-M and OSM-Receptor Feed-Forward Activation of MAPK Induces Separable Stem-like and Mesenchymal Programs.Molecular cancer research : MCR · 2023Article
- Pancreatic ductal adenocarcinoma: tumor microenvironment and problems in the development of novel therapeutic strategies.Clinical and experimental medicine · 2023Review
- Simultaneous targeting of PD-1 and IL-2Rβγ with radiation therapy inhibits pancreatic cancer growth and metastasis.Cancer cell · 2023Article
- Pancreatic Tumor Microenvironment Factor Promotes Cancer Stemness via SPP1-CD44 Axis.Gastroenterology · 2021Article
- Crosstalk between MMP-13, CD44, and TWIST1 and its role in regulation of EMT in patients with esophageal squamous cell carcinoma.Molecular and cellular biochemistry · 2021Article
- Fraction B From Catfish Epidermal Secretions Kills Pancreatic Cancer Cells, Inhibits CD44 Expression and Stemness, and Alters Cancer Cell Metabolism.Frontiers in pharmacology · 2021Article
- Role of eIF4E on epithelial-mesenchymal transition, invasion, and chemoresistance of prostate cancer cells.Cancer communications (London, England) · 2020Article
- Novel prognostic markers within the CD44-stromal ligand network in pancreatic cancer.The journal of pathology. Clinical research · 2019Article
- Bitter melon juice exerts its efficacy against pancreatic cancer via targeting both bulk and cancer stem cells.Molecular carcinogenesis · 2018Article
- Photodynamic Priming Mitigates Chemotherapeutic Selection Pressures and Improves Drug Delivery.Cancer research · 2018Article
- TNFα and TGFβ-1 synergistically increase the cancer stem cell properties of MiaPaCa-2 cells.Oncology letters · 2017Article
- Article
- The Aurora-A-Twist1 axis promotes highly aggressive phenotypes in pancreatic carcinoma.Journal of cell science · 2017Article
- CD44 Expression Level and Isoform Contributes to Pancreatic Cancer Cell Plasticity, Invasiveness, and Response to Therapy.Clinical cancer research : an official journal of the American Association for Cancer Research · 2016Article
- Heterogeneity of metastatic pancreatic adenocarcinoma: Lung metastasis show better prognosis than liver metastasis-a case control study.Oncotarget · 2016Article
- Role of hyaluronan in pancreatic cancer biology and therapy: Once again in the spotlight.Cancer science · 2016Review
Corrections and comments
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Authors and funding
15 authors at 7 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
It has been commonly found that in patients presenting Pancreatic Ductal Adenocarcinoma (PDAC), after a period of satisfactory response to standard treatments, the tumor becomes non-responsive and patient death quickly follows. This phenomenon is mainly due to the rapid and uncontrolled development of the residual tumor. The origin and biological characteristics of residual tumor cells in PDAC still remain unclear. In this work, using PDACs from patients, preserved as xenografts in nude mice, we demonstrated that a residual PDAC tumor originated from a small number of CD44+ cells present in the tumor. During PDAC relapse, proliferating CD44+ cells decrease expression of ZEB1, while overexpressing the MUC1 protein, and gain morphological and biological characteristics of differentiation. Also, we report that CD44+ cells, in primary and residual PDAC tumors, are part of a heterogeneous population, which includes variable numbers of CD133+ and EpCAM+ cells. We confirmed the propagation of CD44+ cells in samples from cases of human relapse, following standard PDAC treatment. Finally, using systemic administration of anti-CD44 antibodies in vivo, we demonstrated that CD44 is an efficient therapeutic target for treating tumor relapse, but not primary PDAC tumors. We conclude that CD44+ cells generate the relapsing tumor and, as such, are themselves promising therapeutic targets for treating patients with recurrent PDAC.
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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.