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BIOMARKER:

CD44 expression

i
Other names: CD44, CD44R, CSPG8, HCELL, IN, MC56, MDU2, MDU3, MIC4, Pgp1
Related biomarkers:
2d
P2, N=45, Active, not recruiting, Mayo Clinic | Suspended --> Active, not recruiting | N=96 --> 45
Enrollment closed • Enrollment change
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HER-2 (Human epidermal growth factor receptor 2) • ER (Estrogen receptor) • CD24 (CD24 Molecule) • CD44 • SOX2
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HER-2 amplification • ER positive • HER-2 negative • HER-2 expression • ER negative • CD44 expression
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fulvestrant • alisertib (MLN8237)
5d
In a summary, circHIF1A from hypoxic CAFs exosomes played an important role in stem cell properties of breast cancer. CircHIF1A may act as a target molecule of breast cancer therapy.
Journal
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CD44
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HIF1A expression • CD44 expression
9d
The long non-coding RNA (lncRNA) imatinib-upregulated (IUR) has been recently reported as a tumor suppressor in leukemia...However, CD44 overexpression played an opposite role and attenuated the effects of IUR and miR-34a overexpression. In conclusion, the results from this study demonstrated that IUR may upregulate miR-34a expression in order to inhibit PAAD cell migration and invasion by downregulating CD44.
Journal
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MIR34A (MicroRNA 34a-5p) • CD44
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CD44 expression • miR-34a expression • miR-34a overexpression
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imatinib
9d
Finally, we developed a novel AML xenograft model in zebrafish, showing that CD44 knockout sensitizes OCI-AML3 cells to venetoclax treatment in vivo. Our study shows that CD44 is a potential molecular target to sensitize AML cells to venetoclax-based therapies.
Journal
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CXCR4 (Chemokine (C-X-C motif) receptor 4) • CXCL12 (C-X-C Motif Chemokine Ligand 12) • POU5F1 (POU Class 5 Homeobox 1) • CD44 • NANOG (Nanog Homeobox) • SOX2
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CD44 expression
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Venclexta (venetoclax)
11d
OV IgG level together with CSC markers can be used as the prognostic markers for CCA patients' survival. The study of the CD44 pathway is promising for adjuvant treatment.
Clinical • Journal
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CD44 • NES (Nestin)
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CD44 expression • NES expression
11d
Univariate and multivariate analysis showed that history of diabetes &lsqb;HR 2.656 (1.194-5.908), P = 0.017], numbers of positive lymph nodes &lsqb;HR 1.871 (1.388-2.522), P < 0.001], preoperative numbers of CD44+ CTECs &lsqb;HR 1.216 (1.064-1.390), P = 0.004], and POM1 CA19-9 level &lsqb;HR 1.002 (1.001-1.002), P < 0.001] were independent prognostic factors for DFS. The detection of CD44+CTECs in patients with resectable PDAC preoperatively could be an independent predictor of shorter DFS after radical surgery.
Clinical • Journal
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CD44 • VIM (Vimentin) • Cancer antigen 19-9
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CD44 expression • VIM expression
11d
The combination of GAPDH and NDRG1 is an independent risk factor and predictor for patient survival. This study delineates heterogeneity of hepatobiliary tumor organoids and proposes that the collaboration of intratumoral heterogenic subpopulations renders malignant phenotypes and drug resistance.
Journal
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MYCN (MYCN Proto-Oncogene BHLH Transcription Factor) • CTNNB1 (Catenin (cadherin-associated protein), beta 1) • EPCAM (Epithelial cell adhesion molecule) • CA9 (Carbonic anhydrase 9) • CD44 • NDRG1 (N-Myc Downstream Regulated 1) • ALDOA (Aldolase Fructose-Bisphosphate A) • GAPDH (Glyceraldehyde-3-Phosphate Dehydrogenase)
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CD44 expression
12d
Our results indicate that TDO2 might take an essential part in BC progression and could be a potential marker for targeted therapy in BC.
Journal
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CD44 • ALDH1A1 (Aldehyde Dehydrogenase 1 Family Member A1)
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CD44 expression
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Erbitux (cetuximab)
12d
This method could also be applied to other types of cancer approachable with endoscopy. Supporting information.
Preclinical • Journal
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EGFR (Epidermal growth factor receptor) • CD44
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CD44 expression
13d
The results suggest that hypoxia-induced ERS and UPR might be associated with APVTs formation in PCNSL and its poor clinical outcomes. The results will help us better understand the progression of PCNSL with APVTs feature in daily pathological work and could be valuable for future target treatment of PCNSLs.
Journal
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CXCR4 (Chemokine (C-X-C motif) receptor 4) • CD44 • XBP1 (X-box-binding protein 1)
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CD44 expression
13d
Under-expression of onco-miRs (miR-21, miR-155, and miR-221), over-expression of several apoptotic potential targets of oncomiRs (Bax, Casp-9, and P53), over-expression of tumor suppressive-miRs (let-7b, miR-34a, and miR-126), and under-expression of Bcl-2 was found in SPNs-treated cells. We suggest that silybin encapsulated in polymersomes (SPNs) may be useful as a complementary agent for destroying both pancreatic cancer cells and pancreatic CSCs along with chemotherapeutic agents.
Journal • IO biomarker
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BCL2 (B-cell CLL/lymphoma 2) • MIR155 (MicroRNA 155) • CD133 • MIR21 (MicroRNA 21) • CD24 (CD24 Molecule) • MIR34A (MicroRNA 34a-5p) • CD44 • CASP9 (Caspase 9) • MIR126 (MicroRNA 126) • MIR221 (MicroRNA 221)
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BCL2 expression • TP53 overexpression • miR-155 expression • miR-21 overexpression • BCL2 underexpression • CD133 expression • CD44 expression
17d
Stem-like cells in OC ascites are heterogeneous and are present even at an early stage of the disease. It seems promising to study cell populations and cytokine profile of ascites together, to assess the biomarker potential of their combination.
Clinical • Journal
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CD133 • MUC16 (Mucin 16, Cell Surface Associated) • PTPRC (Protein Tyrosine Phosphatase Receptor Type C) • CD44 • IL10 (Interleukin 10) • IL18 (Interleukin 18) • IL1B (Interleukin 1, beta) • IL4 (Interleukin 4)
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CD133 expression • CD44 expression
18d
By using pantoprazole, we reduced the biogenesis of EVs and their pro-tumor functions. In conclusion, our findings provided evidence of underlying mechanisms of CRC dissemination driven by the interaction of peritoneal MCs and tumor cells via the EVs released in the peritoneal cavity, which may have important implications for the clinical management of patients.
Journal
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CASP3 (Caspase 3) • CD44 • MMP2 (Matrix metallopeptidase 2) • TGFB1 (Transforming Growth Factor Beta 1) • MMP9 (Matrix metallopeptidase 9)
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CD44 expression
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pantoprazole
18d
Glioma stem cells (GSCs) are tumour initiating cells which contribute to treatment resistance, temozolomide (TMZ) chemotherapy and radiotherapy, in glioblastoma (GBM), the most aggressive adult brain tumour. Apoptotic cell death in GSC subpopulations and non-stem tumour cells resulted in sphere disruption. Collectively, our study highlights the potential of these novel CKIs to induce cell death in GSCs from recurrent tumours, warranting further clinical investigation.
Journal
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CD133 • CD44
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CD44 expression
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temozolomide • fadraciclib (CYC065)
18d
Thus, we used an MEK/ERK inhibitor, PD98059, to block the MEK/ERK pathway and to identify the role of MAPK1 in the radio-resistance of RT-R-MDA-MB-231 cells...In addition, MEK/ERK inhibition reversed the radio-resistance of RT-R-MDA-MB-231 cells and suppressed the increased expression of CSC markers (CD44 and OCT3/4) and the EMT phenotype (β-catenin and N-cadherin/E-cadherin). Taken together, this study suggests that activated ERK signaling is one of the major hub signals related to the radio-resistance of MDA-MB-231 breast cancer cells.
Journal • PARP Biomarker
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CDH1 (Cadherin 1) • MAPK1 (Mitogen-activated protein kinase 1) • CD44
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CD44 expression
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PD98059
18d
Allicin inhibited both gene and protein expression of TNF-alpha, IL-8, and endothelin in both cancer cells and cancer stem cells. Allicin is more likely to be a promising treatment in alleviating the levels of pain and inflammation in OSCCs.
Journal
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CXCL8 (Chemokine (C-X-C motif) ligand 8) • TNFA (Tumor Necrosis Factor-Alpha) • CD133 • CD44
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CD133 expression • CD44 expression • CXCL8 expression
18d
In conclusion, BMX overcomes TMZ resistance by enhancing TMZ-mediated cytotoxic effect by downregulating the β-catenin/c-Myc/SOX2 signaling pathway and upregulating WT-p53 mediated MGMT inhibition. These findings indicate a promising drug combination for precision personal treating of TMZ-resistant WT-p53 GBM cells.
Journal
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MYC (V-myc avian myelocytomatosis viral oncogene homolog) • CCND1 (Cyclin D1) • CD133 • CASP3 (Caspase 3) • CD44 • GSK3B (Glycogen Synthase Kinase 3 Beta) • SOX2
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MYC expression • CCND1 expression • CD133 expression • CD44 expression
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temozolomide
18d
Collectively, our data demonstrate that Onco-P20, exerting both a direct and an NHF-mediated indirect effect on carcinoma cells, is a candidate for an innovative therapy alternative to surgery for the treatment of NMSC.
Preclinical • Journal
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CD44
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CD44 expression
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paclitaxel • Oncofid-P (hyaluronic acid paclitaxel conjugate)
19d
Taken together, we demonstrate that LSD1-loaded sEVs can promote stemness and chemoresistance to oxaliplatin. These findings suggest that the LSD1 content of sEV could serve as a biomarker to predict oxaliplatin response in gastric cancer patients.
Journal
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POU5F1 (POU Class 5 Homeobox 1) • CD44 • NANOG (Nanog Homeobox) • SOX2
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CD44 expression • POU5F1 expression
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oxaliplatin
20d
In this subgroup none of the CSCs biomarkers evaluated in the study had any impact on OS or DFS. In patients with HPV16-positive oropharyngeal cancer, lack of CD44 overexpression and application of CisPt-CRT were found to be positive prognostic factors.
Clinical • Retrospective data • Journal
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SLC3A2 (Solute Carrier Family 3 Member 2) • CD44 • ALDH1A1 (Aldehyde Dehydrogenase 1 Family Member A1)
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CD44 expression
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cisplatin
20d
In contrast, siRNA-mediated silencing of the osteopontin gene decreased GSC proliferation. These results suggest that interaction between CD44 and osteopontin plays a key role in tumor progression in GBM; inhibition of both CD44 and osteopontin may represent an effective therapeutic approach for suppressing tumor progression, thus resulting in a better prognosis for patients with GBM.
Journal
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HIF1A (Hypoxia inducible factor 1, alpha subunit) • SPP1 (Secreted Phosphoprotein 1) • EPAS1 (Endothelial PAS domain protein 1) • CD44
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HIF1A expression • CD44 expression
20d
Conclusion  We can correlate CD44 positive cancer stem cells with grade of ovarian carcinomas, but for prognostic significance and therapeutic applications, more corroborative and multicentric works in this field are needed. CD44 can be targeted for therapy in recurrent and resistant cases of ovarian cancer.
Journal
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TP53 (Tumor protein P53) • CD44
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TP53 expression • CD44 expression
20d
To conclude, we report the expression of CD71, CD81, CD44 and CD39 by FC in B cell lymphomas. Further studies will have to determine the value they add to specific FC panels.
Journal
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CD44 • ENTPD1 (Ectonucleoside Triphosphate Diphosphohydrolase 1) • TFRC • MME (Membrane metallo-endopeptidase)
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CD44 expression
20d
Furthermore, it was shown that the co-formulation with or without aptamer renders the formulation specific tumor accumulation in vivo 24 h post-administration, assisting the combination synergy observed in vitro to be translated to in vivo antitumor efficacy. This combinatorial delivery platform strongly offers a novel approach for the synergistic controlled transportation of several chemotherapeutics for the treatment of non-small cell lung cancer.
Journal
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CD44 • FOXM1 (Forkhead Box M1)
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CD44 expression
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doxorubicin hydrochloride • irinotecan
22d
EMP3 promotes CD44-dependent signaling by initiating complex formation between CD44 and various CD44 interactors, including RhoGTPase signaling effectors and the receptor tyrosine kinase MET. Such a mechanism may be pathologically relevant in MES IDH-wt GBMs, as the signaling pathways induced by these membrane complexes stimulate cellular proliferation, migration, and other oncogenic hallmarks.
CD44
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CD44 expression
22d
The effect of adipocyte conditioned media/EVs on PCa cell resistance to docetaxel was evaluated by Trypan blue exclusion assay and Annexin V/PI assay; Western blot analysis of caspase 3 and PARP levels as well as of CD44 expression was also performed...Conclusion These results highlight that an EV-mediated cross-talk exists between adipocytes and PCa, driving tumor aggressiveness. Further studies will be performed to identify the adipocyte EV molecular cargo responsible for the modulation of this dialog.
PARP Biomarker
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CASP3 (Caspase 3) • CD44 • MMP2 (Matrix metallopeptidase 2) • PARP1 (Poly(ADP-Ribose) Polymerase 1)
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CD44 expression
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Decipher Prostate Cancer Test
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docetaxel
22d
EMP3 promotes CD44-dependent signaling by initiating complex formation between CD44 and various CD44 interactors, including RhoGTPase signaling effectors and the receptor tyrosine kinase MET. Such a mechanism may be pathologically relevant in MES IDH-wt GBMs, as the signaling pathways induced by these membrane complexes stimulate cellular proliferation, migration, and other oncogenic hallmarks.
CD44
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CD44 expression
22d
The effect of adipocyte conditioned media/EVs on PCa cell resistance to docetaxel was evaluated by Trypan blue exclusion assay and Annexin V/PI assay; Western blot analysis of caspase 3 and PARP levels as well as of CD44 expression was also performed...Conclusion These results highlight that an EV-mediated cross-talk exists between adipocytes and PCa, driving tumor aggressiveness. Further studies will be performed to identify the adipocyte EV molecular cargo responsible for the modulation of this dialog.
PARP Biomarker
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CASP3 (Caspase 3) • CD44 • MMP2 (Matrix metallopeptidase 2) • PARP1 (Poly(ADP-Ribose) Polymerase 1)
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CD44 expression
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Decipher Prostate Cancer Test
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docetaxel
22d
The effect of adipocyte conditioned media/EVs on PCa cell resistance to docetaxel was evaluated by Trypan blue exclusion assay and Annexin V/PI assay; Western blot analysis of caspase 3 and PARP levels as well as of CD44 expression was also performed...Conclusion These results highlight that an EV-mediated cross-talk exists between adipocytes and PCa, driving tumor aggressiveness. Further studies will be performed to identify the adipocyte EV molecular cargo responsible for the modulation of this dialog.
PARP Biomarker
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CASP3 (Caspase 3) • CD44 • MMP2 (Matrix metallopeptidase 2) • PARP1 (Poly(ADP-Ribose) Polymerase 1)
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CD44 expression
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Decipher Prostate Cancer Test
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docetaxel
22d
The effect of adipocyte conditioned media/EVs on PCa cell resistance to docetaxel was evaluated by Trypan blue exclusion assay and Annexin V/PI assay; Western blot analysis of caspase 3 and PARP levels as well as of CD44 expression was also performed...Conclusion These results highlight that an EV-mediated cross-talk exists between adipocytes and PCa, driving tumor aggressiveness. Further studies will be performed to identify the adipocyte EV molecular cargo responsible for the modulation of this dialog.
PARP Biomarker
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CASP3 (Caspase 3) • CD44 • MMP2 (Matrix metallopeptidase 2) • PARP1 (Poly(ADP-Ribose) Polymerase 1)
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CD44 expression
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Decipher Prostate Cancer Test
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docetaxel
22d
EMP3 promotes CD44-dependent signaling by initiating complex formation between CD44 and various CD44 interactors, including RhoGTPase signaling effectors and the receptor tyrosine kinase MET. Such a mechanism may be pathologically relevant in MES IDH-wt GBMs, as the signaling pathways induced by these membrane complexes stimulate cellular proliferation, migration, and other oncogenic hallmarks.
CD44
|
CD44 expression
22d
EMP3 promotes CD44-dependent signaling by initiating complex formation between CD44 and various CD44 interactors, including RhoGTPase signaling effectors and the receptor tyrosine kinase MET. Such a mechanism may be pathologically relevant in MES IDH-wt GBMs, as the signaling pathways induced by these membrane complexes stimulate cellular proliferation, migration, and other oncogenic hallmarks.
CD44
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CD44 expression
22d
We also observed, for CAL27 CisR cells, a high in vivo tumorigenic potential. Conclusion Taken all together, our results suggest that a reprogramming in the expression of genes signaling stemness and tumor aggressiveness drives chemoresistance induced by cisplatin.
Preclinical
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CDH1 (Cadherin 1) • CD44 • TGFB1 (Transforming Growth Factor Beta 1) • VIM (Vimentin)
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CD44 expression
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cisplatin
22d
In the transcriptomic profiling of NCAM1-overepressing vs. control LNCaP cells, Notch emerged as one of the most upregulated pathways, whose pharmacological inhibition, in functional in vitro studies, reverted NCAM1-dependent ADT resistance. Conclusion NCAM1 is a bona fide PCSC marker that could be exploited as a prognostic biomarker and a therapeutic target for the personalized management of PCa patients.
Clinical • IO biomarker
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KIT (KIT proto-oncogene, receptor tyrosine kinase) • CD133 • CD44 • NCAM1 (Neural cell adhesion molecule 1)
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KIT expression • CD133 expression • CD44 expression
22d
Conclusion We anticipate that the results from these studies have will have an immediate impact on developing a new and effective treatment for metastatic breast cancer. The outcome of this study, therefore may help to improve the quality of life and mortality rate of the cancer patients.
AKT1 (V-akt murine thymoma viral oncogene homolog 1) • CD44 • VIM (Vimentin)
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CD44 expression • VIM expression
22d
We also observed, for CAL27 CisR cells, a high in vivo tumorigenic potential. Conclusion Taken all together, our results suggest that a reprogramming in the expression of genes signaling stemness and tumor aggressiveness drives chemoresistance induced by cisplatin.
Preclinical
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CDH1 (Cadherin 1) • CD44 • TGFB1 (Transforming Growth Factor Beta 1) • VIM (Vimentin)
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CD44 expression
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cisplatin
22d
Conclusion We anticipate that the results from these studies have will have an immediate impact on developing a new and effective treatment for metastatic breast cancer. The outcome of this study, therefore may help to improve the quality of life and mortality rate of the cancer patients.
AKT1 (V-akt murine thymoma viral oncogene homolog 1) • CD44 • VIM (Vimentin)
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CD44 expression • VIM expression
22d
Conclusion We anticipate that the results from these studies have will have an immediate impact on developing a new and effective treatment for metastatic breast cancer. The outcome of this study, therefore may help to improve the quality of life and mortality rate of the cancer patients.
AKT1 (V-akt murine thymoma viral oncogene homolog 1) • CD44 • VIM (Vimentin)
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CD44 expression • VIM expression
22d
In the transcriptomic profiling of NCAM1-overepressing vs. control LNCaP cells, Notch emerged as one of the most upregulated pathways, whose pharmacological inhibition, in functional in vitro studies, reverted NCAM1-dependent ADT resistance. Conclusion NCAM1 is a bona fide PCSC marker that could be exploited as a prognostic biomarker and a therapeutic target for the personalized management of PCa patients.
Clinical • IO biomarker
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KIT (KIT proto-oncogene, receptor tyrosine kinase) • CD133 • CD44 • NCAM1 (Neural cell adhesion molecule 1)
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KIT expression • CD133 expression • CD44 expression
22d
We also observed, for CAL27 CisR cells, a high in vivo tumorigenic potential. Conclusion Taken all together, our results suggest that a reprogramming in the expression of genes signaling stemness and tumor aggressiveness drives chemoresistance induced by cisplatin.
Preclinical
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CDH1 (Cadherin 1) • CD44 • TGFB1 (Transforming Growth Factor Beta 1) • VIM (Vimentin)
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CD44 expression
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cisplatin
22d
In the transcriptomic profiling of NCAM1-overepressing vs. control LNCaP cells, Notch emerged as one of the most upregulated pathways, whose pharmacological inhibition, in functional in vitro studies, reverted NCAM1-dependent ADT resistance. Conclusion NCAM1 is a bona fide PCSC marker that could be exploited as a prognostic biomarker and a therapeutic target for the personalized management of PCa patients.
Clinical • IO biomarker
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KIT (KIT proto-oncogene, receptor tyrosine kinase) • CD133 • CD44 • NCAM1 (Neural cell adhesion molecule 1)
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KIT expression • CD133 expression • CD44 expression
22d
Conclusion We anticipate that the results from these studies have will have an immediate impact on developing a new and effective treatment for metastatic breast cancer. The outcome of this study, therefore may help to improve the quality of life and mortality rate of the cancer patients.
AKT1 (V-akt murine thymoma viral oncogene homolog 1) • CD44 • VIM (Vimentin)
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CD44 expression • VIM expression
22d
Etoposide-sensitive and -resistant NB CSCs were long-term treated with Etoposide given alone or in combination with Sulfasalazine (SSZ) or with an inhibitor of PKC-alpha (C2-4), which target xCT directly or indirectly, respectively. These results confirm that SSZ is a ferroptotic-inducer and demonstrate, for the first time, that C2-4, a PKC-alpha inhibitor, is able to trigger a similar response in ER-CSCs. Conclusion Altogether these results suggest that PKC-alpha might be a new molecular target able to fight CSC chemoresistance by counteracting drug-induced metabolic adaptation and triggering lipoperoxidative death.
CD44 • GPX4 (Glutathione Peroxidase 4) • PRKCA (Protein Kinase C Alpha) • ZEB1 (Zinc Finger E-box Binding Homeobox 1)
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CD44 expression • ZEB1 expression
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etoposide IV • sulfasalazine
22d
Etoposide-sensitive and -resistant NB CSCs were long-term treated with Etoposide given alone or in combination with Sulfasalazine (SSZ) or with an inhibitor of PKC-alpha (C2-4), which target xCT directly or indirectly, respectively. These results confirm that SSZ is a ferroptotic-inducer and demonstrate, for the first time, that C2-4, a PKC-alpha inhibitor, is able to trigger a similar response in ER-CSCs. Conclusion Altogether these results suggest that PKC-alpha might be a new molecular target able to fight CSC chemoresistance by counteracting drug-induced metabolic adaptation and triggering lipoperoxidative death.
CD44 • GPX4 (Glutathione Peroxidase 4) • PRKCA (Protein Kinase C Alpha) • ZEB1 (Zinc Finger E-box Binding Homeobox 1)
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CD44 expression • ZEB1 expression
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etoposide IV • sulfasalazine
22d
Etoposide-sensitive and -resistant NB CSCs were long-term treated with Etoposide given alone or in combination with Sulfasalazine (SSZ) or with an inhibitor of PKC-alpha (C2-4), which target xCT directly or indirectly, respectively. These results confirm that SSZ is a ferroptotic-inducer and demonstrate, for the first time, that C2-4, a PKC-alpha inhibitor, is able to trigger a similar response in ER-CSCs. Conclusion Altogether these results suggest that PKC-alpha might be a new molecular target able to fight CSC chemoresistance by counteracting drug-induced metabolic adaptation and triggering lipoperoxidative death.
CD44 • GPX4 (Glutathione Peroxidase 4) • PRKCA (Protein Kinase C Alpha) • ZEB1 (Zinc Finger E-box Binding Homeobox 1)
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CD44 expression • ZEB1 expression
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etoposide IV • sulfasalazine
22d
In the transcriptomic profiling of NCAM1-overepressing vs. control LNCaP cells, Notch emerged as one of the most upregulated pathways, whose pharmacological inhibition, in functional in vitro studies, reverted NCAM1-dependent ADT resistance. Conclusion NCAM1 is a bona fide PCSC marker that could be exploited as a prognostic biomarker and a therapeutic target for the personalized management of PCa patients.
Clinical • IO biomarker
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KIT (KIT proto-oncogene, receptor tyrosine kinase) • CD133 • CD44 • NCAM1 (Neural cell adhesion molecule 1)
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KIT expression • CD133 expression • CD44 expression
22d
Etoposide-sensitive and -resistant NB CSCs were long-term treated with Etoposide given alone or in combination with Sulfasalazine (SSZ) or with an inhibitor of PKC-alpha (C2-4), which target xCT directly or indirectly, respectively. These results confirm that SSZ is a ferroptotic-inducer and demonstrate, for the first time, that C2-4, a PKC-alpha inhibitor, is able to trigger a similar response in ER-CSCs. Conclusion Altogether these results suggest that PKC-alpha might be a new molecular target able to fight CSC chemoresistance by counteracting drug-induced metabolic adaptation and triggering lipoperoxidative death.
CD44 • GPX4 (Glutathione Peroxidase 4) • PRKCA (Protein Kinase C Alpha) • ZEB1 (Zinc Finger E-box Binding Homeobox 1)
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CD44 expression • ZEB1 expression
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etoposide IV • sulfasalazine
22d
We also observed, for CAL27 CisR cells, a high in vivo tumorigenic potential. Conclusion Taken all together, our results suggest that a reprogramming in the expression of genes signaling stemness and tumor aggressiveness drives chemoresistance induced by cisplatin.
Preclinical
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CDH1 (Cadherin 1) • CD44 • TGFB1 (Transforming Growth Factor Beta 1) • VIM (Vimentin)
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CD44 expression
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cisplatin
22d
The effect of autophagy inducers 2DG and rapamycin, GLI1 inhibitor GANT61, Smoothened inhibitor cyclopamine, EGFR inhibitor erlotinib, TGFbetaR inhibitor SD208 and DNA damage-inducing chemotherapy FOLFOX (5-fluorouracil/lecovorin/oxaliplatin) was investigated in CTD mutant and wild type cells. GANT61 reduced viability and colony formation in mutant clones, while erlotinib decreased colony formation. Conclusion These findings reveal the oncogenic role of mutations in the PTCH1 CTD present in a subset of CRC cases and reveal specific vulnerabilities that could be exploited therapeutically.
PARP Biomarker
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PTCH1 (Patched 1) • CDH1 (Cadherin 1) • GLI1 (GLI Family Zinc Finger 1) • EREG (Epiregulin) • CD44 • TGFB1 (Transforming Growth Factor Beta 1) • VIM (Vimentin) • GLI2 (GLI Family Zinc Finger 2) • VCAN (Versican)
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PTCH1 mutation • CD44 expression
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erlotinib • 5-fluorouracil • oxaliplatin • sirolimus • cyclopamine
22d
The effect of autophagy inducers 2DG and rapamycin, GLI1 inhibitor GANT61, Smoothened inhibitor cyclopamine, EGFR inhibitor erlotinib, TGFbetaR inhibitor SD208 and DNA damage-inducing chemotherapy FOLFOX (5-fluorouracil/lecovorin/oxaliplatin) was investigated in CTD mutant and wild type cells. GANT61 reduced viability and colony formation in mutant clones, while erlotinib decreased colony formation. Conclusion These findings reveal the oncogenic role of mutations in the PTCH1 CTD present in a subset of CRC cases and reveal specific vulnerabilities that could be exploited therapeutically.
PARP Biomarker
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PTCH1 (Patched 1) • CDH1 (Cadherin 1) • GLI1 (GLI Family Zinc Finger 1) • EREG (Epiregulin) • CD44 • TGFB1 (Transforming Growth Factor Beta 1) • VIM (Vimentin) • GLI2 (GLI Family Zinc Finger 2) • VCAN (Versican)
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PTCH1 mutation • CD44 expression
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erlotinib • 5-fluorouracil • oxaliplatin • sirolimus • cyclopamine
22d
The effect of autophagy inducers 2DG and rapamycin, GLI1 inhibitor GANT61, Smoothened inhibitor cyclopamine, EGFR inhibitor erlotinib, TGFbetaR inhibitor SD208 and DNA damage-inducing chemotherapy FOLFOX (5-fluorouracil/lecovorin/oxaliplatin) was investigated in CTD mutant and wild type cells. GANT61 reduced viability and colony formation in mutant clones, while erlotinib decreased colony formation. Conclusion These findings reveal the oncogenic role of mutations in the PTCH1 CTD present in a subset of CRC cases and reveal specific vulnerabilities that could be exploited therapeutically.
PARP Biomarker
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PTCH1 (Patched 1) • CDH1 (Cadherin 1) • GLI1 (GLI Family Zinc Finger 1) • EREG (Epiregulin) • CD44 • TGFB1 (Transforming Growth Factor Beta 1) • VIM (Vimentin) • GLI2 (GLI Family Zinc Finger 2) • VCAN (Versican)
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PTCH1 mutation • CD44 expression
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erlotinib • 5-fluorouracil • oxaliplatin • sirolimus • cyclopamine
22d
Material and Methods We used breast cancer EMT+ (MDA-MB-231, Hs578T), EMT- (MCF7, T47D) and EMT inducible (EGF-treated MDA-MB-468, MDA-MB-468 harboring a doxycycline-inducible snail expression vector) cellular models...Mutations in the Sp1 binding sites inhibited the ability of CD44 to regulate the activity of the reporter vector, pointing out to Sp1 as a key transcription factor implicated in TF regulation by CD44. Conclusion Our results demonstrate a crucial role of CD44 in regulating the TF/coagulation axis known to support the survival and pro-metastatic abilities of the EMT+ CTCs.
CD44 • EGF (Epidermal growth factor) • VIM (Vimentin)
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CD44 expression • VIM expression
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doxycycline
22d
Material and Methods We used breast cancer EMT+ (MDA-MB-231, Hs578T), EMT- (MCF7, T47D) and EMT inducible (EGF-treated MDA-MB-468, MDA-MB-468 harboring a doxycycline-inducible snail expression vector) cellular models...Mutations in the Sp1 binding sites inhibited the ability of CD44 to regulate the activity of the reporter vector, pointing out to Sp1 as a key transcription factor implicated in TF regulation by CD44. Conclusion Our results demonstrate a crucial role of CD44 in regulating the TF/coagulation axis known to support the survival and pro-metastatic abilities of the EMT+ CTCs.
CD44 • EGF (Epidermal growth factor) • VIM (Vimentin)
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CD44 expression • VIM expression
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doxycycline
22d
Material and Methods We used breast cancer EMT+ (MDA-MB-231, Hs578T), EMT- (MCF7, T47D) and EMT inducible (EGF-treated MDA-MB-468, MDA-MB-468 harboring a doxycycline-inducible snail expression vector) cellular models...Mutations in the Sp1 binding sites inhibited the ability of CD44 to regulate the activity of the reporter vector, pointing out to Sp1 as a key transcription factor implicated in TF regulation by CD44. Conclusion Our results demonstrate a crucial role of CD44 in regulating the TF/coagulation axis known to support the survival and pro-metastatic abilities of the EMT+ CTCs.
CD44 • EGF (Epidermal growth factor) • VIM (Vimentin)
|
CD44 expression • VIM expression
|
doxycycline
22d
The effect of autophagy inducers 2DG and rapamycin, GLI1 inhibitor GANT61, Smoothened inhibitor cyclopamine, EGFR inhibitor erlotinib, TGFbetaR inhibitor SD208 and DNA damage-inducing chemotherapy FOLFOX (5-fluorouracil/lecovorin/oxaliplatin) was investigated in CTD mutant and wild type cells. GANT61 reduced viability and colony formation in mutant clones, while erlotinib decreased colony formation. Conclusion These findings reveal the oncogenic role of mutations in the PTCH1 CTD present in a subset of CRC cases and reveal specific vulnerabilities that could be exploited therapeutically.
PARP Biomarker
|
PTCH1 (Patched 1) • CDH1 (Cadherin 1) • GLI1 (GLI Family Zinc Finger 1) • EREG (Epiregulin) • CD44 • TGFB1 (Transforming Growth Factor Beta 1) • VIM (Vimentin) • GLI2 (GLI Family Zinc Finger 2) • VCAN (Versican)
|
PTCH1 mutation • CD44 expression
|
erlotinib • 5-fluorouracil • oxaliplatin • sirolimus • cyclopamine
22d
Material and Methods We used breast cancer EMT+ (MDA-MB-231, Hs578T), EMT- (MCF7, T47D) and EMT inducible (EGF-treated MDA-MB-468, MDA-MB-468 harboring a doxycycline-inducible snail expression vector) cellular models...Mutations in the Sp1 binding sites inhibited the ability of CD44 to regulate the activity of the reporter vector, pointing out to Sp1 as a key transcription factor implicated in TF regulation by CD44. Conclusion Our results demonstrate a crucial role of CD44 in regulating the TF/coagulation axis known to support the survival and pro-metastatic abilities of the EMT+ CTCs.
CD44 • EGF (Epidermal growth factor) • VIM (Vimentin)
|
CD44 expression • VIM expression
|
doxycycline
23d
Strikingly, overexpression of NUMB in CD44 PCSCs overcame all of the above PCSC properties enforced by miR-9-5p. Taken together, our results suggest that inhibiting the expression of the oncomiR miR-9-5p and overexpressing NUMB may represent novel therapeutic strategies to target PCSCs and PCa metastasis.
Journal
|
CD44
|
CD44 expression
26d
The levels of the expressed CD44 gene significantly changed under different stages of lung adenocarcinoma cancer. All these results demonstrate that the Tim4@ILI-01 immunoaffinity flake is a robust enrichment material and has a good potential in practical clinical applications.
Journal
|
CD44
|
CD44 expression
26d
V1/Chase drives Gemcitabine resistance and potentially predicts Gemcitabine+Cisplatin failure. CDA inhibition re-sensitizes V1-expressing tumors to Gemcitabine. Since several chemotherapy regimens include Gemcitabine, our study could have broad significance.
Clinical • Journal
|
CD44
|
CD44 expression
|
cisplatin • gemcitabine
27d
Although CD44 is regarded to be associated with more prognostic parameters compared to CD133, both immunohistochemical stains were shown to be related to pathological stage. Thus, these may be guiding for determining the tumour depth. Key Words: Gastric adenocarcinoma, CD44, CD133, Stem cell marker, Prognosis.
Journal
|
CD133 • CD44
|
CD133 expression • CD44 expression
1m
CD44v8-10 could represent a marker of a more aggressive bone metastatic PC population exerting a driver role in osteomimicry in bone. A novel link between TAZ and CD44v8-10 is also shown.
Clinical • Journal • PD(L)-1 Biomarker
|
PD-L1 (Programmed death ligand 1) • IL6 (Interleukin 6) • CD44
|
PD-L1 expression • CD44 expression
1m
Finally, minigene -MS2 mutation experiments showed that mutation of the SRA1 exon 3 binding site for SRSF1 prevented the binding of SRA1 pre-mRNA. In summary, our results provide experimental evidence that SRA1 exon 3 inclusion is up regulated by SRSF1 to promote tumor invasion and metastasis in hepatocellular carcinoma.
Journal
|
SOX9 (SRY-Box Transcription Factor 9) • CD44
|
CD44 expression • SOX9 expression
1m
In this small study, there was a statistical increase in CD4, CD14, CD68, CD8A, B7-H3, PDL-1, CD19, FOXP3, CD44, and STAT3 protein expression in methylated versus unmethylated GBM tumour core; however, this requires larger cohort validation. Advanced multiplex immunooncological biomarker analysis may be useful in identifying biomarkers for novel immunotherapeutic agents in GBMs.
Journal • PD(L)-1 Biomarker • IO biomarker
|
PD-L1 (Programmed death ligand 1) • PTEN (Phosphatase and tensin homolog) • BCL2 (B-cell CLL/lymphoma 2) • CD20 (Membrane Spanning 4-Domains A1) • CD8 (cluster of differentiation 8) • PD-1 (Programmed cell death 1) • CD19 (CD19 Molecule) • CTNNB1 (Catenin (cadherin-associated protein), beta 1) • CD276 (CD276 Molecule) • B2M (Beta-2-microglobulin) • STAT3 (Signal Transducer And Activator Of Transcription 3) • CD14 • GZMB (Granzyme B) • PTPRC (Protein Tyrosine Phosphatase Receptor Type C) • CD44 • NCAM1 (Neural cell adhesion molecule 1) • CD68 (CD68 Molecule) • MS4A1 (Membrane Spanning 4-Domains A1) • FOXP3 (Forkhead Box P3)
|
CD44 expression • STAT3 expression
1m
In conclusion, MLCK1/2 variants are novel tumor suppressors by downregulating the TEAD4/CD44 axis via reducing nuclear translocation of distinct transcriptional coactivators. The reduction of epithelial MLCKs, especially isoform 2, may drive cancer stemness and tumorigenesis.
Journal
|
CD133 • YAP1 (Yes associated protein 1) • CD44 • LCK (LCK Proto-Oncogene, Src Family Tyrosine Kinase)
|
CD133 expression • CD44 expression
1m
However, the expression of CD44 and Ki67 is significantly higher in reproductive age patients, compared to patients in menopause and post-menopause. In addition, the expression of CD44 and Ki67 is significantly higher in PTC and Hashimoto's thyroiditis co-occurred cases, compared to cases with PTC only.
Clinical • Journal • IO biomarker
|
BCL2 (B-cell CLL/lymphoma 2) • CD44 • NCAM1 (Neural cell adhesion molecule 1) • KRT19 (Keratin 19)
|
CD44 expression
1m
More importantly, 4-methylumbelliferone (4-MU), a small competitive inhibitor of Uridine diphosphate (UDP) with the ability to penetrate the blood-brain barrier (BBB), also inhibited glioma cell proliferation in vitro and in vivo. Thus, approaches that interfere with HA metabolism by altering the expression of HAS3 and CD44 and the administration of 4-MU potentially represent effective strategies for glioma treatment.
Journal
|
CD44 • HAS3 (Hyaluronan Synthase 3)
|
CD44 expression • HAS3 expression
1m
Conclusion Our data indicate that discordant expression of CD56, CD44 and CD38 may occur in EMD lesions compared to BM. The possible lack of CD38 expression in EMD was highlighted for the first time and it should be considered for its therapeutic impact.
Clinical • IO biomarker
|
CD38 (CD38 Molecule) • CD44 • NCAM1 (Neural cell adhesion molecule 1)
|
CD38 expression • NCAM1 expression • CD44 expression • CD8 negative
1m
Some drugs inhibit hyaluronan-producing cells such as pirfenidone...We present a hypothesis, sustained by hard experimental evidence, suggesting that the simultaneous use of these nontoxic drugs can achieve synergistic or added effects in reducing invasion and metastatic potential, in PDAC. A non-toxic, low-cost scheme for inhibiting this pathway may offer an additional weapon for treating pancreatic cancer.
Journal
|
CD44
|
CD44 expression
|
Esbriet (pirfenidone)
1m
CD44 expression was associated with high-risk of tumor recurrence and metastasis (P = 0.01) in HPV-cases. In summary, genes regulated by methylation play a modulatory function in HNC susceptibility and it represent a critical therapeutic target to manage patients with advanced disease.
Journal • Epigenetic controller
|
TP53 (Tumor protein P53) • RB1 (RB Transcriptional Corepressor 1) • CDH1 (Cadherin 1) • CD44 • RASSF1 (Ras Association Domain Family Member 1)
|
CD44 expression
1m
These data indicate PCSCs may have an important role in stroma differentiation in PDAC. Our results further suggest that tumor stroma may influence the recurrence pattern in PDAC patients.
Journal
|
CD44
|
CD44 expression
1m
CD44v9-positive expression was associated with chemotherapeutic resistance by controlling intracellular accumulated ROS, suggesting that CD44v9 may be a predictive biomarker for chemotherapy in GC.
Journal
|
CD44 • GPX2 (Glutathione peroxidase 2 (gastrointestinal))
|
ROS1 positive • CD44 expression
|
5-fluorouracil
1m
Kyoto Encyclopedia of Genes and Genomes pathway analysis revealed that these genes play key roles in biological adhesion, cell component organization, locomotion, G-α-signaling, and the response to stimulus. In summary, these findings lend evidence for the multiple key roles played by CD44 in tumorigenesis and suggest that CD44 is considered further in future studies of cancer pathogenesis and the search for novel molecular targets and personalized medicine biomarkers in clinical oncology.
Journal • Tumor Mutational Burden
|
TMB (Tumor Mutational Burden) • CD44
|
TMB-H • CD44 expression
2ms
In addition, the drug combination decreased phosphorylated ERK level, indicating inhibition of the mitogenic signaling pathway MEK/ERK. Taken together, the resminostat plus sorafenib combination counteracts platelet-mediated cancer promoting effects in HCC cells.
Journal • Combination therapy • Epigenetic controller
|
CD44
|
CD44 expression
|
Nexavar (sorafenib) • resminostat (4SC-201)
2ms
Our data indicated that autophagy is not necessarily associated with CSC-like cells' radiosensitivity, emphasizing that careful assessment of other milestone processes (such as senescence and autophagy-p53-Zeb1 axis) of primary radiation responses may provide new potential targets modulated for therapeutic benefit through radiosensitizing cancer cells while rescuing normal tissue. Our findings also shed light on the intricate crosstalk between autophagy and the p53-related EMT, by which MFR-surviving cells might obtain an invasive phenotype and metastatic potential.
Clinical • Journal
|
TP53 (Tumor protein P53) • RAD51 (RAD51 Homolog A) • CDH1 (Cadherin 1) • CD44 • VIM (Vimentin) • ZEB1 (Zinc Finger E-box Binding Homeobox 1)
|
CDH1 expression • CD44 expression • VIM expression
2ms
Mechanistically, KDM4A/4C inhibition downregulated granulocyte-macrophage colony-stimulating factor (GM-CSF) expression and prevented GM-CSF-dependent Lepto cell proliferation. Collectively, these results establish KDM4A/4C as a viable therapeutic target in HER2+ LC and spotlight the benefits of targeting the tumorigenic transcriptional network.
Journal • Epigenetic controller
|
HER-2 (Human epidermal growth factor receptor 2) • CD24 (CD24 Molecule) • CD44 • ITGA6 (Integrin, alpha 6)
|
HER-2 expression • CSF2 expression • CD24 expression • CD44 expression
2ms
This study revealed miR-98 inhibits gastric cancer cell stemness and chemoresistance by targeting BCAT1, suggesting that this miR-98/BCAT1 axis represents a potential therapeutic target in gastric cancer.
Journal
|
CD44 • BCAT1 (Branched Chain Amino Acid Transaminase 1 )
|
BCAT1 expression • CD44 expression
|
cisplatin • paclitaxel
2ms
In summary, both cellular and gene expression studies suggest the attenuated cytotoxicity of cisplatin in CSC-like cells as compared to parental cells. Understanding the role of dysregulated putative target genes induced by cisplatin in CSCs may aid in the potential development of therapeutic targets for cisplatin-resistant breast cancer.
Journal
|
CD24 (CD24 Molecule) • CD44
|
CD44 expression
|
cisplatin
2ms
In this study, Etoposide-sensitive and -resistant neuroblastoma CSCs were chronically treated with Etoposide, given alone or in combination with Sulfasalazine (SSZ) or with an inhibitor of PKCα (C2-4), which target xCT directly or indirectly, respectively. Both combined approaches are able to sensitize CSCs to Etoposide by decreasing intracellular GSH levels, inducing a metabolic switch from OXPHOS to aerobic glycolysis, down-regulating glutathione-peroxidase-4 activity and stimulating lipid peroxidation, thus leading to ferroptosis. Our results suggest, for the first time, that PKCα inhibition inducing ferroptosis might be a useful strategy with which to fight CSC chemoresistance.
Journal
|
CD44 • GPX4 (Glutathione Peroxidase 4)
|
CD44 expression
|
etoposide IV • sulfasalazine
2ms
Finally, we provide evidence that ITIH5 increase sensitivity of SCaBER cells to chemotherapeutical agents (cisplatin and gemcitabine), whereas responsiveness of HT1376 cells was not affected by ITIH5 expression. Thus, we gain further insights into the putative role of ITIH5 as tumor suppressor highlighting an impact on drug response potentially via the HA-CD44 axis in BASQ-type BLCA.
Journal
|
CD44
|
CD44 expression
|
cisplatin • gemcitabine
2ms
Ad-CD44-N-HIF3α4 inhibited the both signaling pathways of CD44 and HIF-1α in MDA-MB-231 cells under conditions of hypoxia with HA in vitro, and significantly suppressed tumor growth in vivo. These findings indicated that Ad-CD44-N-HIF3α4 has a high clinical applicability for invasive types of TNBC.
Preclinical
|
HIF1A (Hypoxia inducible factor 1, alpha subunit) • BIRC5 (Baculoviral IAP repeat containing 5) • CCL2 (Chemokine (C-C motif) ligand 2) • CD44
|
BIRC5 expression • CD44 expression • VEGFA expression
2ms
Both single and combined expression of CD44 and CD133 should be considered when validating the detection of prostate cancer cells in circulating tumor cells.
Preclinical • Journal
|
CD133 • CD44
|
CD133 expression • CD44 expression
2ms
Ectopic expression of miR-138 also increased survival rates in mice that had an intracranial xenograft tumor derived from human patient-derived primary GBM cells. In conclusion, we demonstrated a therapeutic potential of tumor suppressive miR-138 through direct downregulation of CD44 for the treatment of primary GBM.
Journal
|
CD44
|
CD44 expression
2ms
Using primary human HNSCC cells in combination with CRISPR/Cas9 and overexpression approaches allowed us to confirm the high specificity of our CAR construct for the tumor-associated CD44v6 as target antigen and to demonstrate a direct correlation between CD44v6 expression levels and cytotoxicity of the CAR T-cells. Importantly, the design of our clinically applicable lentiviral vector facilitates to co-express a second transgene for in vivo control of CAR T-cells, if undesired side-effects or toxicities occur.
Journal • CAR T-Cell Therapy • IO biomarker
|
CD44
|
CD44 expression
2ms
CD44 & ALDH1 expressions, histologic grade, tumor size were the independent predictors of DFS and three years OS. CD44 and ALDH1 expressions are valuable prognostic factors in OSCC and could be well considered predictors for patients' 3 years OS and DFS.
Clinical • Journal
|
CD44 • ALDH1A1 (Aldehyde Dehydrogenase 1 Family Member A1)
|
CD44 expression
2ms
Nanoparticles were fabricated and loaded with chemotherapeutic drug docetaxel (DTX) by physical encapsulation...In vivo anti-tumor experiments proved that DTX/CHD nanoparticles had the best antitumor response versus DTX and CHD nanoparticles under near-infrared (NIR) irradiation. These studies revealed that redox-responsive DTX-loaded CHD nanoparticles held great potential for the treatment of breast cancer.
Journal
|
CD44
|
CD44 expression
|
docetaxel
2ms
Preclinical • Journal
|
CD34 (CD34 molecule) • PTPRC (Protein Tyrosine Phosphatase Receptor Type C) • CD44 • ENG (Endoglin)
|
CD44 expression
2ms
The potential utility of the monoclonal antibodies in blocking tumorigenesis was tested by co-injection of cells of the breast cancer-derived tumorigenic cell line MDA-MB-231 with the anti-CD44 monoclonal antibody P3D2 into the mammary fat pads of mice. All five control mice injected with MDA-MB-231 cells plus anti-IgG formed palpable tumors, while only one of the six test mice injected with MDA-MB-231 cells plus P3D2 formed a tiny tumor, while the remaining five were tumor-free, indicating that the four anti-CD44 mAbs may be useful therapeutically.
Preclinical • Journal
|
CD44
|
CD44 expression
2ms
Finally, we studied the effects of the lncRNA-cCSC1/miR-124-3p axis on CD44. These results indicate that lncRNA-cCSC1 promotes cell proliferation of CRC through sponging miR-124-3p and upregulating CD44.
Journal
|
CD44
|
CD44 expression
2ms
Furthermore, we confirmed that HET0016 suppressed CYP4Z1 activity, and HET0016-induced inhibition on the stemness and metastasis of breast cancer cells was rescued by CYP4Z1 overexpression. Thus, our results demonstrate that HET0016 can attenuate the stemness of breast cancer cells through targeting CYP4Z1.
Journal
|
CD24 (CD24 Molecule) • CD44
|
CD24 expression • CD44 expression
2ms
These results suggest that BUB1B plays an oncogenic role and may be a promising predictive biomarker for survival in RCC.
Journal • PD(L)-1 Biomarker • IO biomarker
|
PD-L1 (Programmed death ligand 1) • CD8 (cluster of differentiation 8) • IFNG (Interferon, gamma) • CD44 • BUB1B (BUB1 Mitotic Checkpoint Serine/Threonine Kinase B)
|
TP53 expression • CD44 expression
|
Opdivo (nivolumab)
2ms
Apatinib inhibited stem property and malignant biological behaviors of BCSCs by blocking Wnt/β-catenin signal pathway through down-regulating lncRNA ROR.
Journal
|
ABCG2 • CDH1 (Cadherin 1) • CD24 (CD24 Molecule) • CD44 • MMP2 (Matrix metallopeptidase 2) • VIM (Vimentin) • MMP9 (Matrix metallopeptidase 9)
|
CD44 expression
|
AiTan (rivoceranib)
2ms
Capan-26 is a unique cell line that may be used to study the mechanism of pancreatic cancer.
Preclinical • Journal
|
KRAS (KRAS proto-oncogene GTPase) • TP53 (Tumor protein P53) • POU5F1 (POU Class 5 Homeobox 1) • CD44 • CEACAM6 (CEA Cell Adhesion Molecule 6) • ZEB1 (Zinc Finger E-box Binding Homeobox 1) • Cancer antigen 19-9
|
TP53 mutation • KRAS mutation • CD44 expression • KRAS deletion • ZEB1 expression
|
gemcitabine
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