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BIOMARKER:

CD9 expression

i
Other names: CD9, BA2, MIC3, MRP-1, P24, TSPAN29
Entrez ID:
27d
An early T-cell precursor lymphoblastic leukemia was raised in the differential diagnosis, but lack of CD2 and CD7 and bright CD56 expression makes this later diagnosis less likely. AML with “RAM” phenotype (bright CD56, dim to negative CD45 and CD38, HLA-DR negative) has been reported with a median age at diagnosis of 1.26 years and is associated with inv(16)(p13.3q24.3) CBFA2T3-GLIS2 fusion protein.
Clinical • IO biomarker
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KIT (KIT proto-oncogene, receptor tyrosine kinase) • CD20 (Membrane Spanning 4-Domains A1) • CD8 (cluster of differentiation 8) • CD19 (CD19 Molecule) • CD38 (CD38 Molecule) • CD79B (CD79b Molecule) • CD34 (CD34 molecule) • CD36 (thrombospondin receptor) • CD123 (Interleukin 3 Receptor Subunit Alpha) • CD5 (CD5 Molecule) • CD14 • CD9 • PTPRC (Protein Tyrosine Phosphatase Receptor Type C) • CBFA2T3 (CBFA2/RUNX1 Partner Transcriptional Co-Repressor 3) • CD22 (CD22 Molecule) • CD33 (CD33 Molecule) • CD7 (CD7 Molecule) • GLIS2 (GLIS Family Zinc Finger 2) • NCAM1 (Neural cell adhesion molecule 1) • ITGAM (Integrin, alpha M) • MME (Membrane metallo-endopeptidase)
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CD38 expression • CD9 expression • CBFA2T3 - GLIS2 fusion • NCAM1 expression
1m
An increased CD9 expression was associated with favorable survival in cancer patients suggesting that CD9 expression could be a valuable survival factor in cancer patients.
Retrospective data • Review • Journal
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CD9
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CD9 expression
1m
Cytotoxicity in these cocultures is restored with a CD9-blocking antibody or CD9 CRISPR knockout, thereby identifying mechanisms of immune suppression in HGSC. CD9 is widely expressed in HGSC tumors and so represents an important new therapeutic target with immediate relevance for NK immunotherapy.
Journal • IO biomarker
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CD9 • NCAM1 (Neural cell adhesion molecule 1) • VIM (Vimentin) • CXCR3 (C-X-C Motif Chemokine Receptor 3)
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CD9 expression • VIM expression
1m
Panobinostat exposure elevated CD9 expression (3.1-32.2-fold) and restored activating histone marks in AML samples...Preliminary data showed that CD9 could enhance BM infiltration of cytotoxic T cells and thereby mount an effective immunity against AML in humanized NSG mice. Conclusions Our data established CD9 as a novel tumor suppressor and immune regulator in pediatric AML, and inspired a new combinatorial epigenetic/immunotherapy for this rare but aggressive malignancy.
Clinical • IO biomarker
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CD9
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CD9 expression
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Farydak (panobinostat)
3ms
The expression of the exosomal markers (CD63 and CD9) increased in patients with rectal adenocarcinoma after treatment with NCCR. The exosomal markers (CD63 and CD9) may have a prognostic significance. There was a trend for higher CD63 and CD9 expression in patients with high NAR score compared with low-intermediate NAR scores. The lack of statistical significance is likely due to the small sample size.
Clinical • Journal
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CD9
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CD9 expression
4ms
Furthermore, in SW962 particularly, CD63-siRNA also remarkably inhibited cell migration. Altogether, our data suggest that the differential expression of TSPANs represents an important feature for prognosis of VSCC patients and indicates that CD63 and CD82 are likely potential therapeutic targets in VSCC.
Journal
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CD9
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CD9 expression
5ms
Material and Methods 14 patients (pts) harboring BRAFV600 mutation were enrolled (NCT03149029), and treated with 2 weeks (wks) of MTT (dabrafenib plus trametinib) then 6 wks of concomitant MTT and pembrolizumab, followed by single-agent pembrolizumab thereafter. It is theorized that the tumor’s ability to create a unique microenvironment by producing certain factors (e.g. TGFβ), modifies the immune system and may tilt its path into immune suppression thereby reducing the efficacy of this combinatorial therapy in melanoma pts with metastatic disease. These results may help identify pts most likely to benefit from combined MTT plus ICB and new targets to overcome resistance to these regimens.
Clinical • Checkpoint inhibition • PD(L)-1 Biomarker • IO biomarker
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CD8 (cluster of differentiation 8) • IFNG (Interferon, gamma) • CD9 • PTPRC (Protein Tyrosine Phosphatase Receptor Type C) • TGFB1 (Transforming Growth Factor Beta 1)
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BRAF V600 • CD9 expression
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Keytruda (pembrolizumab) • Mekinist (trametinib) • Tafinlar (dabrafenib)
5ms
Material and Methods 14 patients (pts) harboring BRAFV600 mutation were enrolled (NCT03149029), and treated with 2 weeks (wks) of MTT (dabrafenib plus trametinib) then 6 wks of concomitant MTT and pembrolizumab, followed by single-agent pembrolizumab thereafter. It is theorized that the tumor’s ability to create a unique microenvironment by producing certain factors (e.g. TGFβ), modifies the immune system and may tilt its path into immune suppression thereby reducing the efficacy of this combinatorial therapy in melanoma pts with metastatic disease. These results may help identify pts most likely to benefit from combined MTT plus ICB and new targets to overcome resistance to these regimens.
Clinical • Checkpoint inhibition • PD(L)-1 Biomarker • IO biomarker
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CD8 (cluster of differentiation 8) • IFNG (Interferon, gamma) • CD9 • PTPRC (Protein Tyrosine Phosphatase Receptor Type C) • TGFB1 (Transforming Growth Factor Beta 1)
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BRAF V600 • CD9 expression
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Keytruda (pembrolizumab) • Mekinist (trametinib) • Tafinlar (dabrafenib)
5ms
Material and Methods 14 patients (pts) harboring BRAFV600 mutation were enrolled (NCT03149029), and treated with 2 weeks (wks) of MTT (dabrafenib plus trametinib) then 6 wks of concomitant MTT and pembrolizumab, followed by single-agent pembrolizumab thereafter. It is theorized that the tumor’s ability to create a unique microenvironment by producing certain factors (e.g. TGFβ), modifies the immune system and may tilt its path into immune suppression thereby reducing the efficacy of this combinatorial therapy in melanoma pts with metastatic disease. These results may help identify pts most likely to benefit from combined MTT plus ICB and new targets to overcome resistance to these regimens.
Clinical • Checkpoint inhibition • PD(L)-1 Biomarker • IO biomarker
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CD8 (cluster of differentiation 8) • IFNG (Interferon, gamma) • CD9 • PTPRC (Protein Tyrosine Phosphatase Receptor Type C) • TGFB1 (Transforming Growth Factor Beta 1)
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BRAF V600 • CD9 expression
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Keytruda (pembrolizumab) • Mekinist (trametinib) • Tafinlar (dabrafenib)
5ms
Material and Methods 14 patients (pts) harboring BRAFV600 mutation were enrolled (NCT03149029), and treated with 2 weeks (wks) of MTT (dabrafenib plus trametinib) then 6 wks of concomitant MTT and pembrolizumab, followed by single-agent pembrolizumab thereafter. It is theorized that the tumor’s ability to create a unique microenvironment by producing certain factors (e.g. TGFβ), modifies the immune system and may tilt its path into immune suppression thereby reducing the efficacy of this combinatorial therapy in melanoma pts with metastatic disease. These results may help identify pts most likely to benefit from combined MTT plus ICB and new targets to overcome resistance to these regimens.
Clinical • Checkpoint inhibition • PD(L)-1 Biomarker • IO biomarker
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CD8 (cluster of differentiation 8) • IFNG (Interferon, gamma) • CD9 • PTPRC (Protein Tyrosine Phosphatase Receptor Type C) • TGFB1 (Transforming Growth Factor Beta 1)
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BRAF V600 • CD9 expression
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Keytruda (pembrolizumab) • Mekinist (trametinib) • Tafinlar (dabrafenib)
6ms
This could explain the refractoriness observed by some groups of expanded stem cells to repairing efficiently damaged tissue when used as a source in cell therapies. Understanding the function of the CD9 receptor in normal and malignant CD34 and VSELs, along with its relationship with the CXCR4/SDF-1 pathway, will enable advances in the field of adult pluripotent cell usage in regenerative medicine and in their role in leukemia.
Journal
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CXCR4 (Chemokine (C-X-C motif) receptor 4) • CD34 (CD34 molecule) • CD9 • CXCL12 (C-X-C Motif Chemokine Ligand 12)
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CD9 expression
8ms
In conclusion, in glioblastoma patients, GSCs are present at distance from the glioblastoma tumor in the SVZ. These findings suggest that GSCs in the SVZ niche are protected against radiotherapy and chemotherapy and protected against surgical resection due to their distant localization and thus may contribute to tumor recurrence after therapy.
Clinical • Journal
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CXCR4 (Chemokine (C-X-C motif) receptor 4) • CD133 • CD44 • SPP1 (Secreted Phosphoprotein 1) • CD9 • SOX2
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CD9 expression
8ms
The silencing of CD9 demonstrated an inhibitory role of cellular CD9 in CCL21 expression in hMSCs, suggesting that ionomycin could upregulate cellular CD9 to decrease CCL21 expression and secretion of hMSCs, which would reduce the migration of B16F10, A549 and U87MG cancer cell lines due to chemoattraction reduction of CCL21. The present study not only highlights the important role of bone marrow-derived hMSCs' CD9-mediated CCL21 regulation in cancer bone metastasis but also suggests a new distinct pharmaceutical strategy for prevention or/and therapy of cancer metastasis.
Journal
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CD9
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CD9 expression
9ms
Our findings suggest that CD9 is a new biomarker of AML LSCs and is a promising therapeutic target.
Journal
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CD9
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CD9 expression
10ms
Xenograft assays showed that the combinations of ALDH1A1 + cells co-expressing CD9, CD24 or EPHA1 were more tumorigenic and aggressive with respect to ALDH1A1-cells. These data suggest that a combined approach could be more useful in identifying CSCs in HGSOC.
Journal
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KIT (KIT proto-oncogene, receptor tyrosine kinase) • CD133 • CD44 • CD24 (CD24 Molecule) • CD9 • ALDH1A1 (Aldehyde Dehydrogenase 1 Family Member A1)
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CD9 expression • CD24 expression
10ms
In patients with LARC, the expression of exosomal markers (CD63 and CD9) increased after treatment with NCCR. Our results show that the expression of CD63 and CD9 is relatively higher in rectal cancer specimens treated with NCCR and thus suggest a possible role of these exosomes in adaptive response to NCCR. Further follow-up and laboratory studies are required to precisely understand the underlying mechanism(s).
Clinical
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CD9
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CD9 expression
11ms
No significant differences were observed in the CD9, CD36, and CD68 gene expression and at the protein levels between opium-treated THP-1 cells and controls. In conclusion, cigarettes by increasing the levels of CD36, CD68, and CD9 can be a risk factor in the development of many inflammatory diseases, including cardiovascular diseases, chronic obstructive pulmonary disease (COPD) and lung carcinoma.
Journal
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CD36 (thrombospondin receptor) • CD9 • CD68 (CD68 Molecule)
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CD9 expression
11ms
We have developed a labelling and stringent gating strategy which is able to explore EV marker expression (CD63, CD9, and LAMP1) on individual EVs within a widely heterogeneous population. Taken together, data presented here strongly support the value of exploring large EVs in clinical samples for potential biomarkers, useful in diagnostic screening and disease monitoring.
Journal
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CD9
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CD9 expression
1year
Finally, CD9 antibody showed anti-tumor effects in cell proliferation MTT assay, transwell migration assay and colony formation assay. Our study reveals a novel CD9/ADAM/Notch signaling network in PDAC and it supports that targeting CD9-ADAM interaction with antibody may be a potential therapeutic intervention for PDAC.
Journal
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ADAM9 (ADAM Metallopeptidase Domain 9) • CD9
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CD9 expression
1year
In addition, we observed that small-interfering RNAs against Cd9 and Cd81 inhibited estrogen-induced proliferation of CD9-positive mammary epithelial cells. Our current findings may provide novel insights into the proliferation of mammary epithelial cells during pregnancy and lactation as well as in pathological processes associated with breast cancer.
Journal
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ER (Estrogen receptor) • CD9
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CD9 expression
1year
Methods A drug sensitivity profiling, comprising 7 standard chemotherapeutic agents (6-mercaptopurine, cytarabine, daunorubicin, vincristine, methotrexate, prednisone, dexamethasone), was performed on 4 CD9+ (697, BV-173, RS4;11, SUP-B15) and 3 CD9- (Reh, SEM, KOPN-8) B-ALL cell lines...Conclusions Our results indicate that CD9 negativity was definitively linked to glucocorticoid resistance, which could be reversed by CD9 reactivation through a receptor-independent mechanism. Comprehensive understanding of the interaction between CD9 and glucocorticoid susceptibility could lead to improved therapeutic strategies for resistant pediatric B-ALL.
Clinical
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CEBPA (CCAAT Enhancer Binding Protein Alpha) • IRS2 (Insulin receptor substrate 2) • STAT5B (Signal Transducer And Activator Of Transcription 5B) • CD9 • IR (Insulin receptor) • SGK1 (Serum/Glucocorticoid Regulated Kinase 1) • ZBTB16 (Zinc Finger And BTB Domain Containing 16)
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CD9 expression
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cytarabine • prednisone • vincristine • methotrexate • daunorubicin • dexamethasone • mercaptopurine delayed release (DR6MP)
1year
Epigenetic control of CD9 was investigated by bisulfite sequencing, and confirmed by decitabine treatment...Overexpression of CD9 reduced proliferation, division and clonogenicity of MV4-11 cells, and enhanced cytarabine-induced apoptosis...Reexpression of CD9 substantially suppressed leukemia progression via immune sensitization. Our data established CD9 as a novel tumor suppressor in pediatric AML, which endow a huge translational potential.
Clinical
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CD9
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CD9 expression
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cytarabine • decitabine
1year
PPDU was an efficient and practical method to enrich EVs from body fluids and cell culture supernatant. The characteristic expression of ITGαV, β1 and β3 in ascites and plasma EVs of patients with HGSC provided useful information on the development of EVs in HGSC.
Journal
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CD9
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CD9 expression
1year
Trial completion
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CD9
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CD9 expression
1year
Herein, we report an additional maxillary intraosseous B-cell LBL, affecting a 14-year-old girl, which also showed positivity for CD9, Bcl-6 and MUM1/IRF4. Aiming at diagnostic and prognostic criteria, further studies focusing CD9 expression in LBL is recommended.
Clinical • Journal
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BCL6 (B-cell CLL/lymphoma 6) • CD9 • IRF4 (Interferon regulatory factor 4)
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CD9 expression