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BIOMARKER:

CARD11 mutation

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Other names: CARD11, Caspase Recruitment Domain Family Member 11, CARMA1, Caspase Recruitment Domain-Containing Protein 11, Bcl10-Interacting Maguk Protein 3, CARD-Containing MAGUK Protein 1, Carma 1, BIMP3, Caspase Recruitment Domain Family, Member 11, Card-Maguk Protein 1, IMD11A, CARD11, BENTA, IMD11, PPBL
Entrez ID:
Related biomarkers:
1m
Of note, EBVnegative PBL cases had higher mutational and copy-number load and more frequent TP53, CARD11 and MYC mutations, whereas EBV-positive PBL tended to have more mutations affecting the JAK-STAT pathway. In conclusion, these findings further unravel the distinctive molecular heterogeneity of PBL identifying novel molecular targets and the different genetic profile of these tumors related to EBV infection.
Journal
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TP53 (Tumor protein P53) • NRAS (Neuroblastoma RAS viral oncogene homolog) • MYC (V-myc avian myelocytomatosis viral oncogene homolog) • TET2 (Tet Methylcytosine Dioxygenase 2) • CARD11 (Caspase Recruitment Domain Family Member 11) • STAT3 (Signal Transducer And Activator Of Transcription 3) • EP300 (E1A binding protein p300) • SOCS1 (Suppressor Of Cytokine Signaling 1)
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TP53 mutation • NRAS mutation • CARD11 mutation • MYC translocation • STAT3 mutation • MYC mutation
2ms
Following relapse after initial CHOP chemotherapy, the patient was successfully treated with cyclosporine A and has remained in remission since, with prophylactic TMP-SMX and no infections. After a poor response to multiple rounds of chemotherapy, she required autologous bone marrow transplant and has been in remission since, with no infectious complications. These cases illuminate an unusual pathological manifestation for BENTA disease, and further suggest that CARD11 GOF mutations can contribute to the development of cutaneous T cell dyscrasias and/or malignancies involving both CD4+ (Sézary syndrome) and CD8+ (SPTCL) lineages, or both (ALLP).
Clinical • IO biomarker
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CD8 (cluster of differentiation 8) • CARD11 (Caspase Recruitment Domain Family Member 11) • HAVCR2 (Hepatitis A Virus Cellular Receptor 2) • CD4 (CD4 Molecule)
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CARD11 mutation • HAVCR2 expression
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cyclosporin A microemulsion • trimethoprim/sulfamethoxazole
3ms
Taken together, the in vitro and in vivo data for JNJ‑67856633 and JNJ-64264681 suggest that combination therapy can increase the anti-tumor effect of the monotherapies and provide a more sustained response, offering strong support for clinical investigation of the combination of these two novel agents. A phase 1b combination study is scheduled to initiate.
Combination therapy
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CD79B (CD79b Molecule) • CARD11 (Caspase Recruitment Domain Family Member 11) • IL2RA (Interleukin 2 receptor, alpha) • MALT1 (MALT1 Paracaspase) • CD4 (CD4 Molecule) • FOXP3 (Forkhead Box P3)
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CARD11 mutation • CD79B mutation • CD79B mutation
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JNJ-67856633 • JNJ-64264681
4ms
Journal
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CARD11 (Caspase Recruitment Domain Family Member 11)
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CARD11 mutation
4ms
This was associated with improved in vivo potency in a mechanistic model of B cell activation. The optimized compound led to tumor regression in a CARD11 mutant ABC-DLBCL lymphoma xenograft model.
Preclinical • Journal
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CARD11 (Caspase Recruitment Domain Family Member 11)
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CARD11 mutation
4ms
CARD11 mutation is associated with longer OS and a better prognosis after ICI treatment. Therefore, the CARD11 gene can be used as a biomarker for predicting the efficacy of ICIs in SKCM patients.
Journal • Checkpoint inhibition • IO biomarker
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CARD11 (Caspase Recruitment Domain Family Member 11)
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CARD11 mutation
6ms
He will further discuss the underlying molecular and pathophysiological mechanisms of these different mutations and their association with clinical phenotypes. Sponsor: Joint Session: Scientific Committee on Blood Disorders in Childhood & Scientific Committee on Immunology and Host Defense
Clinical
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IKZF1 (IKAROS Family Zinc Finger 1) • PIK3CD (Phosphatidylinositol-4 5-Bisphosphate 3-Kinase Catalytic Subunit Delta) • CARD11 (Caspase Recruitment Domain Family Member 11) • PIK3CG (Phosphatidylinositol-4,5-Bisphosphate 3-Kinase Catalytic Subunit Gamma) • GATA2 (GATA Binding Protein 2)
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CARD11 mutation • IKZF1 mutation
7ms
Importantly, mouse-based mutant MyD88- and CARD11-derived signatures marked DLBCL subgroups exhibiting mirroring phenotypes with respect to the triad of senescence induction, macrophage attraction, and evasion of cytotoxic T-cell immunity. Complementing genomic subclassification approaches, our functional, cross-species investigation unveils pathogenic principles and therapeutic vulnerabilities applicable to and testable in human DLBCL subsets that may inform future personalized treatment strategies.
Journal • PD(L)-1 Biomarker
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PD-L1 (Programmed death ligand 1) • MYD88 (MYD88 Innate Immune Signal Transduction Adaptor) • CD79B (CD79b Molecule) • CARD11 (Caspase Recruitment Domain Family Member 11)
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CARD11 mutation
7ms
Taken together, our findings support use of cytogenetic profiles combined with GPS and subsequent use of an AI system to predict MYC status in DLBCL.
MYD88 (MYD88 Innate Immune Signal Transduction Adaptor) • CD79B (CD79b Molecule) • CARD11 (Caspase Recruitment Domain Family Member 11) • FOXP1 • PIM1 (Pim-1 Proto-Oncogene)
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MYC rearrangement • CARD11 mutation • CD79B mutation • PIM1 mutation
7ms
In summary, the novel, selective, small-molecule MALT1 inhibitor CTX-177 demonstrated preclinical efficacy along with target engagement in several lymphoma models with activated antigen receptor signaling and NF-κB pathway. Our results underscore the preclinical therapeutic potential of CTX-177 as a single-agent or in combination with other inhibitors like BTK inhibitor for the treatment of malignant lymphomas.
Preclinical
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CARD11 (Caspase Recruitment Domain Family Member 11) • IRF4 (Interferon regulatory factor 4)
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CARD11 mutation
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CTX-177
7ms
In addition to ABC-DLBCL, a MALT1 inhibitor is a promising treatment option for patients with CLL, MCL, WM, and FL whose tumors have been shown to be sensitive to inhibition of BTK. MALT lymphomas, characterized by MALT1 and BCL10 translocation, represent another attractive target for MALT1 inhibition.
IO biomarker
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IL6 (Interleukin 6) • CD79B (CD79b Molecule) • CARD11 (Caspase Recruitment Domain Family Member 11) • IL2RA (Interleukin 2 receptor, alpha) • IL10 (Interleukin 10) • FOXP3 (Forkhead Box P3)
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CARD11 mutation • CD79B mutation
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JNJ-67856633
7ms
Among the 15 pts who progressed on acalabrutinib, 14 pts received systemic therapies for MCL [eight received ibrutinib based therapies (4 non responders, 3 achieved CR and 1 were PR and all pts progressed subsequently), 5 got chemo-immunotherapy, bortezomib, lenalidomide and progressed and one pt did not receive any treatment and was lost to follow up and died. In this small cohort, we did not observe BTK mutations associated with acalabrutinib resistance in MCL pts. Further studies are ongoing to determine acalabrutinib resistance mechanism in MCL.
IO biomarker
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TP53 (Tumor protein P53) • NOTCH1 (Notch 1) • MYD88 (MYD88 Innate Immune Signal Transduction Adaptor) • MYCN (MYCN Proto-Oncogene BHLH Transcription Factor) • KMT2C (Lysine Methyltransferase 2C) • B2M (Beta-2-microglobulin) • CARD11 (Caspase Recruitment Domain Family Member 11) • PLCG2 (Phospholipase C Gamma 2) • NOTCH3 (Notch Receptor 3)
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TP53 mutation • ATM mutation • CARD11 mutation • BTK mutation • MSLN positive
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ibrutinib • Revlimid (lenalidomide) • bortezomib • Calquence (acalabrutinib)
7ms
The clonality assay using the TCR repertoires exhibited an oligoclonal pattern in 4 of 4 splenic CD4+ cells, and 2 of 2 LNs CD4+ cells from compound mice. These results suggest that CARD11 mutant-induced NFkB activation and constant HBZ expression may have similar effects, such as T-cell infiltration into organs and LN adenopathy, and that the simultaneous occurrence of both may have additive effects.
Combination therapy • IO biomarker
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CARD11 (Caspase Recruitment Domain Family Member 11) • CD4 (CD4 Molecule) • FOXP3 (Forkhead Box P3)
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CARD11 mutation
8ms
He will further discuss the underlying molecular and pathophysiological mechanisms of these different mutations and their association with clinical phenotypes. Sponsor: Joint Session: Scientific Committee on Blood Disorders in Childhood & Scientific Committee on Immunology and Host Defense
Clinical
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IKZF1 (IKAROS Family Zinc Finger 1) • PIK3CD (Phosphatidylinositol-4 5-Bisphosphate 3-Kinase Catalytic Subunit Delta) • CARD11 (Caspase Recruitment Domain Family Member 11) • PIK3CG (Phosphatidylinositol-4,5-Bisphosphate 3-Kinase Catalytic Subunit Gamma) • GATA2 (GATA Binding Protein 2)
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CARD11 mutation • IKZF1 mutation
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