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BIOMARKER:

B2M mutation

i
Other names: B2M, Beta-2-microglobulin
Entrez ID:
Related biomarkers:
3ms
Eighteen patients received ICB with pembrolizumab and one patient with nivolumab/ipilimumab. Among metastatic MSI GI cancers, B2M-mutant tumors represent a biologically distinct disease with distinct metastatic patterns. To assess ICB response in B2M-mutant MSI cancer patients, future studies need to account for the fact that baseline survival of patients with B2M-mutant MSI cancer may be longer than of patients with B2M-wild type MSI cancer.
Journal • PD(L)-1 Biomarker
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B2M (Beta-2-microglobulin)
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B2M mutation
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Keytruda (pembrolizumab) • Opdivo (nivolumab) • Yervoy (ipilimumab)
4ms
We highlight the role of tumor associated effector CD4+ T cells in pre-clinical models and patients with impaired APM. Overall, our findings highlight that the absence of B2M in MMRd cancers, does not prevent clinic response to immune checkpoint blockade.
Preclinical • Mismatch repair • PD(L)-1 Biomarker • IO biomarker
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CD8 (cluster of differentiation 8) • MLH1 (MutL homolog 1) • B2M (Beta-2-microglobulin) • CTLA4 (Cytotoxic T-Lymphocyte Associated Protein 4) • CD4 (CD4 Molecule)
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MSI-H/dMMR • B2M mutation • MLH1 deletion
10ms
Our findings thus contribute to an improved understanding of the biological behavior of multiple ENI and provide a clinical rationale for targeting ENI in DLBCL.
Journal
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ARID1A (AT-rich interaction domain 1A) • MYD88 (MYD88 Innate Immune Signal Transduction Adaptor) • CXCR4 (Chemokine (C-X-C motif) receptor 4) • CD79B (CD79b Molecule) • B2M (Beta-2-microglobulin) • FOXO1 (Forkhead box O1) • PIM1 (Pim-1 Proto-Oncogene)
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ARID1A mutation • MYD88 mutation • CD79B mutation • B2M mutation • PIM1 mutation
11ms
For the first time, our data have unveiled the nature of the T cell repertoire in cHL at single cell resolution. Our results reveal a recurrent pattern of clonal expansion within effector CD8+ cells, which may be the HRS antigen-specific T cells that mediate response to PD-1 blockade. This hypothesis requires confirmation through similar analyses of pre- and on-treatment biopsies of cHL patients receiving anti-PD-1 therapy.
Clinical • PD(L)-1 Biomarker • IO biomarker
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PD-L1 (Programmed death ligand 1) • CD8 (cluster of differentiation 8) • CD19 (CD19 Molecule) • IFNG (Interferon, gamma) • B2M (Beta-2-microglobulin) • HAVCR2 (Hepatitis A Virus Cellular Receptor 2) • GZMA (Granzyme A)
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PD-L1 overexpression • PD-L1 amplification • B2M mutation
12ms
Importantly, certain outlier mutations are common in MSI cancers despite being related to frameshift peptides with functionally confirmed immunogenicity, suggesting a possible driver role during MSI tumor evolution. Neoantigens resulting from shared mutations represent promising vaccine candidates for prevention of MSI cancers.
Journal
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MSI (Microsatellite instability) • B2M (Beta-2-microglobulin)
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B2M mutation
12ms
Methylation of the promoter region of the B2M gene was observed in one patient with MSI-H colorectal cancer. Detection of genetic and epigenetic changes in B2M gene could be important in personalized therapy for CRC patients as these changes may be one of the mechanisms of secondary resistance of MSI positive tumors to immunotherapy.
Journal • MSi-H Biomarker
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BRAF (B-raf proto-oncogene) • KRAS (KRAS proto-oncogene GTPase) • MSI (Microsatellite instability) • B2M (Beta-2-microglobulin)
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KRAS mutation • MSI-H/dMMR • BRAF mutation • B2M mutation • TILs
over1year
The quantitative and qualitative differences clearly indicate a distinct biology of sporadic and hereditary MSI tumors. Clinically, these findings underline the need for differentiating sporadic and hereditary tumors in basic science studies and clinical trials, including trials evaluating immune checkpoint blockade therapy in MSI tumors.
Review • Journal
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MSI (Microsatellite instability) • B2M (Beta-2-microglobulin)
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MSI-H/dMMR • B2M mutation
over1year
Next, we investigated mutation landscape in patients with wild-type (WT) TP53 (n = 58) and found that patients harboring MYD88 L265P had significantly inferior TTP than those with WT or non-265P (P = 0.046). This study reveals the mutation spectrum of treatment-naive Chinese DLBCL patients.It also confirms the clinical significance of TP53 mutations and indicates the prognostic value of MYD88 L265P in TP53 WT patients.
Clinical • Journal
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TP53 (Tumor protein P53) • BCL2 (B-cell CLL/lymphoma 2) • MYD88 (MYD88 Innate Immune Signal Transduction Adaptor) • KMT2D (Lysine Methyltransferase 2D) • B2M (Beta-2-microglobulin)
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TP53 mutation • B2M mutation
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Rituxan (rituximab)
over1year
(1) Targeting EGFR L858R mutation in patients with HLA-A*33:03 allele appeared to be valuable for the neoantigen-based vaccine designed for Chinese NSCLC patients. (2) The specific immunogenicity of L858R seemed to be little influenced by B2M mutation and HLA-I LOH which were important factors for neoantigen presentation. (3) High pDC and low neutrophils infiltration might contribute to the inhibitive microenvironment associated with L858R mutation.
Clinical
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EGFR (Epidermal growth factor receptor) • B2M (Beta-2-microglobulin)
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EGFR mutation • EGFR L858R • EGFR exon 19 deletion • B2M mutation • EGFR L858R + EGFR exon 19 deletion
over1year
Here, we describe a patient with BRAF-V600E-positive metastatic melanoma who was sequentially treated with BRAF/MEK inhibitors (dabrafenib/trametinib) and checkpoint inhibitor immunotherapy (nivolumab, followed by pembrolizumab). After the emergence of resistance, whole exome sequencing was performed, implicating MAP2K2 and B2M mutations in loss of response to anti-BRAF/MEK and anti-PD1 therapies, respectively.
Journal • Checkpoint inhibition • PD(L)-1 Biomarker
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BRAF (B-raf proto-oncogene) • B2M (Beta-2-microglobulin)
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BRAF V600 • B2M mutation
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Keytruda (pembrolizumab) • Opdivo (nivolumab) • Mekinist (trametinib) • Tafinlar (dabrafenib)