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BIOMARKER:

PD-L1 amplification

i
Other names: PD-L1, CD274, HPD-L1, PD-L1, B7H1, PDL1, Programmed death ligand 1, B7-H1, B7-H, PDCD1L1, PDCD1LG1, PDCD1 Ligand 1, B7 homolog 1, CD274 Antigen, Programmed cell death 1 ligand 1, CD274 molecule
Entrez ID:
Related biomarkers:
11ms
CRAFT: The NCT-PMO-1602 Phase II Trial (clinicaltrials.gov)
P2, N=72, Completed, German Cancer Research Center | Active, not recruiting --> Completed | N=175 --> 72 | Trial completion date: Jun 2025 --> Dec 2024 | Trial primary completion date: Jun 2025 --> Dec 2024
Trial completion • Enrollment change • Trial completion date • Trial primary completion date • Tumor mutational burden
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HER-2 (Human epidermal growth factor receptor 2) • BRAF (B-raf proto-oncogene) • ALK (Anaplastic lymphoma kinase) • PIK3CA (Phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha) • TMB (Tumor Mutational Burden) • RET (Ret Proto-Oncogene) • PTEN (Phosphatase and tensin homolog) • PI3K (Phosphoinositide 3-kinases)
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BRAF V600E • TMB-H • PD-L1 overexpression • HER-2 overexpression • HER-2 amplification • PIK3CA mutation • BRAF V600 • RET fusion • ALK rearrangement • BRAF V600K • AKT1 mutation • PD-L1 amplification • ALK rearrangement + PIK3CA mutation
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Herceptin (trastuzumab) • Tecentriq (atezolizumab) • Zelboraf (vemurafenib) • Alecensa (alectinib) • Perjeta (pertuzumab) • Cotellic (cobimetinib) • ipatasertib (RG7440) • Itovebi (inavolisib)
12ms
Evaluation of immune checkpoint inhibitor efficacy for solid tumors with CD274 (PD-L1 gene) amplification identified by comprehensive genomic profiling: retrospective study based on a nationwide database. (PubMed, J Immunother Cancer)
The number of patients with solid tumors positive for CD274 amplification in this analysis is the largest to date, and our results suggest that such gene amplification may be associated with the outcome of ICI treatment in such individuals. CD274 amplification identified by CGP may therefore be a predictor of ICI efficacy for solid tumors.
Retrospective data • Journal • Checkpoint inhibition • PD(L)-1 Biomarker • IO biomarker
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PD-L1 (Programmed death ligand 1)
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PD-L1 amplification
12ms
If it is a solid tumor target, then it may be a hematologic cancer target: Bridging the great divide. (PubMed, Med)
They include larotrectinib/entrectinib/repotrectinib (NTRK fusions), selpercatinib (RET fusions), dabrafenib/trametinib (BRAFV600E mutations), pembrolizumab/dostarlimab (microsatellite instability), pembrolizumab (high tumor mutational burden), and trastuzumab deruxtecan (HER2 3+ expression) (all solid cancers). Pemigatinib is approved for FGFR1-rearranged myeloid/lymphoid neoplasms...For example, BRAFV600E and IDH1/2 mutations; ALK, FGFR, and NTRK fusions; PD-L1 amplification; and CD70 antigens are druggable in both solid and blood malignancies by gene-/immune-targeted therapies/chimeric antigen receptor T cells. Future biomarker-based tissue-agnostic basket studies/approvals should bridge the great divide and include both solid and hematologic cancers.
Review • Journal • Tumor mutational burden • PD(L)-1 Biomarker • IO biomarker
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HER-2 (Human epidermal growth factor receptor 2) • PD-L1 (Programmed death ligand 1) • ALK (Anaplastic lymphoma kinase) • TMB (Tumor Mutational Burden) • MSI (Microsatellite instability) • RET (Ret Proto-Oncogene) • IDH1 (Isocitrate dehydrogenase (NADP(+)) 1) • IDH2 (Isocitrate Dehydrogenase (NADP(+)) 2) • FGFR1 (Fibroblast growth factor receptor 1) • CD70 (CD70 Molecule) • NTRK (Neurotrophic receptor tyrosine kinase)
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BRAF V600E • TMB-H • BRAF V600 • HER-2 expression • RET fusion • FGFR mutation • FGFR fusion • PD-L1 amplification • FGFR1 expression • IDH mutation + BRAF V600E • IDH mutation + NTRK fusion • NTRK fusion
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Keytruda (pembrolizumab) • Mekinist (trametinib) • Tafinlar (dabrafenib) • Vitrakvi (larotrectinib) • Rozlytrek (entrectinib) • Enhertu (fam-trastuzumab deruxtecan-nxki) • Retevmo (selpercatinib) • Jemperli (dostarlimab-gxly) • Pemazyre (pemigatinib) • Augtyro (repotrectinib)
12ms
CRAFT: the NCT-PMO-1602 Phase II Trial (clinicaltrials.gov)
P2, N=175, Active, not recruiting, German Cancer Research Center | Recruiting --> Active, not recruiting
Enrollment closed • Tumor mutational burden
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HER-2 (Human epidermal growth factor receptor 2) • BRAF (B-raf proto-oncogene) • ALK (Anaplastic lymphoma kinase) • PIK3CA (Phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha) • TMB (Tumor Mutational Burden) • RET (Ret Proto-Oncogene) • PTEN (Phosphatase and tensin homolog) • PI3K (Phosphoinositide 3-kinases)
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BRAF V600E • TMB-H • PD-L1 overexpression • HER-2 overexpression • HER-2 amplification • PIK3CA mutation • BRAF V600 • RET fusion • ALK rearrangement • BRAF V600K • AKT1 mutation • PD-L1 amplification • ALK rearrangement + PIK3CA mutation
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Herceptin (trastuzumab) • Tecentriq (atezolizumab) • Zelboraf (vemurafenib) • Alecensa (alectinib) • Perjeta (pertuzumab) • Cotellic (cobimetinib) • ipatasertib (RG7440) • Itovebi (inavolisib)
1year
Decoding the pathological and genomic profile of epithelial ovarian cancer. (PubMed, Sci Rep)
We observed that OC clinical and pathological characteristics of these patients from Tunisia were similar to those of Caucasian patients. We identified frequent CNA in this population that need to be confirmed in other sets from Africa.
Journal • BRCA Biomarker • PD(L)-1 Biomarker • IO biomarker
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HER-2 (Human epidermal growth factor receptor 2) • PD-L1 (Programmed death ligand 1) • HRD (Homologous Recombination Deficiency) • BRCA (Breast cancer early onset) • H2AX (H2A.X Variant Histone)
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PD-L1 expression • PD-L1 overexpression • HER-2 amplification • HER-2 expression • HRD • PD-L1 amplification • HER-2 amplification + PD-L1 expression
1year
Combination therapy • New P1/2 trial • Metastases
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EGFR (Epidermal growth factor receptor) • PD-L1 (Programmed death ligand 1) • ALK (Anaplastic lymphoma kinase)
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PD-L1 expression • EGFR mutation • ALK mutation • PD-L1 amplification
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PD-L1 IHC 22C3 pharmDx
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cisplatin • carboplatin • Enshuxing (enlonstobart)
1year
THE GENOMIC AND IMMUNE LANDSCAPE OF LIPOSARCOMA AND ITS SUBTYPES (CTOS 2024)
There is significant heterogeneity in the TME and mutational profiles across LPS subtypes. MLS has a particularly immune-cold TME shown by lower infiltration of lymphocytes, T cell-inflamed scores, and PDL1+ prevalence, while DDLS has a relatively immune-hot profile. These findings are critical to develop immune modulatory strategies for LPS and provide novel insights for future studies.
Tumor mutational burden • PD(L)-1 Biomarker • MSi-H Biomarker • IO biomarker
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PD-L1 (Programmed death ligand 1) • TP53 (Tumor protein P53) • PIK3CA (Phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha) • TMB (Tumor Mutational Burden) • RB1 (RB Transcriptional Corepressor 1) • CD8 (cluster of differentiation 8) • TERT (Telomerase Reverse Transcriptase) • CDK4 (Cyclin-dependent kinase 4) • ATRX (ATRX Chromatin Remodeler) • FUS (FUS RNA Binding Protein) • HMGA2 (High mobility group AT-hook 2) • DDIT3 (DNA-damage-inducible transcript 3)
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PD-L1 expression • TP53 mutation • TMB-H • MSI-H/dMMR • PIK3CA mutation • PD-L1 amplification • TERT mutation • TERT promoter mutation
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VENTANA PD-L1 (SP142) Assay
1year
Vogt-Koyanagi-Harada-Like Uveitis Secondary to Pembrolizumab in Metastatic Gastric Cancer: A Case Report and Review of the Literature. (PubMed, Case Rep Oncol)
She continues on trastuzumab maintenance, and most recent imaging shows no evidence of disease. Oncologists should be aware of VKH-like disease as a possible immune-related adverse event and seek urgent ophthalmologic consultation when such symptoms arise.
Review • Journal • Metastases
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HER-2 (Human epidermal growth factor receptor 2) • PD-L1 (Programmed death ligand 1)
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HER-2 amplification • PD-L1 amplification
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Keytruda (pembrolizumab) • Herceptin (trastuzumab) • 5-fluorouracil • leucovorin calcium
1year
HER2 amplification and PD-L1 expression in invasive stratified mucin-producing carcinoma of the cervix: a clinicopathological analysis of eighteen cases (PubMed, Zhonghua Bing Li Xue Za Zhi)
PD-L1 is positive in most of the ISMC cases, while HER2 is amplified or lowly expressed in a small portion of them. Thus, it is possible to treat ISMC patients with therapies targeting PD-L1 and therapy targeting HER2.
Retrospective data • Journal • PD(L)-1 Biomarker • IO biomarker
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HER-2 (Human epidermal growth factor receptor 2) • PD-L1 (Programmed death ligand 1)
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PD-L1 expression • HER-2 amplification • HER-2 expression • PD-L1 amplification • HER-2 amplification + PD-L1 expression • PD-L1 expression + HER-2 overexpression
1year
Molecular pathogenesis of adult T-cell leukemia/lymphoma (PubMed, Rinsho Ketsueki)
Here we summarize the current understanding of the molecular pathogenesis of ATLL, focusing on recent progress made by genetic, epigenetic, and single-cell analyses. These findings not only provide a deeper understanding of the molecular pathobiology of ATLL, but also have significant implications for diagnostic and therapeutic strategies.
Review • Journal • PD(L)-1 Biomarker • IO biomarker
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PD-L1 (Programmed death ligand 1) • CDKN2A (Cyclin Dependent Kinase Inhibitor 2A) • IRF4 (Interferon regulatory factor 4) • PRKCB (Protein Kinase C Beta)
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CDKN2A deletion • PD-L1 amplification • IRF4 mutation • PD-L1 mutation
1year
Dendritic Cell-Targeted Nanoparticles Enhance T Cell Activation and Antitumor Immune Responses by Boosting Antigen Presentation and Blocking PD-L1 Pathways. (PubMed, ACS Appl Mater Interfaces)
MSNP-MaN-PDL1bp/CLT treatment upregulated the levels of effector molecules such as granzyme B and proinflammatory cytokines (IFNγ and INFα) in the tumor tissue, indicating antitumoral T cell responses. This strategy of utilizing nanoparticles to trigger DC activation while promoting T cell stimulation can be used to amplify the antitumor T cell responses and represents a promising alternative to anti-PD-L1 immunotherapy.
Journal
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PD-1 (Programmed cell death 1) • IFNG (Interferon, gamma) • GZMB (Granzyme B) • MRC1 (Mannose Receptor C-Type 1) • CD80 (CD80 Molecule)
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PD-L1 expression • PD-L1 amplification • PD-1 positive
1year
MET and concomitant mutations in pulmonary adenocarcinomas (ECP 2024)
Oncogenic activation of genes-drivers are responsible for resistance mechanisms either understood has resistance to METtargeted therapies and as primary resistance. Recently it has been reported that PI3K pathway alteration is common in concomitancy with METex14 and believed that confers primary resistance to MET TKI. Early identification of alterations in MET kinase domain at diagnosis, is crucial for understanding progression and resistance mechanism, to develop novel therapies or to design treatment strategies in order to improve patient outcomes.
EGFR (Epidermal growth factor receptor) • HER-2 (Human epidermal growth factor receptor 2) • PD-L1 (Programmed death ligand 1) • KRAS (KRAS proto-oncogene GTPase) • ALK (Anaplastic lymphoma kinase) • TP53 (Tumor protein P53) • PIK3CA (Phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha) • MET (MET proto-oncogene, receptor tyrosine kinase) • PTEN (Phosphatase and tensin homolog) • SMO (Smoothened Frizzled Class Receptor)
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TP53 mutation • KRAS mutation • EGFR mutation • HER-2 amplification • PIK3CA mutation • HER-2 mutation • PTEN mutation • MET exon 14 mutation • ALK mutation • MET mutation • PD-L1 amplification • SMO mutation • PIK3CA mutation + PTEN mutation
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Oncomine Precision Assay