Integrative analysis reveals selective 9p24.1 amplification, increased PD-1 ligand expression, and further induction via JAK2 in nodular sclerosing Hodgkin lymphoma and primary mediastinal large…

By Michael R. Green, Stefano Monti, S. Rodig, P. Juszczyński, Treeve Currie, Evan O’Donnell, B. Chapuy, K. Takeyama, D. Neuberg, Todd R. Golub and 2 more. Blood, 2010

1,237 citations recorded by the source corpus.

Subfields: Gastroenterology, Pathology and Forensic Medicine

View Paper: https://www.semanticscholar.org/paper/34a1685d4ef555e7873471a32da1a32a57a4e94f

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

In Pathology and Forensic Medicine

Citations in the corpus

Nivolumab in Patients With Relapsed or Refractory Hematologic Malignancy: Preliminary Results of a Phase Ib Study. (2016, neutral): “Lipase increased 3 (4) 1 (1) Mucosal inflammation 3 (4) 1 (1) Stomatitis 2 (2) 1 (1) Diplopia 1 (1) 1 (1) Pneumonia 1 (1) 1 (1) Pulmonary embolism 1 (1) 1 (1) Rash pustular 1 (1) 1 (1) Sepsis 1 (1) 1 (1) ARDS† 1 (1) 1 (1) Hematologic Anemia 5 (6) 3 (4) Leukopenia 4 (5) 3 (4) Lymphopenia 3 (4) 1 (1) ”
Mechanisms controlling PD-L1 expression in cancer (2019, background): “1, and genomic rearrangements in this region, including amplification and translocation, have been shown to upregulate its expression, leading to enhanced immune escape as reported for cHL, primary mediastinal large B-cell lymphoma (PMBCL), NSCLC, squamous cell carcinoma, and gastric adenocarcinoma ”
Analysis of the Coding Genome of Diffuse Large B-Cell Lymphoma (2011, background): “More recently, chromosomal translocations involving CIITA and amplifications or rearrangements of the genes encoding for the CD274 (also known as PDL1) and CD273 (also known as PDL2) ligands have been reported as recurrent events in PMBC”
Combining Immunotherapy and Targeted Therapies in Cancer Treatment (2012, background): “and decrease tumour cell PDL1 expression at the level of transcriptio”
Radiation and Dual Checkpoint Blockade Activates Non-Redundant Immune Mechanisms in Cancer (2015, neutral): “To confirm specificity, the anti-PD-L1 antibody was validated by staining Hodgkin’s lymphoma cells 25 and placenta 26 .”
Constitutive AP-1 Activity and EBV Infection Induce PD-L1 in Hodgkin Lymphomas and Post-transplant Lymphoproliferative Disorders: Implications for Targeted Therapy (2012, methodology): “STAT activity in these cell lines was assessed by intracellular phospho-specific flow cytometry using anti-phospho (Tyr701)-STAT1, anti-phospho(Ser727)-STAT3, anti-phospho(Tyr694)-STAT5, and anti-phospho(Tyr641)-STAT6 (all from BD Biosciences), as previously described (9), with reference to fixed an”
PD-L1 Expression is Characteristic of a Subset of Aggressive B-Cell Lymphomas and Virus-Associated Malignancies (2013, neutral): “Cytokines, such as IFN-g , can upregulate PD-L1 on macrophages, potentially via the ISRE/IRF1 motif in the CD274 promoter (5, 34).”
PD-L1 Expression as a Predictive Biomarker in Cancer Immunotherapy (2015, background): “1 amplification, which contains an amplicon containing PD-L1, PD-L2, and JAK2 (31).”
Control of PD-L1 Expression by Oncogenic Activation of the AKT-mTOR Pathway in Non-Small Cell Lung Cancer. (2016, background): “Expressions of PD-L1 and PD-L2 (another ligand for PD-1) are increased inHodgkin's disease andmediastinal large Bcell lymphoma through chromosomal amplification (12).”
PD-L1 and PD-L2 Genetic Alterations Define Classical Hodgkin Lymphoma and Predict Outcome. (2016, neutral): “(%) Nodular sclerosis 93 (86) 25 (76) 39 (95) 29 (85) Mixed cellularity 12 (11) 8 (24) 1 (2) 3 (9) cHL, not otherwise specified 3 (3) — 1 (2) 2 (6)”
The 5th edition of the World Health Organization Classification of Haematolymphoid Tumours: Lymphoid Neoplasms (2022, background): “While the basic description has not changed substantially since the last century, WHO-HAEM5 includes a comprehensive section on the etiology and pathogenesis of CHL, in particular incorporating new data on the crucial role of the microenvironment in modulating the disease [172, 173].”