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Disease Info Card
Nodular Sclerosis Classical Hodgkin Lymphoma
Information about Nodular Sclerosis Classical Hodgkin Lymphoma: characteristics, related genes and pathways, plus antibodies you can use for research. This page is being enriched constantly, if you see some information you would like this page to include please send your suggestions to us.
Overview of Nodular Sclerosis Classical Hodgkin Lymphoma
Most recent studies have shown that Nodular Sclerosis Classical Hodgkin Lymphoma shares some biological mechanisms with b-cell-lymphomas, childhood-hodgkin-lymphoma, classical-hodgkins-lymphoma, complete-hearing-loss, diffuse-large-b-cell-lymphoma, epstein-barr-virus-infections, hodgkin-disease, hyperplasia, leukemia, lymphoma, lymphoma-follicular, lymphoma-non-hodgkin, malignant-neoplasms, malignant-paraganglionic-neoplasm, mediastinal-neoplasms, mixed-cellularity-hodgkin-lymphoma, neoplasms, sclerosis, sensorineural-hearing-loss-(disorder), t-cell-lymphoma.
Among the many pathways, these few ones have gauged particular interests from scientists studying Nodular Sclerosis Classical Hodgkin Lymphoma, and have been seen in publications frequently: Angiogenesis, Cell Activation, Cell Adhesion, Cell Cycle, Cell Death, Cell Growth, Cell Proliferation, Coagulation, Cytokine Secretion, Dna Methylation, Drug Resistance, Hypersensitivity, Immune Response, Localization, Methylation, Mitosis, Oncogenesis, Pathogenesis, Reflex, Secretion
Quite a number of genes have been found to play important roles in Nodular Sclerosis Classical Hodgkin Lymphoma, such as CTLA4, FMN1, FOXC2, FUT4, GJB2, GJB6, GNL3, HES1, HLA-DQA1, HMGCL, HTT, KRAS, KRT20, LIPC, MS4A1, NOD2, PDLIM7, PTPRC, SEPSECS, TNFRSF8. See what Boster has to offer for the research of these genes by clicking the gene name links below and view a more detailed info card/product listing for that gene.
In a later update, we will include information such as current drugs and therapy solutions as well as on-going and past clinical trials for this disease. Plesae stay updated.