hg u133 plus 2.0 microarray assay (Thermo Fisher)
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hg u133 plus 2.0 microarray assay
Hg U133 Plus 2.0 Microarray Assay, supplied by Thermo Fisher, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/hg+u133+plus+2%2E0+microarray+assay/pm39305307-77-22-21
Average 90 stars, based on 1 article reviews
Hg U133 Plus 2.0 Microarray Assay, supplied by Thermo Fisher, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/hg+u133+plus+2%2E0+microarray+assay/pm39305307-77-22-21
Average 90 stars, based on 1 article reviews
hg u133 plus 2.0 microarray assay - by Bioz Stars,
2026-09
90/100 stars
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Expressing:Article Title: Distinct pathway activities are associated with prognosis and response to bortezomib-containing treatment in MCL1-M based molecular subtypes of multiple myeloma. Article Snippet: 1 Department of Biology, Beijing Key Laboratory of Gene Resource and Molecular Development, School of Life Sciences, Key Laboratory of Cell Proliferation and Regulation Biology, School of Life Sciences, Ministry of Education, Beijing Normal University, Beijing, China 2 Clinical Research Center, The Affiliated Hospital of Guizhou Medical University, Guiyang, China 3 Department of Hematology, Beijing Chao-Yang Hospital Capital Medical University, Beijing, China 4 College of Life Sciences, Sichuan Normal University, Chengdu, China 5 Department of Pathology, Capital Medical University Sanbo Brain Hospital, Beijing, China 6 Institute of Biomedical Sciences, Henan Academy of Sciences, Zhengzhou, China 7 Department of Physiology, University of Sindh, Jamshoro, Pakistan 8 Department of Hematology, Changzhou Second People’s Hospital of Nanjing Medical University, Changzhou, China Abstract Multiple myeloma (MM) is the second most prevalent hematological malignancy and remains incurable with remarkable heterogeneity in prognosis and treatment response across the patients.. Clinical diagnosis and the existing molecular classification systems are inadequate for predicting treatment responses.. Based on the convergence between plasma cell development and MM pathogenesis, we identified a gene co-expression module centered on the plasma cell survival regulator MCL1 (MCL1 module, MCL1-M) in the transcriptomes of pre-treated MM, which enabled stratification of MM patients into MCL1-M high and MCL1-M low molecular subtypes with subtype-specific prognosis and response to bortezomib-containing treatment. Microarray:Article Title: Distinct pathway activities are associated with prognosis and response to bortezomib-containing treatment in MCL1-M based molecular subtypes of multiple myeloma. Article Snippet: 1 Department of Biology, Beijing Key Laboratory of Gene Resource and Molecular Development, School of Life Sciences, Key Laboratory of Cell Proliferation and Regulation Biology, School of Life Sciences, Ministry of Education, Beijing Normal University, Beijing, China 2 Clinical Research Center, The Affiliated Hospital of Guizhou Medical University, Guiyang, China 3 Department of Hematology, Beijing Chao-Yang Hospital Capital Medical University, Beijing, China 4 College of Life Sciences, Sichuan Normal University, Chengdu, China 5 Department of Pathology, Capital Medical University Sanbo Brain Hospital, Beijing, China 6 Institute of Biomedical Sciences, Henan Academy of Sciences, Zhengzhou, China 7 Department of Physiology, University of Sindh, Jamshoro, Pakistan 8 Department of Hematology, Changzhou Second People’s Hospital of Nanjing Medical University, Changzhou, China Abstract Multiple myeloma (MM) is the second most prevalent hematological malignancy and remains incurable with remarkable heterogeneity in prognosis and treatment response across the patients.. Clinical diagnosis and the existing molecular classification systems are inadequate for predicting treatment responses.. Based on the convergence between plasma cell development and MM pathogenesis, we identified a gene co-expression module centered on the plasma cell survival regulator MCL1 (MCL1 module, MCL1-M) in the transcriptomes of pre-treated MM, which enabled stratification of MM patients into MCL1-M high and MCL1-M low molecular subtypes with subtype-specific prognosis and response to bortezomib-containing treatment. |