<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Aktas Samur A</submitter><funding>U.S. Department of Health &amp; Human Services | NIH | NCI | Division of Cancer Epidemiology and Genetics, National Cancer Institute (National Cancer Institute Division of Cancer Epidemiology and Genetics)</funding><funding>Health Services Research and Development</funding><funding>Health Services Research and Development (VA Health Services Research and Development Service)</funding><funding>Paula and Rodger Riney foundation</funding><funding>U.S. Department of Health &amp;amp; Human Services | NIH | NCI | Division of Cancer Epidemiology and Genetics, National Cancer Institute</funding><funding>Paula and Rodger Riney foundation grant</funding><pagination>171</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC9763261</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>12(12)</volume><pubmed_abstract>Splicing changes are common in cancer and are associated with dysregulated splicing factors. Here, we analyzed RNA-seq data from 323 newly diagnosed multiple myeloma (MM) patients and described the alternative splicing (AS) landscape. We observed a large number of splicing pattern changes in MM cells compared to normal plasma cells (NPC). The most common events were alterations of mutually exclusive exons and exon skipping. Most of these events were observed in the absence of overall changes in gene expression and often impacted the coding potential of the alternatively spliced genes. To understand the molecular mechanisms driving frequent aberrant AS, we investigated 115 splicing factors (SFs) and associated them with the AS events in MM. We observed that ~40% of SFs were dysregulated in </pubmed_abstract><journal>Blood cancer journal</journal><pubmed_title>In-depth analysis of alternative splicing landscape in multiple myeloma and potential role of dysregulated splicing factors.</pubmed_title><pmcid>PMC9763261</pmcid><funding_grant_id>P01CA155258</funding_grant_id><funding_grant_id>5I01BX001584</funding_grant_id><funding_grant_id>SPORE-P50CA100707</funding_grant_id><pubmed_authors>Lopez MA</pubmed_authors><pubmed_authors>Samur MK</pubmed_authors><pubmed_authors>Corre J</pubmed_authors><pubmed_authors>Aktas Samur A</pubmed_authors><pubmed_authors>Derebail S</pubmed_authors><pubmed_authors>Moreau P</pubmed_authors><pubmed_authors>Fulciniti M</pubmed_authors><pubmed_authors>Anderson KC</pubmed_authors><pubmed_authors>Parmigiani G</pubmed_authors><pubmed_authors>Munshi NC</pubmed_authors><pubmed_authors>Avet-Loiseau H</pubmed_authors><pubmed_authors>Magrangeas F</pubmed_authors><pubmed_authors>Minvielle S</pubmed_authors></additional><is_claimable>false</is_claimable><name>In-depth analysis of alternative splicing landscape in multiple myeloma and potential role of dysregulated splicing factors.</name><description>Splicing changes are common in cancer and are associated with dysregulated splicing factors. Here, we analyzed RNA-seq data from 323 newly diagnosed multiple myeloma (MM) patients and described the alternative splicing (AS) landscape. We observed a large number of splicing pattern changes in MM cells compared to normal plasma cells (NPC). The most common events were alterations of mutually exclusive exons and exon skipping. Most of these events were observed in the absence of overall changes in gene expression and often impacted the coding potential of the alternatively spliced genes. To understand the molecular mechanisms driving frequent aberrant AS, we investigated 115 splicing factors (SFs) and associated them with the AS events in MM. We observed that ~40% of SFs were dysregulated in </description><dates><release>2022-01-01T00:00:00Z</release><publication>2022 Dec</publication><modification>2025-04-26T09:44:54.174Z</modification><creation>2025-04-06T13:09:31.28Z</creation></dates><accession>S-EPMC9763261</accession><cross_references><pubmed>36535935</pubmed><doi>10.1038/s41408-022-00759-6</doi></cross_references></HashMap>