<HashMap><database>biostudies-literature</database><scores/><additional><omics_type>Unknown</omics_type><volume>21(12)</volume><submitter>Iqbal Z</submitter><pubmed_abstract>&lt;h4>Objective&lt;/h4>BCR-ABL fusion oncogene is the hallmark of chronic myeloid leukemia (CML), causing genomic instability which leads to accumulation of mutations in BCR-ABL as well as other genes. BCR-ABL mutations are the cause of tyrosine kinase inhibitors (TKIs) resistance in CML. Recently, compound BCR-ABL mutations have been reported to resist all FDA approved TKIs. Therefore, finding novel compound BCR-ABL mutations can help and clinically manage CML. Therefore, our objective was to find out novel drug-resistant compound BCR-ABL mutations in CML and carry out their protein modelling studies.&lt;h4>Methodology&lt;/h4>Peripheral blood samples were collected from ten imatinib resistant CML patients receiving nilotinib treatment. BCR-ABL transcript mutations were investigated by employing capi</pubmed_abstract><journal>Asian Pacific journal of cancer prevention : APJCP</journal><pagination>3517-3526</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC8046299</full_dataset_link><repository>biostudies-literature</repository><pubmed_title>Discovery and Protein Modeling Studies of Novel Compound Mutations Causing Resistance to Multiple Tyrosine Kinase Inhibitors in Chronic Myeloid Leukemia.</pubmed_title><pmcid>PMC8046299</pmcid><pubmed_authors>Akram AM</pubmed_authors><pubmed_authors>Shah IH</pubmed_authors><pubmed_authors>Absar M</pubmed_authors><pubmed_authors>Karim S</pubmed_authors><pubmed_authors>Iqbal J</pubmed_authors><pubmed_authors>Jameel A</pubmed_authors><pubmed_authors>Alanazi N</pubmed_authors><pubmed_authors>Khalid AM</pubmed_authors><pubmed_authors>Aljarrah K</pubmed_authors><pubmed_authors>Sabar MF</pubmed_authors><pubmed_authors>Iqbal Z</pubmed_authors><pubmed_authors>Mahmood A</pubmed_authors><pubmed_authors>Akhtar T</pubmed_authors><pubmed_authors>Khalid M</pubmed_authors><pubmed_authors>Mirza Z</pubmed_authors><pubmed_authors>Aleem A</pubmed_authors><pubmed_authors>Iqbal M</pubmed_authors><pubmed_authors>Rasool M</pubmed_authors></additional><is_claimable>false</is_claimable><name>Discovery and Protein Modeling Studies of Novel Compound Mutations Causing Resistance to Multiple Tyrosine Kinase Inhibitors in Chronic Myeloid Leukemia.</name><description>&lt;h4>Objective&lt;/h4>BCR-ABL fusion oncogene is the hallmark of chronic myeloid leukemia (CML), causing genomic instability which leads to accumulation of mutations in BCR-ABL as well as other genes. BCR-ABL mutations are the cause of tyrosine kinase inhibitors (TKIs) resistance in CML. Recently, compound BCR-ABL mutations have been reported to resist all FDA approved TKIs. Therefore, finding novel compound BCR-ABL mutations can help and clinically manage CML. Therefore, our objective was to find out novel drug-resistant compound BCR-ABL mutations in CML and carry out their protein modelling studies.&lt;h4>Methodology&lt;/h4>Peripheral blood samples were collected from ten imatinib resistant CML patients receiving nilotinib treatment. BCR-ABL transcript mutations were investigated by employing capi</description><dates><release>2020-01-01T00:00:00Z</release><publication>2020 Dec</publication><modification>2025-04-19T17:04:02.214Z</modification><creation>2022-02-09T16:04:09.812Z</creation></dates><accession>S-EPMC8046299</accession><cross_references><pubmed>33369447</pubmed><doi>10.31557/APJCP.2020.21.12.3517</doi></cross_references></HashMap>