Description of PTPRG genetic variants identified in a cohort of Chronic Myeloid Leukemia patients and their ability to influence response to Tyrosine kinase Inhibitors

<p dir="ltr">Tyrosine kinase inhibitors (TKIs) have remarkably transformed Ph+ chronic myeloid leukemia (CML) management; however, TKI resistance remains a major clinical challenge. Mutations in <i>BCR-ABL1</i> are well studied but fail to explain 20–40% of resistant case...

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Main Author: Mohamed A. Ismail (418629) (author)
Other Authors: Gheyath K. Nasrallah (9200525) (author), Maria Monne (4166524) (author), Ali AlSayab (17150992) (author), Mohamed A. Yassin (8361183) (author), Govindarajulu Varadharaj (14778931) (author), Salma Younes (6424865) (author), Claudio Sorio (212799) (author), Richard Cook (70389) (author), Helmout Modjtahedi (532099) (author), Nader I. Al-Dewik (14152884) (author)
Published: 2022
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author Mohamed A. Ismail (418629)
author2 Gheyath K. Nasrallah (9200525)
Maria Monne (4166524)
Ali AlSayab (17150992)
Mohamed A. Yassin (8361183)
Govindarajulu Varadharaj (14778931)
Salma Younes (6424865)
Claudio Sorio (212799)
Richard Cook (70389)
Helmout Modjtahedi (532099)
Nader I. Al-Dewik (14152884)
author2_role author
author
author
author
author
author
author
author
author
author
author_facet Mohamed A. Ismail (418629)
Gheyath K. Nasrallah (9200525)
Maria Monne (4166524)
Ali AlSayab (17150992)
Mohamed A. Yassin (8361183)
Govindarajulu Varadharaj (14778931)
Salma Younes (6424865)
Claudio Sorio (212799)
Richard Cook (70389)
Helmout Modjtahedi (532099)
Nader I. Al-Dewik (14152884)
author_role author
dc.creator.none.fl_str_mv Mohamed A. Ismail (418629)
Gheyath K. Nasrallah (9200525)
Maria Monne (4166524)
Ali AlSayab (17150992)
Mohamed A. Yassin (8361183)
Govindarajulu Varadharaj (14778931)
Salma Younes (6424865)
Claudio Sorio (212799)
Richard Cook (70389)
Helmout Modjtahedi (532099)
Nader I. Al-Dewik (14152884)
dc.date.none.fl_str_mv 2022-03-01T00:00:00Z
dc.identifier.none.fl_str_mv 10.1016/j.gene.2021.146101
dc.relation.none.fl_str_mv https://figshare.com/articles/journal_contribution/Description_of_PTPRG_genetic_variants_identified_in_a_cohort_of_Chronic_Myeloid_Leukemia_patients_and_their_ability_to_influence_response_to_Tyrosine_kinase_Inhibitors/24314257
dc.rights.none.fl_str_mv CC BY 4.0
info:eu-repo/semantics/openAccess
dc.subject.none.fl_str_mv Biological sciences
Genetics
Biomedical and clinical sciences
Cardiovascular medicine and haematology
Clinical sciences
Chronic Myeloid Leukemia
Protein Tyrosine Phosphatase Receptor Type G
BCR-ABL1
Single Nucleotide Polymorphisms
Tyrosine Kinase Inhibitors
Therapeutic Modalities
dc.title.none.fl_str_mv Description of PTPRG genetic variants identified in a cohort of Chronic Myeloid Leukemia patients and their ability to influence response to Tyrosine kinase Inhibitors
dc.type.none.fl_str_mv Text
Journal contribution
info:eu-repo/semantics/publishedVersion
text
contribution to journal
description <p dir="ltr">Tyrosine kinase inhibitors (TKIs) have remarkably transformed Ph+ chronic myeloid leukemia (CML) management; however, TKI resistance remains a major clinical challenge. Mutations in <i>BCR-ABL1</i> are well studied but fail to explain 20–40% of resistant cases, suggesting the activation of alternative, <i>BCR-ABL1</i>-independent pathways. Protein Tyrosine Phosphatase Receptor Gamma (<i>PTPRG</i>), a tumor suppressor, was found to be well expressed in CML patients responsive to TKIs and remained at low level in resistant patients. In this study, we aimed to identify genetic variants in <i>PTPRG</i> that could potentially modulate TKIs response in CML patients. DNA was extracted from peripheral blood samples collected from two CML cohorts (Qatar and Italy) and targeted exome sequencing was performed. Among 31 CML patients, six were TKI-responders and 25 were TKI-non-responsive. Sequencing identified ten variants, seven were annotated and three were novel SNPs (c.1602_1603insC, c.85+14412delC, and c.2289-129delA). Among them, five variants were identified in 15 resistant cases. Of these, one novel exon variant (c.1602_1603insC), c.841-29C>T (rs199917960) and c.1378-224A>G (rs2063204) were found to be significantly different between the resistant cases compared to responders. Our findings suggest that <i>PTPRG</i> variants may act as an indirect resistance mechanism of <i>BCR-ABL1</i> to affect TKI treatment.</p><h2>Other Information</h2><p dir="ltr">Published in: Gene<br>License: <a href="http://creativecommons.org/licenses/by/4.0/" target="_blank">http://creativecommons.org/licenses/by/4.0/</a><br>See article on publisher's website: <a href="https://dx.doi.org/10.1016/j.gene.2021.146101" target="_blank">https://dx.doi.org/10.1016/j.gene.2021.146101</a></p>
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identifier_str_mv 10.1016/j.gene.2021.146101
network_acronym_str Manara2
network_name_str Manara2
oai_identifier_str oai:figshare.com:article/24314257
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spelling Description of PTPRG genetic variants identified in a cohort of Chronic Myeloid Leukemia patients and their ability to influence response to Tyrosine kinase InhibitorsMohamed A. Ismail (418629)Gheyath K. Nasrallah (9200525)Maria Monne (4166524)Ali AlSayab (17150992)Mohamed A. Yassin (8361183)Govindarajulu Varadharaj (14778931)Salma Younes (6424865)Claudio Sorio (212799)Richard Cook (70389)Helmout Modjtahedi (532099)Nader I. Al-Dewik (14152884)Biological sciencesGeneticsBiomedical and clinical sciencesCardiovascular medicine and haematologyClinical sciencesChronic Myeloid LeukemiaProtein Tyrosine Phosphatase Receptor Type GBCR-ABL1Single Nucleotide PolymorphismsTyrosine Kinase InhibitorsTherapeutic Modalities<p dir="ltr">Tyrosine kinase inhibitors (TKIs) have remarkably transformed Ph+ chronic myeloid leukemia (CML) management; however, TKI resistance remains a major clinical challenge. Mutations in <i>BCR-ABL1</i> are well studied but fail to explain 20–40% of resistant cases, suggesting the activation of alternative, <i>BCR-ABL1</i>-independent pathways. Protein Tyrosine Phosphatase Receptor Gamma (<i>PTPRG</i>), a tumor suppressor, was found to be well expressed in CML patients responsive to TKIs and remained at low level in resistant patients. In this study, we aimed to identify genetic variants in <i>PTPRG</i> that could potentially modulate TKIs response in CML patients. DNA was extracted from peripheral blood samples collected from two CML cohorts (Qatar and Italy) and targeted exome sequencing was performed. Among 31 CML patients, six were TKI-responders and 25 were TKI-non-responsive. Sequencing identified ten variants, seven were annotated and three were novel SNPs (c.1602_1603insC, c.85+14412delC, and c.2289-129delA). Among them, five variants were identified in 15 resistant cases. Of these, one novel exon variant (c.1602_1603insC), c.841-29C>T (rs199917960) and c.1378-224A>G (rs2063204) were found to be significantly different between the resistant cases compared to responders. Our findings suggest that <i>PTPRG</i> variants may act as an indirect resistance mechanism of <i>BCR-ABL1</i> to affect TKI treatment.</p><h2>Other Information</h2><p dir="ltr">Published in: Gene<br>License: <a href="http://creativecommons.org/licenses/by/4.0/" target="_blank">http://creativecommons.org/licenses/by/4.0/</a><br>See article on publisher's website: <a href="https://dx.doi.org/10.1016/j.gene.2021.146101" target="_blank">https://dx.doi.org/10.1016/j.gene.2021.146101</a></p>2022-03-01T00:00:00ZTextJournal contributioninfo:eu-repo/semantics/publishedVersiontextcontribution to journal10.1016/j.gene.2021.146101https://figshare.com/articles/journal_contribution/Description_of_PTPRG_genetic_variants_identified_in_a_cohort_of_Chronic_Myeloid_Leukemia_patients_and_their_ability_to_influence_response_to_Tyrosine_kinase_Inhibitors/24314257CC BY 4.0info:eu-repo/semantics/openAccessoai:figshare.com:article/243142572022-03-01T00:00:00Z
spellingShingle Description of PTPRG genetic variants identified in a cohort of Chronic Myeloid Leukemia patients and their ability to influence response to Tyrosine kinase Inhibitors
Mohamed A. Ismail (418629)
Biological sciences
Genetics
Biomedical and clinical sciences
Cardiovascular medicine and haematology
Clinical sciences
Chronic Myeloid Leukemia
Protein Tyrosine Phosphatase Receptor Type G
BCR-ABL1
Single Nucleotide Polymorphisms
Tyrosine Kinase Inhibitors
Therapeutic Modalities
status_str publishedVersion
title Description of PTPRG genetic variants identified in a cohort of Chronic Myeloid Leukemia patients and their ability to influence response to Tyrosine kinase Inhibitors
title_full Description of PTPRG genetic variants identified in a cohort of Chronic Myeloid Leukemia patients and their ability to influence response to Tyrosine kinase Inhibitors
title_fullStr Description of PTPRG genetic variants identified in a cohort of Chronic Myeloid Leukemia patients and their ability to influence response to Tyrosine kinase Inhibitors
title_full_unstemmed Description of PTPRG genetic variants identified in a cohort of Chronic Myeloid Leukemia patients and their ability to influence response to Tyrosine kinase Inhibitors
title_short Description of PTPRG genetic variants identified in a cohort of Chronic Myeloid Leukemia patients and their ability to influence response to Tyrosine kinase Inhibitors
title_sort Description of PTPRG genetic variants identified in a cohort of Chronic Myeloid Leukemia patients and their ability to influence response to Tyrosine kinase Inhibitors
topic Biological sciences
Genetics
Biomedical and clinical sciences
Cardiovascular medicine and haematology
Clinical sciences
Chronic Myeloid Leukemia
Protein Tyrosine Phosphatase Receptor Type G
BCR-ABL1
Single Nucleotide Polymorphisms
Tyrosine Kinase Inhibitors
Therapeutic Modalities