GSTM1 and GSTT1 double null genotypes determining cell fate and proliferation as potential risk factors of relapse in children with hematological malignancies after hematopoietic stem cell transplantation

Purpose This study aimed to retrospectively evaluate the genetic association of null variants of glutathione S-transferases GSTM1 and GSTT1 with relapse incidence in children with hematological malignancies (HMs) undergoing busulfan (BU)- containing allogeneic hematopoietic stem cell transplantation...

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Published inJournal of cancer research and clinical oncology Vol. 148; no. 1; pp. 71 - 86
Main Authors Jurkovic Mlakar, Simona, Uppugunduri, Satyanarayana Chakradhara Rao, Nava, Tiago, Mlakar, Vid, Golay, Hadrien, Robin, Shannon, Waespe, Nicolas, Rezgui, Mohamed Aziz, Chalandon, Yves, Boelens, Jaap Jan, Bredius, Robert G. M., Dalle, Jean-Hugues, Peters, Christina, Corbacioglu, Selim, Bittencourt, Henrique, Krajinovic, Maja, Ansari, Marc
Format Journal Article
LanguageEnglish
Published Berlin/Heidelberg Springer Berlin Heidelberg 01.01.2022
Springer Nature B.V
Subjects
Adolescent
Apoptosis
Biomarkers, Tumor - genetics
Busulfan
Busulfan - therapeutic use
Cancer Research
Cell culture
Cell death
Cell fate
Cell Line, Tumor
Cell proliferation
Cell Proliferation - genetics
Child
Child, Preschool
Children
CRISPR
Cytotoxicity
Drug Resistance, Neoplasm - genetics
Female
Gene Deletion
Genetic Predisposition to Disease - genetics
Genotype
Genotypes
Glutathione
Glutathione - analysis
Glutathione - metabolism
Glutathione Transferase - genetics
GSTM1 protein
GSTT1 protein
Hematologic Neoplasms - genetics
Hematologic Neoplasms - pathology
Hematologic Neoplasms - therapy
Hematology
Hematopoietic Stem Cell Transplantation
Hematopoietic stem cells
Humans
Infant
Internal Medicine
Leukemia - genetics
Leukemia - pathology
Leukemia - therapy
Lymphoblastoid cell lines
Male
Medicine
Medicine & Public Health
NCT
NCT01257854
Neoplasm Recurrence, Local - genetics
Null cells
Oncology
Original Article – Cancer Research
Original – Cancer Research
Retrospective Studies
Risk Factors
Stem cell transplantation
Tumor cell lines
Tumors
Post-transplant relapse
Acute leukemia
genotypes of glutathione S-transferases
Hematological malignancies
Hematopoietic stem cell transplantation
Busulfan resistance
Null genotypes of glutathione S-transferases
Online AccessGet full text
ISSN0171-5216
1432-1335
1432-1335
DOI10.1007/s00432-021-03769-2

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Abstract Purpose This study aimed to retrospectively evaluate the genetic association of null variants of glutathione S-transferases GSTM1 and GSTT1 with relapse incidence in children with hematological malignancies (HMs) undergoing busulfan (BU)- containing allogeneic hematopoietic stem cell transplantation (HSCT) and to assess the impact of these variants on BU-induced cytotoxicity on the immortalized lymphoblastoid cell lines (LCLs) and tumor THP1 GST gene-edited cell models. Methods GSTM1- and GSTT1-null alleles were genotyped using germline DNA from whole blood prior to a conditioning BU-based regimen. Association of GSTM1- and GSTT1-null variants with relapse incidence was analyzed using multivariable competing risk analysis. BU-induced cell death studies were conducted in GSTs - null and non-null LCLs and CRISPR–Cas9 gene-edited THP1 leukemia cell lines. Results Carrying GSTM1/GSTT1 double null genotype was found to be an independent risk factor for post-HSCT relapse in 86 children (adjusted HR: 6.52 [95% Cl, 2.76–15.42; p  = 1.9 × 10 –5 ]). BU-induced cell death preferentially in THP1 GSTM1(non−null) and LCLs GSTM1(non−null) as shown by decreased viability, increased necrosis and levels of the oxidized form of glutathione compared to null cells, while GSTT1 non-null cells showed increased baseline proliferation. Conclusion The clinical association suggests that GSTM1 / GSTT1 double null genotype could serve as genetic stratification biomarker for the high risk of post-HSCT relapse. Functional studies have indicated that GSTM1 status modulates BU-induced cell death. On the other hand, GSTT1 is proposed to be involved in baseline cell proliferation.
AbstractList PurposeThis study aimed to retrospectively evaluate the genetic association of null variants of glutathione S-transferases GSTM1 and GSTT1 with relapse incidence in children with hematological malignancies (HMs) undergoing busulfan (BU)- containing allogeneic hematopoietic stem cell transplantation (HSCT) and to assess the impact of these variants on BU-induced cytotoxicity on the immortalized lymphoblastoid cell lines (LCLs) and tumor THP1 GST gene-edited cell models.MethodsGSTM1- and GSTT1-null alleles were genotyped using germline DNA from whole blood prior to a conditioning BU-based regimen. Association of GSTM1- and GSTT1-null variants with relapse incidence was analyzed using multivariable competing risk analysis. BU-induced cell death studies were conducted in GSTs- null and non-null LCLs and CRISPR–Cas9 gene-edited THP1 leukemia cell lines.ResultsCarrying GSTM1/GSTT1 double null genotype was found to be an independent risk factor for post-HSCT relapse in 86 children (adjusted HR: 6.52 [95% Cl, 2.76–15.42; p = 1.9 × 10–5]). BU-induced cell death preferentially in THP1GSTM1(non−null) and LCLsGSTM1(non−null) as shown by decreased viability, increased necrosis and levels of the oxidized form of glutathione compared to null cells, while GSTT1 non-null cells showed increased baseline proliferation.ConclusionThe clinical association suggests that GSTM1/GSTT1 double null genotype could serve as genetic stratification biomarker for the high risk of post-HSCT relapse. Functional studies have indicated that GSTM1 status modulates BU-induced cell death. On the other hand, GSTT1 is proposed to be involved in baseline cell proliferation.
Purpose This study aimed to retrospectively evaluate the genetic association of null variants of glutathione S-transferases GSTM1 and GSTT1 with relapse incidence in children with hematological malignancies (HMs) undergoing busulfan (BU)- containing allogeneic hematopoietic stem cell transplantation (HSCT) and to assess the impact of these variants on BU-induced cytotoxicity on the immortalized lymphoblastoid cell lines (LCLs) and tumor THP1 GST gene-edited cell models. Methods GSTM1- and GSTT1-null alleles were genotyped using germline DNA from whole blood prior to a conditioning BU-based regimen. Association of GSTM1- and GSTT1-null variants with relapse incidence was analyzed using multivariable competing risk analysis. BU-induced cell death studies were conducted in GSTs - null and non-null LCLs and CRISPR–Cas9 gene-edited THP1 leukemia cell lines. Results Carrying GSTM1/GSTT1 double null genotype was found to be an independent risk factor for post-HSCT relapse in 86 children (adjusted HR: 6.52 [95% Cl, 2.76–15.42; p  = 1.9 × 10 –5 ]). BU-induced cell death preferentially in THP1 GSTM1(non−null) and LCLs GSTM1(non−null) as shown by decreased viability, increased necrosis and levels of the oxidized form of glutathione compared to null cells, while GSTT1 non-null cells showed increased baseline proliferation. Conclusion The clinical association suggests that GSTM1 / GSTT1 double null genotype could serve as genetic stratification biomarker for the high risk of post-HSCT relapse. Functional studies have indicated that GSTM1 status modulates BU-induced cell death. On the other hand, GSTT1 is proposed to be involved in baseline cell proliferation.
This study aimed to retrospectively evaluate the genetic association of null variants of glutathione S-transferases GSTM1 and GSTT1 with relapse incidence in children with hematological malignancies (HMs) undergoing busulfan (BU)- containing allogeneic hematopoietic stem cell transplantation (HSCT) and to assess the impact of these variants on BU-induced cytotoxicity on the immortalized lymphoblastoid cell lines (LCLs) and tumor THP1 GST gene-edited cell models. GSTM1- and GSTT1-null alleles were genotyped using germline DNA from whole blood prior to a conditioning BU-based regimen. Association of GSTM1- and GSTT1-null variants with relapse incidence was analyzed using multivariable competing risk analysis. BU-induced cell death studies were conducted in GSTs- null and non-null LCLs and CRISPR-Cas9 gene-edited THP1 leukemia cell lines. Carrying GSTM1/GSTT1 double null genotype was found to be an independent risk factor for post-HSCT relapse in 86 children (adjusted HR: 6.52 [95% Cl, 2.76-15.42; p = 1.9 × 10 ]). BU-induced cell death preferentially in THP1 and LCLs as shown by decreased viability, increased necrosis and levels of the oxidized form of glutathione compared to null cells, while GSTT1 non-null cells showed increased baseline proliferation. The clinical association suggests that GSTM1/GSTT1 double null genotype could serve as genetic stratification biomarker for the high risk of post-HSCT relapse. Functional studies have indicated that GSTM1 status modulates BU-induced cell death. On the other hand, GSTT1 is proposed to be involved in baseline cell proliferation.
This study aimed to retrospectively evaluate the genetic association of null variants of glutathione S-transferases GSTM1 and GSTT1 with relapse incidence in children with hematological malignancies (HMs) undergoing busulfan (BU)- containing allogeneic hematopoietic stem cell transplantation (HSCT) and to assess the impact of these variants on BU-induced cytotoxicity on the immortalized lymphoblastoid cell lines (LCLs) and tumor THP1 GST gene-edited cell models.PURPOSEThis study aimed to retrospectively evaluate the genetic association of null variants of glutathione S-transferases GSTM1 and GSTT1 with relapse incidence in children with hematological malignancies (HMs) undergoing busulfan (BU)- containing allogeneic hematopoietic stem cell transplantation (HSCT) and to assess the impact of these variants on BU-induced cytotoxicity on the immortalized lymphoblastoid cell lines (LCLs) and tumor THP1 GST gene-edited cell models.GSTM1- and GSTT1-null alleles were genotyped using germline DNA from whole blood prior to a conditioning BU-based regimen. Association of GSTM1- and GSTT1-null variants with relapse incidence was analyzed using multivariable competing risk analysis. BU-induced cell death studies were conducted in GSTs- null and non-null LCLs and CRISPR-Cas9 gene-edited THP1 leukemia cell lines.METHODSGSTM1- and GSTT1-null alleles were genotyped using germline DNA from whole blood prior to a conditioning BU-based regimen. Association of GSTM1- and GSTT1-null variants with relapse incidence was analyzed using multivariable competing risk analysis. BU-induced cell death studies were conducted in GSTs- null and non-null LCLs and CRISPR-Cas9 gene-edited THP1 leukemia cell lines.Carrying GSTM1/GSTT1 double null genotype was found to be an independent risk factor for post-HSCT relapse in 86 children (adjusted HR: 6.52 [95% Cl, 2.76-15.42; p = 1.9 × 10-5]). BU-induced cell death preferentially in THP1GSTM1(non-null) and LCLsGSTM1(non-null) as shown by decreased viability, increased necrosis and levels of the oxidized form of glutathione compared to null cells, while GSTT1 non-null cells showed increased baseline proliferation.RESULTSCarrying GSTM1/GSTT1 double null genotype was found to be an independent risk factor for post-HSCT relapse in 86 children (adjusted HR: 6.52 [95% Cl, 2.76-15.42; p = 1.9 × 10-5]). BU-induced cell death preferentially in THP1GSTM1(non-null) and LCLsGSTM1(non-null) as shown by decreased viability, increased necrosis and levels of the oxidized form of glutathione compared to null cells, while GSTT1 non-null cells showed increased baseline proliferation.The clinical association suggests that GSTM1/GSTT1 double null genotype could serve as genetic stratification biomarker for the high risk of post-HSCT relapse. Functional studies have indicated that GSTM1 status modulates BU-induced cell death. On the other hand, GSTT1 is proposed to be involved in baseline cell proliferation.CONCLUSIONThe clinical association suggests that GSTM1/GSTT1 double null genotype could serve as genetic stratification biomarker for the high risk of post-HSCT relapse. Functional studies have indicated that GSTM1 status modulates BU-induced cell death. On the other hand, GSTT1 is proposed to be involved in baseline cell proliferation.
Author Chalandon, Yves
Uppugunduri, Satyanarayana Chakradhara Rao
Robin, Shannon
Jurkovic Mlakar, Simona
Rezgui, Mohamed Aziz
Bittencourt, Henrique
Mlakar, Vid
Golay, Hadrien
Bredius, Robert G. M.
Krajinovic, Maja
Waespe, Nicolas
Boelens, Jaap Jan
Peters, Christina
Ansari, Marc
Corbacioglu, Selim
Nava, Tiago
Dalle, Jean-Hugues
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BackLink https://www.ncbi.nlm.nih.gov/pubmed/34499222$$D View this record in MEDLINE/PubMed
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CitedBy_id crossref_primary_10_1038_s41409_023_01963_z
crossref_primary_10_2174_1568009623666221027103845
crossref_primary_10_34067_KID_0004552022
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Copyright The Author(s) 2021. corrected publication 2021
2021. The Author(s).
Copyright Springer Nature B.V. Jan 2022
The Author(s) 2021, corrected publication 2021
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CorporateAuthor the paediatric diseases working party of the European society for blood and marrow transplantation
paediatric diseases working party of the European society for blood and marrow transplantation
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Issue 1
Keywords Post-transplant relapse
Acute leukemia
genotypes of glutathione S-transferases
Hematological malignancies
Hematopoietic stem cell transplantation
Busulfan resistance
Null genotypes of glutathione S-transferases
Language English
License 2021. The Author(s).
Open AccessThis article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/.
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Snippet Purpose This study aimed to retrospectively evaluate the genetic association of null variants of glutathione S-transferases GSTM1 and GSTT1 with relapse...
This study aimed to retrospectively evaluate the genetic association of null variants of glutathione S-transferases GSTM1 and GSTT1 with relapse incidence in...
PurposeThis study aimed to retrospectively evaluate the genetic association of null variants of glutathione S-transferases GSTM1 and GSTT1 with relapse...
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Enrichment Source
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StartPage 71
SubjectTerms Adolescent
Apoptosis
Biomarkers, Tumor - genetics
Busulfan
Busulfan - therapeutic use
Cancer Research
Cell culture
Cell death
Cell fate
Cell Line, Tumor
Cell proliferation
Cell Proliferation - genetics
Child
Child, Preschool
Children
CRISPR
Cytotoxicity
Drug Resistance, Neoplasm - genetics
Female
Gene Deletion
Genetic Predisposition to Disease - genetics
Genotype
Genotypes
Glutathione
Glutathione - analysis
Glutathione - metabolism
Glutathione Transferase - genetics
GSTM1 protein
GSTT1 protein
Hematologic Neoplasms - genetics
Hematologic Neoplasms - pathology
Hematologic Neoplasms - therapy
Hematology
Hematopoietic Stem Cell Transplantation
Hematopoietic stem cells
Humans
Infant
Internal Medicine
Leukemia - genetics
Leukemia - pathology
Leukemia - therapy
Lymphoblastoid cell lines
Male
Medicine
Medicine & Public Health
NCT
NCT01257854
Neoplasm Recurrence, Local - genetics
Null cells
Oncology
Original Article – Cancer Research
Original – Cancer Research
Retrospective Studies
Risk Factors
Stem cell transplantation
Tumor cell lines
Tumors
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Title GSTM1 and GSTT1 double null genotypes determining cell fate and proliferation as potential risk factors of relapse in children with hematological malignancies after hematopoietic stem cell transplantation
URI https://link.springer.com/article/10.1007/s00432-021-03769-2
https://www.ncbi.nlm.nih.gov/pubmed/34499222
https://www.proquest.com/docview/2618749632
https://www.proquest.com/docview/2571049384
https://pubmed.ncbi.nlm.nih.gov/PMC8752561
Volume 148
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