'Evaluation of adverse prognostic gene alterations & MRD positivity in BCR::ABL1-like B-lineage acute lymphoblastic leukaemia patients, in a resource-constrained setting.


Journal

British journal of cancer
ISSN: 1532-1827
Titre abrégé: Br J Cancer
Pays: England
ID NLM: 0370635

Informations de publication

Date de publication:
07 2023
Historique:
received: 01 11 2022
accepted: 21 04 2023
revised: 12 04 2023
pmc-release: 08 05 2024
medline: 30 6 2023
pubmed: 9 5 2023
entrez: 8 5 2023
Statut: ppublish

Résumé

Early detection of BCR::ABL1-like ALL could impact treatment management and improve the overall survival/outcome. BCR::ABL1-like ALL cases are characterised by diverse genetic alterations activating cytokine receptors and kinase signalling. Its detection is still an unmet need in low-middle-income countries due to the unavailability of a patented TLDA assay. This study's rationale is to identify BCR::ABL1-like ALLs using the PHi-RACE classifier, followed by the characterisation of underlying adverse genetic alterations in recurrent gene abnormalities negative (RGA We identified 34.25% (37/108) BCR::ABL1-like ALLs using PHi-RACE classifier, characterised by TSLPR/CRLF2 expression (11.58%), IKZF1 (Δ4-7) deletion (18.9%) and chimeric gene fusions (34.61%). In overexpressed TSLPR/CRLF2 BCR::ABL1-like ALLs, we identified 33.33% (1/3) CRLF2::IGH and 33.33% (1/3) EPOR::IGH rearrangements with concomitant JAK2 mutation R683S (50%). We identified 18.91% CD13 (P = 0.02) and 27.02% CD33 (P = 0.05) aberrant myeloid markers positivity, which was significantly higher in BCR::ABL1-like ALLs compared to non-BCR::ABL1-like ALLs. MRD positivity was considerably higher (40% in BCR::ABL1-like vs. 19.29% in non-BCR::ABL1-like ALLs). With this practical approach, we reported a high incidence of BCR::ABL1-like ALLs, and a lower frequency of CRLF2 alteration & associated CGFs. Recognising this entity, early at diagnosis is crucial to optimise personalised treatment strategies.

Sections du résumé

BACKGROUND
Early detection of BCR::ABL1-like ALL could impact treatment management and improve the overall survival/outcome. BCR::ABL1-like ALL cases are characterised by diverse genetic alterations activating cytokine receptors and kinase signalling. Its detection is still an unmet need in low-middle-income countries due to the unavailability of a patented TLDA assay.
METHODS
This study's rationale is to identify BCR::ABL1-like ALLs using the PHi-RACE classifier, followed by the characterisation of underlying adverse genetic alterations in recurrent gene abnormalities negative (RGA
RESULTS
We identified 34.25% (37/108) BCR::ABL1-like ALLs using PHi-RACE classifier, characterised by TSLPR/CRLF2 expression (11.58%), IKZF1 (Δ4-7) deletion (18.9%) and chimeric gene fusions (34.61%). In overexpressed TSLPR/CRLF2 BCR::ABL1-like ALLs, we identified 33.33% (1/3) CRLF2::IGH and 33.33% (1/3) EPOR::IGH rearrangements with concomitant JAK2 mutation R683S (50%). We identified 18.91% CD13 (P = 0.02) and 27.02% CD33 (P = 0.05) aberrant myeloid markers positivity, which was significantly higher in BCR::ABL1-like ALLs compared to non-BCR::ABL1-like ALLs. MRD positivity was considerably higher (40% in BCR::ABL1-like vs. 19.29% in non-BCR::ABL1-like ALLs).
CONCLUSIONS
With this practical approach, we reported a high incidence of BCR::ABL1-like ALLs, and a lower frequency of CRLF2 alteration & associated CGFs. Recognising this entity, early at diagnosis is crucial to optimise personalised treatment strategies.

Identifiants

pubmed: 37156894
doi: 10.1038/s41416-023-02294-y
pii: 10.1038/s41416-023-02294-y
pmc: PMC10307811
doi:

Substances chimiques

Fusion Proteins, bcr-abl EC 2.7.10.2

Types de publication

Journal Article Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

143-152

Informations de copyright

© 2023. The Author(s), under exclusive licence to Springer Nature Limited.

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Auteurs

Dikshat Gopal Gupta (DG)

Department of Urology, The Robert H. Lurie Comprehensive Cancer Center, Northwestern University Feinberg School of Medicine, Chicago, IL, 60611, USA.

Neelam Varma (N)

Department of Hematology, Post Graduate Institute of Medical Education and Research, Chandigarh, Chandigarh, 160012, India. varmaneelam@yahoo.com.

Sreejesh Sreedharanunni (S)

Department of Hematology, Post Graduate Institute of Medical Education and Research, Chandigarh, Chandigarh, 160012, India.

Sarki Abba Abdulkadir (SA)

Department of Urology, The Robert H. Lurie Comprehensive Cancer Center, Northwestern University Feinberg School of Medicine, Chicago, IL, 60611, USA.

Shano Naseem (S)

Department of Hematology, Post Graduate Institute of Medical Education and Research, Chandigarh, Chandigarh, 160012, India.

Man Updesh Singh Sachdeva (MUS)

Department of Hematology, Post Graduate Institute of Medical Education and Research, Chandigarh, Chandigarh, 160012, India.

Jogeshwar Binota (J)

Department of Hematology, Post Graduate Institute of Medical Education and Research, Chandigarh, Chandigarh, 160012, India.

Parveen Bose (P)

Department of Hematology, Post Graduate Institute of Medical Education and Research, Chandigarh, Chandigarh, 160012, India.

Pankaj Malhotra (P)

Department of Clinical Hematology & Medical Oncology, Post Graduate Institute of Medical Education and Research, Chandigarh, Chandigarh, 160012, India.

Alka Khadwal (A)

Department of Clinical Hematology & Medical Oncology, Post Graduate Institute of Medical Education and Research, Chandigarh, Chandigarh, 160012, India.

Subhash Varma (S)

Department of Internal Medicine, Post Graduate Institute of Medical Education and Research, Chandigarh, Chandigarh, 160012, India.

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