dic(7;9)(p11.1;p11.1) and del(7)(q36) as a Primary Abnormality in Childhood B-cell Precursor ALL: A Case Report

Dhanlaxmi Shetty1, Elizabeth Talker1, Kruti Chaubal1

  • 1Department of Cancer Cytogenetics, Advanced Centre for Treatment, Research and Education in Cancer (ACTREC), Tata Memorial Centre, Kharghar, Navi Mumbai, India.

Insights

This study details a pediatric B-cell acute lymphoblastic leukemia case with a rare dic(7;9) chromosomal abnormality. Despite poor prognostic indicators, the patient achieved a positive response to standard induction therapy.

Area of Science:

  • Hematology
  • Genetics
  • Pediatric Oncology

Background:

  • B-cell acute lymphoblastic leukemia (B-ALL) involves abnormal B-lymphoblast proliferation.
  • FAB classification (L1/L2) describes B-ALL cell morphology.
  • Genetic classification of B-ALL relies on molecular cytogenetic and molecular testing.

Purpose of the Study:

  • To report a pediatric B-ALL case with a primary dic(7;9)(p11.1;p11.1) and CUL1 deletion (7q36).
  • To highlight the patient's response to standard risk induction therapy despite poor prognostic markers.

Main Methods:

  • Conventional karyotyping and fluorescence in situ hybridization (FISH) were used for genetic abnormality detection.
  • Minimal residual disease monitoring assessed treatment response.

Main Results:

  • The pediatric B-ALL case presented with dic(7;9)(p11.1;p11.1) and CUL1 deletion (7q36).
  • Both 7p and 9p deletions are typically associated with poor prognosis.
  • The patient exhibited a favorable response to standard risk induction therapy.

Conclusions:

  • This case demonstrates that pediatric B-ALL with dic(7;9) and CUL1 deletion can respond well to standard treatment.
  • Genetic abnormalities, even those linked to poor prognosis, require careful correlation with clinical response.
Abstract

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