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Original Article: Research

Deletion of CDKN2A/B is associated with inferior relapse free survival in pediatric B cell acute lymphoblastic leukemia

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Pages 433-441 | Received 20 Feb 2018, Accepted 19 May 2018, Published online: 03 Jul 2018

References

  • Mullighan CG, Miller CB, Radtke I, et al. BCR-ABL1 lymphoblastic leukaemia is characterized by the deletion of Ikaros. Nature 2008;453:110–114.
  • Schwab CJ, Chilton L, Morrison H, et al. Genes commonly deleted in childhood B-cell precursor acute lymphoblastic leukemia: association with cytogenetics and clinical features. Haematologica 2013;98: 1081–1088.
  • Moorman AV, Enshaei A, Schwab C, et al. A novel integrated cytogenetic and genomic classification refines risk stratification in pediatric acute lymphoblastic leukemia. Blood 2014;124:1434–1444.
  • Krentz S, Hof J, Mendioroz A, et al. Prognostic value of genetic alterations in children with first bone marrow relapse of childhood B-cell precursor acute lymphoblastic leukemia. Leukemia 2013;27:295–304.
  • Braun M, Pastorczak A, Fendler W, et al. Biallelic loss of CDKN2A is associated with poor response to treatment in pediatric acute lymphoblastic leukemia. Leuk Lymphoma. 2017;58:1162–1171.
  • Kim WY, Sharpless NE. The Regulation of INK4/ARF in Cancer and Aging. Cell 2006;127:265–275.
  • Sharpless NE. INK4a/ARF: a multifunctional tumor suppressor locus. Mutat Res. 2005;576:22–38.
  • Chin L, Pomerantz J, DePinho RA. The INK4a/ARF tumor suppressor: one gene-two products-two pathways. Trends Biochem Sci. 1998;23:291–296.
  • Liggett WH, Sidransky D. Role of the p16 tumor suppressor gene in cancer. J Clin Oncol. 1998;16: 1197–1206.
  • Messina M, Chiaretti S, Fedullo AL, et al. Clinical significance of recurrent copy number aberrations in B-lineage acute lymphoblastic leukaemia without recurrent fusion genes across age cohorts. Br J Haematol. 2017;178:583–587.
  • Gupta SK, Bakhshi S, Kumar L, et al. Gene copy number alteration profile and its clinical correlation in B-cell acute lymphoblastic leukemia. Leuk Lymphoma. 2017;58:333–342.
  • Singh M, Bhatia P, Trehan A, et al. High frequency of intermediate and poor risk copy number abnormalities in pediatric cohort of B-ALL correlate with high MRD post induction. Leuk Res. 2018;66:79–84.
  • Patkar N, Subramanian PG, Tembhare P, et al. An integrated genomic profile that includes copy number alterations is highly predictive of minimal residual disease status in childhood precursor B-lineage acute lymphoblastic leukemia. Indian J Pathol Microbiol. 2017;60:209–213.
  • Irving JA, Enshaei A, Parker CA, et al. Integration of genetic and clinical risk factors improves prognostication in relapsed childhood B-cell precursor acute lymphoblastic leukemia. Blood 2016;128:911–922.
  • Mirebeau D, Acquaviva C, Suciu S, et al. The prognostic significance of CDKN2A, CDKN2B and MTAP inactivation in B-lineage acute lymphoblastic leukemia of childhood. Results of the EORTC studies 58881 and 58951. Haematologica 2006;91:881–885.
  • Takeuchi S, Bartram CR, Seriu T, et al. Analysis of a family of cyclin-dependent kinase inhibitors: p15/MTS2/INK4B, p16/MTS1/INK4A, and p18 genes in acute lymphoblastic leukemia of childhood. Blood 1995;86:755–760.
  • Sulong S, Moorman AV, Irving JAE, et al. A comprehensive analysis of the CDKN2A gene in childhood acute lymphoblastic leukemia reveals genomic deletion, copy number neutral loss of heterozygosity, and association with specific cytogenetic subgroups. Blood 2009;113:100–107.
  • Bertin R, Acquaviva C, Mirebeau D, et al. CDKN2A, CDKN2B, and MTAP gene dosage permits precise characterization of mono- and bi-allelic 9p21 deletions in childhood acute lymphoblastic leukemia. Genes Chromosom Cancer. 2003;37:44–57.
  • Yang JJ, Bhojwani D, Yang W, et al. Genome-wide copy number profiling reveals molecular evolution from diagnosis to relapse in childhood acute lymphoblastic leukemia. Blood 2008;112:4178–4183.
  • van Zutven LJCM, van Drunen E, de Bont JM, et al. CDKN2 deletions have no prognostic value in childhood precursor-B acute lymphoblastic leukaemia. Leukemia 2005;19:1281–1284.
  • Xu N, Li Y-L, Zhou X, et al. CDKN2 Gene Deletion as Poor Prognosis Predictor Involved in the Progression of Adult B-Lineage Acute Lymphoblastic Leukemia Patients. J Cancer. 2015;6:1114–1120.
  • Iacobucci I, Ferrari A, Lonetti A, et al. CDKN2A/B alterations impair prognosis in adult BCR-ABL1-positive acute lymphoblastic leukemia patients. Clin Cancer Res. 2011;17:7413–7423.
  • Kim M, Yim S-H, Cho N-S, et al. Homozygous deletion of CDKN2A (p16, p14) and CDKN2B (p15) genes is a poor prognostic factor in adult but not in childhood B-lineage acute lymphoblastic leukemia: a comparative deletion and hypermethylation study. Cancer Genet Cytogenet. 2009;195:59–65.
  • Trehan A, Bansal D, Varma N, et al. Improving outcome of acute lymphoblastic leukemia with a simplified protocol: report from a tertiary care center in north India. Pediatr Blood Cancer. 2017;64:e26281.
  • Gujral S, Subramanian PG, Patkar N, et al. Report of proceedings of the national meeting on “Guidelines for Immunophenotyping of Hematolymphoid Neoplasms by Flow Cytometry.” Indian J Pathol Microbiol. 2008;51:161–166.
  • Gruszka-Westwood AM, Hamoudi RA, Matutes E, et al. p53 abnormalities in splenic lymphoma with villous lymphocytes. Blood 2001;97:3552–3558.
  • Kwabi-Addo B, Giri D, Schmidt K, et al. Haploinsufficiency of the Pten tumor suppressor gene promotes prostate cancer progression. Proc Natl Acad Sci USA. 2001;98:11563–11568.
  • Fero ML, Randel E, Gurley KE, et al. The murine gene p27Kip1 is haplo-insufficient for tumour suppression. Nature 1998;396:177–180.
  • Tang B, Böttinger EP, Jakowlew SB, et al. Transforming growth factor-beta1 is a new form of tumor suppressor with true haploid insufficiency. Nat Med. 1998;4: 802–807.
  • Carter TL, Watt PM, Kumar R, et al. Hemizygous p16(INK4A) deletion in pediatric acute lymphoblastic leukemia predicts independent risk of relapse. Blood 2001;97:572–574.
  • Carter TL, Terry P, Gottardo N, et al. Deletion of one copy of the p16INK4A tumor suppressor gene is implicated as a predisposing factor in pediatric leukemia. Biochem Biophys Res Commun. 2004;318:852–855.
  • Maloney K, Mcgavran L, Odom L, et al. Different patterns of homozygous p16 INK4A and p15 INK4B deletions in childhood acute lymphoblastic leukemias containing distinct E2A translocations. Leukemia 1998;12:1417–1421.
  • Ohnishi H, Kawamura M, Ida K, et al. Homozygous deletions of p16/MTS1 gene are frequent but mutations are infrequent in childhood T-cell acute lymphoblastic leukemia. Blood 1995;86:1269–1275.
  • Guidal-Giroux C, Gérard B, Cavé H, et al. Deletion mapping indicates that MTS1 is the target of frequent deletions at chromosome 9p21 in paediatric acute lymphoblastic leukaemias. Br J Haematol. 1996;92: 410–419.
  • Kuiper RP, Waanders E, van der Velden VHJ, et al. IKZF1 deletions predict relapse in uniformly treated pediatric precursor B-ALL. Leukemia 2010;24: 1258–1264.
  • Martinelli G, Iacobucci I, Storlazzi CT, et al. IKZF1 (Ikaros) Deletions in BCR-ABL1–positive acute lymphoblastic leukemia are associated with short disease-free survival and high rate of cumulative incidence of relapse: a GIMEMA AL WP report. J Clin Oncol. 2009;27:5202–5207.
  • Gupta SK, Bakhshi S, Kumar L, et al. IKZF1 (IKAROS) deletions in B-ALL and its clinical correlation: a prospective study from a tertiary care centre in Northern India. Leuk Res. 2016;41:7–11.

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