title: Predictive and Prognostic Implications of Variant Philadelphia Translocations in CML: Experience From a Tertiary Oncology Center in Southern India.
abstract: Chronic myeloid leukemia (CML) is a myeloproliferative disorder characterized by Philadelphia (Ph) chromosome with classical t(9;22)(q34;q11) seen in up to 90% of cases. However 5% to 10% of patients who present with variant Ph translocations (vPh) have been an area of research for their significance in predicting response to various therapies including tyrosine kinase inhibitors as well as prognosticating survival outcomes for many years involving varied patient populations, with conflicting results.
  
  
  
  We retrospectively analyzed our data from January 2002 to December 2014. Patients with vPh in chronic phase of CML (CML-CP) were analyzed with respect to their demographic parameters, response to imatinib therapy, and survival and their data were compared with data of patients with classical Ph translocation (cPh).
  
  
  
  Of 615 patients diagnosed with CML-CP, 72 patients (11.7%) showed vPh. Most common chromosomes involved in these translocations were 14 (13.9%), 11 (12.5%), 19 (9.7%), and 7 (8.3%). Rates of complete hematological response, complete cytogenetic response, and major molecular response were not statistically different between the groups. At 5 years, event-free survival, failure-free survival, progression-free survival, and overall survival were 60% versus 67.9%, 62.7% versus 69.7%, 84.7% versus 92.1%, and 87.5% versus 92.4%, respectively, in vPh and cPh. The differences in survival were statistically not significant.
  
  
  
  To our knowledge, this is the largest series of variant translocations in CML-CP, pertaining to the Indian population. Our data suggest that the presence of vPh in CML has no significant effect in predicting response to imatinib as well as in prognosticating survival.
authors.affiliation: Department of Medical Oncology, Kidwai Memorial Institute of Oncology, Bengaluru, India.
authors.forename: Govind Babu
authors.initials: GB
authors.lastname: Kanakasetty
authors.affiliation: Department of Medical Oncology, Kidwai Memorial Institute of Oncology, Bengaluru, India.
authors.forename: Lakshmaiah
authors.initials: L
authors.lastname: Kuntejowdahalli
authors.affiliation: Department of Medical Oncology, Kidwai Memorial Institute of Oncology, Bengaluru, India. Electronic address: aditik2008@yahoo.com.
authors.forename: Aditi Harsh
authors.initials: AH
authors.lastname: Thanky
authors.affiliation: Department of Medical Oncology, Kidwai Memorial Institute of Oncology, Bengaluru, India.
authors.forename: Lokanatha
authors.initials: L
authors.lastname: Dasappa
authors.affiliation: Department of Medical Oncology, Kidwai Memorial Institute of Oncology, Bengaluru, India.
authors.forename: Linu Abraham
authors.initials: LA
authors.lastname: Jacob
authors.affiliation: Department of Medical Oncology, Kidwai Memorial Institute of Oncology, Bengaluru, India.
authors.forename: Suresh Babu
authors.initials: SB
authors.lastname: Mallekavu
authors.affiliation: Department of Cytogenetics, Kidwai Memorial Institute of Oncology, Bengaluru, India.
authors.forename: Prasanna
authors.initials: P
authors.lastname: Kumari
mesh_terms: D000293:Adolescent; D000328:Adult; D000368:Aged; D000970:Antineoplastic Agents / Q000627:therapeutic use*; D018572:Disease-Free Survival; D005260:Female; D006801:Humans; D000068877:Imatinib Mesylate / Q000627:therapeutic use*; D007194:India; D015464:Leukemia, Myelogenous, Chronic, BCR-ABL Positive / Q000188:drug therapy* / Q000235:genetics* / Q000473:pathology; D008297:Male; D008875:Middle Aged; D010677:Philadelphia Chromosome; D011379:Prognosis; D047428:Protein Kinase Inhibitors / Q000627:therapeutic use*; D012189:Retrospective Studies; D014178:Translocation, Genetic / Q000235:genetics*; D055815:Young Adult
chemical_list: D000970:Antineoplastic Agents; D047428:Protein Kinase Inhibitors; D000068877:Imatinib Mesylate
keywords: Chronic myeloid leukemia; Imatinib; Indian population; Prognostic and predictive markers; Variant translocation