title: Deletions and losses in chromosomes 5 or 7 in adult acute lymphocytic leukemia: incidence, associations and implications.
abstract: Deletions or losses in chromosomes 5 or 7 are recurrent non-random abnormalities in acute myeloid leukemia (AML), and are associated with prior exposure to carcinogens or leukemogenic agents, and with poor prognosis. Their occurrence and significance in adult acute lymphocytic leukemia (ALL) is not well described. The aim of the study was to evaluate the incidence, associations and implications of chromosome 5 or 7 abnormalities in adult ALL. Patients with newly diagnosed ALL referred to MD Anderson Cancer Center between 1980 and 1996 were analyzed. Characteristics and outcome of patients with or without chromosome 5 or 7 abnormalities were compared by standard statistical methods. Thirty-one of 468 patients (6.6%) had chromosome 5 or 7 abnormalities. Loss of chromosome 5 occurred in six cases, three of them had both chromosome 5 and 7 abnormalities. Deletion or loss of chromosome 7 occurred as a single abnormality in three patients; in 28 patients it was associated with other abnormalities. The most significant cytogenetic association was with the Philadelphia chromosome (Ph) abnormality occurring in nine patients (29%). Compared with patients without the abnormalities, patients with chromosome 5 or 7 abnormalities tended to express CD34 more frequently (74% vs 54% P = 0.07), to be older (age >60 years 29% vs 18% P = 0.14), and to be associated with Ph (29% vs 11% P = 0.004). With therapy, the complete response (CR) rate with chromosome 5 or 7 abnormalities was lower (64% vs 79% P = 0.038) but the survival rate was similar (3-year survival rate 32% vs 36% P = 0.14). When the 22 patients without Ph were considered separately, the CR and survival rates were similar among patients with or without chromosome 5 or 7 abnormalities. Abnormalities in chromosome 5 or 7 are not specific for AML, and may occur in ALL. Unlike in AML, chromosome 5 or 7 abnormalities in ALL were not predictive of worse prognosis, which is accounted for mostly by the association with Ph.
authors.affiliation: Department of Leukemia, The University of Texas, MD Anderson Cancer Center, Houston 77030, USA.
authors.forename: B S
authors.initials: BS
authors.lastname: Dabaja
authors.forename: S
authors.initials: S
authors.lastname: Faderl
authors.forename: D
authors.initials: D
authors.lastname: Thomas
authors.forename: J
authors.initials: J
authors.lastname: Cortes
authors.forename: S
authors.initials: S
authors.lastname: O'Brien
authors.forename: F
authors.initials: F
authors.lastname: Nasr
authors.forename: S
authors.initials: S
authors.lastname: Pierce
authors.forename: K
authors.initials: K
authors.lastname: Hayes
authors.forename: A
authors.initials: A
authors.lastname: Glassman
authors.forename: M
authors.initials: M
authors.lastname: Keating
authors.forename: H M
authors.initials: HM
authors.lastname: Kantarjian
mesh_terms: D000293:Adolescent; D000328:Adult; D000368:Aged; D002869:Chromosome Aberrations; D002872:Chromosome Deletion; D025063:Chromosome Disorders; D002895:Chromosomes, Human, Pair 5; D002897:Chromosomes, Human, Pair 7; D005260:Female; D006801:Humans; D015994:Incidence; D008297:Male; D008875:Middle Aged; D010641:Phenotype; D054198:Precursor Cell Lymphoblastic Leukemia-Lymphoma / Q000235:genetics* / Q000401:mortality; D015996:Survival Rate; D016896:Treatment Outcome