Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:2.7.10.2 (focal adhesion kinase)
 44,029 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A subset of adult acute lymphoblastic leukemia (ALL) patients have blast cells which co-express myeloid-associated antigens (MY+ ALL). We have analyzed 113 adult ALL cases for expression of MY-associated antigens (MAA). ALL was diagnosed by standard morphology, cytochemistry, and immunophenotype in central review. MY+ ALL was diagnosed when > or = 20% of lymphoblasts co-expressed CD13 and/or CD33. Overall incidence of MY+ was 31/113 (27%). MAA expression was not significantly correlated with WBC, blast count, hemoglobin, or hematocrit. MY+ cases were more likely to express B-associated antigens, especially CALLA, and to be FAB L2, Ph+, or to have the BCR-ABL translocation by PCR, but these differences were not statistically significant. All patients were induced with a L10M regimen, and 67 (59%) achieved CR: 43/66 (65%) of B MY neg; 14/29 (48%) of B MY+; 10/16 (63%) T MY neg; and 0/2 T MY+. In age-adjusted analyses CR rate did not differ significantly between MY+ and MY neg patients or between B- and T-cell patients. Of the 113 patients, 84 have died and the remaining 29 patients have been followed for a median of 49 months. In proportional hazards regression analyses adjusting for age and WBC, heterogeneity of survival among the four groups was statistically significant (p = 0.021), largely due to MY status. The mortality rate was 85% greater for MY+ patients compared to MY neg patients (two-tailed p = 0.013). By contrast, survival did not vary significantly between B- and T-cell patients. The data indicate that MAA expression is useful for predicting overall survival of adult patients with ALL treated in a L10M protocol. As a predictive factor MAA expression is comparable to the WBC and superior to the more standard stratification by B- or T-cell markers for this group of patients.
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PMID:Expression of myeloid antigens by blast cells in acute lymphoblastic leukemia of adults. The Southwest Oncology Group experience. 780 99

Jumping translocations (JT) are rare chromosomal abnormalities in which an identical copy of a chromosomal region (donor) is translocated to a different chromosome (acceptor). Chromosome 1 is often involved as donor chromosome. JTs of the long arm of chromosome 1 (1q) or parts of it are associated with a poor outcome. We report on a 72-year-old male patient with a BCR/ABL1 rearrangement positive acute lymphoblastic leukemia (common ALL, or c-ALL; FAB L2 morphology) and with additional structural and numeric aberrations. Four aberrant clones were observed after conventional cytogenetic analysis. Three of the four clones showed a JT with 1q as donor and 3q, 8q, and 22q as acceptors. To the best of our knowledge, neither JT between 1q and chromosome 3 nor JT between 1q and chromosome 22 have been described in c-ALL. This report emphasizes the frequent involvement of 1q in JT and the association with a poor prognosis.
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PMID:Jumping translocation of 1q in a BCR/ABL-positive acute lymphoblastic leukemia. 1572 38