Deletions of interferon genes in acute lymphoblastic leukemia

Article Abstract:

The pathogenesis of some cancerous diseases has been associated with chromosomal abnormalities. Previous studies have indicated that this results from the loss of dominant tumor-suppressor genes or a modification of the normal gene cells that produce dominant oncogenes (cancer causing genes). Specifically, in patients with acute lymphoblastic leukemia (ALL) the short arm of chromosome 9 has been associated with deletions or unbalanced translocations; these abnormalities have previously been reported to occur in seven to 13 percent of patients with ALL. The chromosome 9 region is known to contain interferon-alpha and interferon-beta-1 genes. Primary leukemia cell samples were analyzed in 62 patients with ALL to further examine the relationship between interferon gene deletion and this disease. The results revealed that the prevalence of both homozygous (similar gene pairs) and hemizygous (single gene pairs) deletions of these interferon genes was greater than previously reported. Twenty-nine percent of the patients had genetic lesions in the chromosome 9 region. No relationship was found between the interferon gene deletion and patient age, sex, immunologic characteristics, or any particular observed clinical feature. The frequency of these deletions in the primary leukemia cells of patients with ALL indicates that the loss of a leukemia suppressor gene may be an important step in the disease process. It was proposed that one of the interferon-alpha genes, or another closely linked gene, is instrumental in the pathogenesis of ALL. (Consumer Summary produced by Reliance Medical Information, Inc.)

Analysis, Causes of, Genetic aspects, Chromosome deletion, Lymphocytic leukemia, Interferon, Human chromosome abnormalities

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Augmented post-induction therapy for children with high-risk acute lymphoblastic leukemia and a slow response to initial therapy

Article Abstract:

An augmented chemotherapy regimen appears to be more effective than the standard regimen in children with acute lymphoblastic leukemia (ALL) who do not respond completely to initial chemotherapy. These children have a high rate of relapse. Researchers compared standard chemotherapy to augmented chemotherapy in 311 children who had received initial treatment and were in remission. Augmented treatment consisted of more vincristine, asparaginase, methotrexate and dexamethasone than the standard treatment. Overall and disease-free survival rates were substantially higher in the children who received augmented treatment.

Evaluation, Chemotherapy, Lymphoblastic leukemia in children, Acute lymphocytic leukemia, Childhood leukemia

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Loss of Smad3 in acute T-cell lymphoblastic leukemia

Article Abstract:

Direct evidence of a tumor-suppressor function for Smad3 in the T-cell lineage is found Smad3 messenger RNA (mRNA) and protein in leukemia cells obtained at diagnosis from 19 children with acute leukemia were measured. A reduction in Smad3 expression and the loss of p27(super Kip1) work synergistically to promote T-cell leukemogenesis in mice.

Science & research, Diagnosis, Tumor suppressor genes, Messenger RNA, Acute leukemia, Tumour suppressor genes

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