Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UNIPROT:Q06643 (non-Hodgkin's lymphoma)
 11,307 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The TAL1 gene is altered as a consequence of t(1;14)(p32;q11) found in T-cell acute lymphoblastic leukemia (ALL) and shows site specific recombination (tald rearrangement). We investigated TAL1 gene alterations in 39 children with T-cell ALL, in 32 with B-precursor ALL, in three with ALL with myeloid-associated antigen, and in 18 with T-non-Hodgkin's lymphoma (T-NHL). tald rearrangement was found in nine of 39 T-cell ALL patients using Southern blot analysis with a TAL1 gene probe. Polymerase chain reaction (PCR) products predicted from the sequences of the corresponding tald alleles were shown in all of these patients. In contrast, no rearranged band was observed in other kinds of leukemia or in T-NHL patients. All of these patients with tald rearrangement had CD1- CD2+ CD4- CD7+ CD10- pheno-type. Of these, seven were classified as stage I thymic differentiation, and eight have survived for three to 59 months remission. Four of seven patients investigated had normal karyotypes, which has been reported to be associated with a good prognosis in T-cell ALL. We conclude that tald rearrangement is restricted to T-cell ALL, for which it provides a useful clonal marker. Such patients with this rearrangement may constitute a subgroup of T-cell ALL with a good prognosis.
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PMID:Clinical significance of TAL1 gene alteration in childhood T-cell acute lymphoblastic leukemia and lymphoma. 832 Oct 44

Site-specific recombination of the TAL1 gene was analyzed by Southern blotting and polymerase chain reaction (PCR) in 44 cases of childhood T-cell acute lymphoblastic leukemia (T-ALL), 20 cases of childhood T-cell non-Hodgkin's lymphoma (T-NHL) and 35 cases of adult T-cell malignancies. This recombination was found in 10 (22.7%) of 44 childhood T-ALL patients, but in none of the T-NHL or adult T-cell malignancies. Recombination of the TAL1 gene was therefore suggested to be specific for childhood T-ALL. The immunophenotypic features of the 10 T-ALL patients with this recombination were CD1-, CD2+, CD4-, CD7+, CD10-, and they had a significantly better outcome than other T-ALL cases without the recombination. The PCR technique revealed minimal residual disease (MRD) in 2 patients. One showed persistent MRD, while in the other MRD was recognized only at initial diagnosis. Further investigation is needed whether T-ALL with this recombination constitutes a distinct clinical subgroup among childhood T-ALL patients.
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PMID:[TAL1 gene analysis in T-cell malignancies]. 959 92

The BCL6 gene, encoding a POZ/Zinc finger protein which acts as a transcriptional repressor, is frequently altered at its 5' non-coding region by 3q27 chromosomal translocations in B-cell non-Hodgkin's lymphoma (NHL). BCL6 rearrangement is one of the most common genetic abnormalities in NHL. As a result of translocations, the regulatory region of the BCL6 gene is replaced by an heterologous reciprocal partner such as the immunoglobulin (IG) genes. Promotor substitution leads to deregulation of the BCL6 expression, which may be associated with lymphomagenesis. Recent studies have shown that the 5' non-coding region of the BCL6 gene is also subject to somatic hypermutation physiologically operating in germinal center (GC) B-cells in a similar pattern to that of the IG genes. There is little evidence to show that structural alterations of the BCL6 gene may be caused by mechanisms other than chromosomal translocations. To date, five cases with NHL exhibiting gross BCL6 deletions of the 1.5-2.4 kb have been reported. These deletions occurred in the same region as translocational breakpoints and the somatic hypermutations cluster, but independently of chromosomal rearrangements. The deletions overlapped at the 270 bp region and this region contains a putative protein-binding sequence which may play a role in the regulation of the BCL6 expression. Small separated deletions of 22-101 bp, which may also contain protein-binding sequences, were evident in another NHL case. In contrast to the TAL1 deletion in T-cell acute lymphoblastic leukemia (ALL), the BCL6 deletion is considered to be mediated by a mechanism other than aberrant activity of the IG recombinase. Internal deletion within the BCL6 gene is a recurrent molecular abnormality in B-cell NHL, which is sometimes indistinguishable from rearrangements by chromosomal translocations. At present, the mechanism of DNA recombination and its role in lymphomagenesis remain unknown.
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PMID:Internal deletions within the BCL6 gene in B-cell non-Hodgkin's lymphoma. 1095 71