bcl-1

CCND1

A gene on chromosome 11q13 that encodes a member of the highly conserved cyclin family, which regulates CDK kinases. Cyclin D1 forms a complex with and is a regulatory subunit of CDK4 or CDK6, which are required for cell cycle G1/S transition; it also interacts with tumour suppressor protein Rb, which regulates the expression of CCND1.
 
Molecular pathology
CCND1 mutations, amplification and overexpression alter cell cycle progression, occur in various tumours and play a role in tumourigenesis.

bcl-1

Proto-ONCOGENEs concerned with the persistence of LYMPHOCYTES. Mutations can cause various kinds of lymphocytic lymphomas and chronic lymphocytic leukaemia. bcl-1 genes are situated at chromocoam sites that break easily.
References in periodicals archive ?
An NR3C1 diallelic single nucleotide polymorphism, Bcl-1, has been reported to distinguish individuals with the highest GC sensitivity.(6) The aim of the present study was to investigate the association between the NR3C1 gen (Bcl-1-CG) polymorphism and the response to therapy among RA patients and healthy control subjects.
The distribution of the NR3C1 Bcl-1 polymorphism in the intron 2 polymorphism were evaluated in RA patients and healthy control populations by using the polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) method.
Digestion of PCR product by the Bcl-1 enzyme generated one fragment for homozygous G/G, three fragments for heterozygote G/C, and two fragments for homozygous C/C (Figure 1).
Genotype frequencies of the NR3C1 Bcl-1 polymorphism did not differ between the patients with RA and the controls (table 2).
Frequency of Bcl-1 genotypes in control and rheumatoid arthritis cases NR3C1 gene Rheumatoid arthritis Healthy OR (n=65) control (n=70) n % n % BCL-1 polymorphism Genotype CC 35 53.8 42 60 3.023* CG 20 30.8 24 34.3 2.933* GG 10 15.4 4 5.7 3.000[dagger] NR3C1 gene 95% CI p BCL-1 polymorphism Genotype CC 0.870-10.506* 0.082* CG 0.795-10.821* 0.106* GG 0.891-10.096[dagger] 0.090[dagger] # High expression; t Low expression; * OR (95%CI) was adjusted by age and sex; t Fisher's Exact Test.
For oral administration, BCL-1, 400 mg/kg; BCL-2, 800 mg/kg; BCL-3, 1600 mg/kg; BCL-4, 3200 mg/kg; BCL-5, 6400 mg/kg.
BCL-1, -2 and -3 were test groups treated with BCL (400, 800 and 1600 mg/kg respectively, p.o.).
We present the lymph node morphology, the incidence and patterns of bone marrow involvement, and the results of available cyclin D1 immunostaining and bcl-1 gene rearrangement analyses in 19 cases of large cell variants of [CD5.sup.+], [CD23.sup.-] BCL/B-cell leukemia.
DNA was extracted from nodal or extranodal tissue and bone marrow aspirate as described previously.[35] Polymerase chain reaction analysis of the translocation involving the major translocation cluster of the bcl-1 gene and the immunoglobulin heavy-chain gene was performed using both primer pairs, mcl-1/[J.sub.h] and mcl-2/[J.sub.h], as previously described.[36]
Bcl-1 analysis was performed in a total of 5 cases (4 blastic [CD5.sup.+], [CD23.sup.-] BCLs and 1 MCL-P).
Mantle cell lymphoma and its leukemic phase constitute a well-studied hematologic malignancy with known overall survival, prognostic indicators, morphologic findings at diagnosis and in bone marrow, and known incidence of bcl-1 immunoglobulin gene rearrangements.
However, the immunophenotypic features and presence of a bcl-1 gene rearrangement supported the mantle cell origin.