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P E Crossen

Publications and source records attributed to P E Crossen.

At least 19 recordsLinked to original sources
PubMed1995

Elevated frequency of a SstI polymorphism of the Ets-1 oncogene in non-Hodgkin's lymphoma patients.

We studied the frequency of a SstI polymorphism of the Ets-1 oncogene in 100 patients with non-Hodgkin's lymphoma, 44 patients with Hodgkin's disease, 49 patients with chronic myeloid leukemia, and 100 controls. There was no difference in the genotype frequency between the controls and patients with either Hodgkin's disease or chronic myeloid leukemia. In contrast, there was a highly significant difference in the distribution of the three genotypes between the patients with non-Hodgkin's lymphoma and the controls (X2 = 10.76, 2df, p = 0.004) with the C2 allele being more frequent in the lymphoma patients. Molecular cloning indicated that the polymorphic SstI site lay 304 bp from exon 7. This is the second association of the SstI polymorphism of the Ets-1 oncogene with a lymphoid disorder and suggests that the presence of the C2 allele is associated with a predisposition to develop a lymphoid malignancy.

Alleles↗
PubMed1994

Increased frequency of the S allele of the L-myc oncogene in non-Hodgkin's lymphoma.

We studied 100 patients with non-Hodgkin's lymphoma, 44 patients with Hodgkin's disease and 100 controls for the prevalence of the EcoRI restriction fragment polymorphism of the L-myc oncogene. No difference in the frequency of the three genotypes (LL, LS, SS) was found between the patient and control groups. However, the S allele was found to occur more frequently in the non-Hodgkin's lymphoma patients (chi 2 = 4.57, P = 0.032). These data confirm an earlier report and suggest that the presence of the S allele is associated with susceptibility to non-Hodgkin's lymphoma.

Adult↗
PubMed1993

Oligoclonal B-cell leukemia characterized by spontaneous cell division and telomere association.

Cytogenetic analysis of unstimulated cultures from a female patient with chronic B-cell leukemia (CLL) revealed three cytogenetically distinct clones, suggesting that the patient's leukemia was oligoclonal. Immunoglobulin heavy chain gene rearrangement studies revealed 1 germline and 4 rearranged bands, indicative of an oligoclonal leukemic population. Further evidence of oligoclonality was provided by X-linked RFLP studies. This is the first report of oligoclonality in CLL demonstrated by cytogenetic, immunoglobulin gene rearrangement, and X-chromosome inactivation studies. In addition to oligoclonality, the patient's leukemic cells exhibited telomere association, a Robertsonian translocation, and clonal evolution, suggesting an underlying genomic instability.

Cell Division↗
PubMed1993

Cloning and sequencing of a t(14;19) breakpoint that involves the C mu switch region.

The t(14;19) is a recurring translocation found in a small number of cases of chronic B-cell leukemia (CLL). We have cloned and sequenced the breakpoint in a patient with a t(14;19) and shown that the breakpoint on chromosome 14 occurred in the C mu switch region, and that the breakpoint on chromosome 19 occurred in the 5' untranslated region of the BCL3 gene. This is in contrast to all the other reported cases with a t(14;19) in which the breakpoints on chromosome 14 occurred in the C alpha 1 or C alpha 2 switch region, and the breakpoints on chromosome 19 occurred upstream of the BCL3 gene. Our results further emphasize the importance of the switch region in the t(14;19) translocation.

Aged↗
PubMed1993

Elevated frequency of an ETS-1 restriction fragment polymorphism in chronic B-cell leukaemia.

We studied the frequency of an SstI polymorphism in 70 patients with chronic B-cell leukaemia (CLL) and 100 normal controls. There was a highly significant difference in the distribution of the three genotypes between the CLL patients and the normal controls (chi 2 = 13.46, 2 df, P < 0.001). The C2 allele was found more frequently in CLL patients and may be a marker for a predisposition to develop CLL.

Adult↗
PubMed1993

Lack of 5' BCL2 rearrangements in B-cell leukemia.

We found no rearrangements in the 5' region of the BCL2 gene in DNA samples from 60 patients with chronic B-cell leukemia (CLL). This compares with the presence of these rearrangements in up to 10% of patients in other reports, and suggests that the incidence of 5' BCL2 rearrangements in CLL is considerably less than 10%.

DNA, Neoplasm↗
PubMed1992

XbaI RFLP of ETS-1 oncogene in chronic B-cell leukaemia.

The influence of a polymorphic variant of the ETS-1 oncogene on the predisposition to develop chronic B-cell leukemia (CLL) was investigated. A total of 59 patients with CLL and 59 controls were examined for the frequency of an XbaI restriction fragment length polymorphism RFLP of the ETS-1 oncogene which has been reported to occur more frequently in patients with hematological malignancies than in normal controls. We found no significant difference in the allele frequency between the CLL patients and the normal controls. These data suggest that the presence of the XbaI RFLP is not associated with CLL.

Adolescent↗
PubMed1991

Molecular definition of interstitial deletions of chromosome 13 in leukemic cells.

Three patients with leukemia and one with a myeloproliferative disorder carried an interstitial deletion of chromosome 13, del(13)(q12q14), in leukemic cells. Proximal and distal breakpoints of the deleted segment were characterized by using DNA restriction fragment length polymorphisms of chromosome 13 supplemented by quantitative densitometry of hybridization signals to determine the copy number of individual loci. Both proximal and distal breakpoints varied between patients, and it is unlikely that a significant hybrid gene was formed by rejoining at the breakpoint junctions. The retinoblastoma gene was encompassed by the deleted segment in all four patients.

Aged↗
PubMed1991

Complex karyotypic evolution in B-cell chronic lymphocytic leukemia.

Cytogenetic analysis at diagnosis in a female patient with chronic B-cell leukemia showed a single abnormal clone with a 4p+ abnormality, 46,XX, -4, +der(4)t(4;?)(p16;?). Six additional clones evolved from this clone during the following 4 1/2 years and showed 3p+, 4p-, and 11q- chromosomes in addition to the 4p+ abnormality. Immunoglobulin heavy chain gene rearrangement studies showed two rearranged bands and a faint germline band. Following splenectomy, a strong germline and faint rearranged bands were seen, suggesting that the majority of cells were normal, whereas cytogenetic studies showed that the karyotypically abnormal cells were still present. The combination of cytogenetic and Ig gene rearrangement studies provides detailed information regarding the number of circulating normal and leukemic cells.

Chromosome Aberrations↗
PubMed1991

Linkage studies in tuberous sclerosis. Chromosome 9?, 11?, or maybe 14!

Published reports show linkage of tuberous sclerosis (TSC) to either chromosome 9 in some families or chromosome 11 in other families. We studied 243 individuals (82 with TSC) from 16 multigenerational TSC families. The diagnosis of TSC conformed to the criteria of Gomez. Penetrance was estimated at 0.90. DNA markers were analyzed using Southern blotting, probe hybridization, autoradiography, and genetic linkage analysis. Two-point lod scores for TSC were calculated for 43 genetic markers distributed over 11 chromosomes. Tests for homogeneity rejected the null hypothesis of homogeneity. Linkage to TSC was excluded (z less than or equal to -2, theta greater than or equal to 0.05) for 23 of these markers including 9q34 and 11q markers. One family gave z(theta max) = 1.8, theta max = 0.001 with ABO (on 9q34), and two other families attained lod scores greater than 1 for 9q34-region markers. The lod score for TSC versus chromosome 14 marker pAW101 (D14S1) was z(theta max) = 1.98, theta max = 0.15. A single large family has overall negative lod scores for markers localized to both chromosome 9 and chromosome 11. These data confirm genetic heterogeneity in TSC and suggest linkage of some families to 9q34. Furthermore, the data suggest that 14q may be an interesting area.

Chromosome Mapping↗
PubMed1990

t(2;14)(q23;q32.3) as the sole abnormality in a patient with acute nonlymphocytic leukemia (FAB-M4).

Cytogenetic analysis of bone marrow cells from a 53-year-old man with acute nonlymphocytic leukemia (FAB-M4) revealed a t(2;14)(q23;q32.3) as the sole cytogenetic abnormality. This is the first report of a t(2;14)(q23;q32.3) as the sole abnormality in acute nonlymphocytic leukemia (M-4). The findings are discussed in relation to the possible role of genes located at 2q23 in acute nonlymphocytic leukemia.

Chromosomes, Human, Pair 14↗
PubMed1989

Absence of linkage of ABO blood group locus to familial tuberous sclerosis.

A mutation leading to tuberous sclerosis was linked to the ABO blood group locus (9q34) on the long arm of chromosome 9. In an effort to confirm this assignment, nine multigenerational families with tuberous sclerosis, comprising 126 sampled individuals, were assessed for linkage of the ABO locus to tuberous sclerosis. Two-point linkage analysis and multilocus linkage analysis were used to evaluate linkage between tuberous sclerosis and the markers ABO, MCT136, and AblK2. Linkage of ABO to tuberous sclerosis was excluded for a distance of 20 centimorgans (cM) encompassing the region of the ABO locus. There was no evidence for genetic heterogeneity within this data set. Using 23 polymorphic markers, exclusion mapping demonstrated only a 1% probability that the tuberous sclerosis locus was on the distal short arm of chromosome 9 and provided no evidence in support of a tuberous sclerosis locus on the remainder of chromosome 9 including the area of the ABO locus.

ABO Blood-Group System↗
PubMed1989

Cytogenetic and molecular changes in chronic B-cell leukemia.

Cytogenetic studies using B-cell mitogens indicate that approximately 50% of patients with chronic B-cell leukemia (CLL) have chromosome abnormalities. The most common abnormality is an additional chromosome 12, either as the sole abnormality or in conjunction with other abnormalities such as 14q+, 6q-, and 11q-. In two instances, the 14q+ is a result of a translocation from either chromosome 11, t(11;14), or chromosome 19, t(14;19). These two translocations led to the identification of the bcl-1 and bcl-3 genes located on chromosomes 11 and 19, respectively. Very few instances of oncogene activation have been described and it does not seem to be an important mechanism in the pathogenesis of CLL. Further cytogenetic and molecular studies may provide clues for the identification of the genes involved in CLL.

B-Lymphocytes↗
PubMed1987

Chromosome abnormalities in chronic lymphocytic leukemia revealed by cytochalasin B and Epstein-Barr virus.

Peripheral blood lymphocytes from eight patients with chronic lymphocytic leukemia (CLL) were cultured with Epstein Barr virus (EBV) and cytochalasin B. All eight cytochalasin B cultures had analyzable metaphases whereas only six of the EBV cultures were successful. Furthermore, the number of abnormal metaphases and the mitotic indices were greater in the cytochalasin B cultures than in the EBV cultures. Trisomy 12, alone or in combination with other abnormalities, was the most frequent cytogenetic finding. Structural abnormalities of chromosomes #6 and #14 were also found. Cytochalasin B appears to be an effective mitogen for demonstrating abnormal metaphases in patients with CLL.

Aged↗
PubMed1986

Cell cycle analysis using bromodeoxyuridine: comparison of methods for analysis of total cell transit time.

Results are presented supporting the study of cellular proliferation utilizing 5-bromodeoxyuridine (BrdU) incorporation followed by sister chromatid differential staining. In order to determine the relative accuracy of this method in estimating total cell transit time (TC), we utilized a thermosensitive rat embryonic cell line to compare measurement of TC based on the percent differentially labeled (PDLM) technique, with cell cycle measurements using [3H]-thymidine [( 3H]-TdR) incorporation and the percent labeled mitoses (PLM) technique. Results of PLM and PDLM analysis were shown to be highly concordant, indicating the utility of the BrdU method for analysis of Tc. Results are presented suggesting the general application of the PDLM method for estimations of TC in cultures of human tumors.

Animals↗