Biomedical subjects

J Henshall

Publications and source records attributed to J Henshall.

5 recordsLinked to original sources

PubMed1991

CD3+, CD4-, CD8- large granular T-cell lymphoproliferative disorder.

Large granular T-cell lymphoproliferative disorder (LGTLD) is a heterogeneous disorder covering a broad spectrum of diseases and requiring further subdivision. Most reported cases emphasized its suppressor phenotype (T gamma cell or CD8+), but we encountered two cases of CD3+, CD4-, CD8- LGTLD. Both cases had a benign clinical course and required no chemotherapy despite persistent lymphocytosis. This unique phenotype has been reported in a few cases of acute lymphoblastic leukemia expressing the T-cell receptor (TcR) gamma chain gene and is considered the counterpart of thymocytes at the intermediate stage between early precursors and mature thymocytes. Our case 1 provides further evidence that the CD3+, CD4-, CD8- phenotype, indeed, expresses the TcR gamma chain gene. However, the negative reaction to terminal deoxynucleotidyl transferase in our case 1 indicates that this phenotype represents proliferation of peripheral T-cells, in which about 2% bear the CD3+, CD4-, CD8- phenotype in the normal population. The selective use of CD3, CD4, CD8, HNK-1 monoclonal antibodies and of cytochemical stains (acid phosphatase and alpha-naphthyl butyrate esterase) for characterization of this disorder is discussed.

Adult↗

PubMed1989

Comparison of phenotyping and genotyping of lymphoid neoplasms.

Comparison of phenotyping (PT) and genotyping (GT) of lymphoid neoplasms was performed on 51 specimens including lymph nodes, bone marrows, and body fluids. PT was performed with a flow cytometer using a large monoclonal antibody panel. GT included the testing for gene rearrangements of heavy chain, kappa and lambda light chains, and T-cell receptor beta-chain genes with DNA probes. The results obtained from these two techniques were generally compatible in terms of clonality and cell lineage. Only one case of B-cell lymphoma was not diagnosed by PT but showed gene rearrangement. For T-cell lymphoma, GT offers a more definitive diagnosis than does PT. Biclonality was demonstrated in one case of hairy cell leukemia by GT only. The rearranged band also offers a definitive clonal identification based on electrophoretic mobility. GT can detect a monoclonal population as small as 5% and can be performed on old or fresh specimens. PT requires 20% abnormal cells and a fresh specimen. It is concluded that GT is superior to PT for lymphoid tumor diagnosis, but it should be reserved as a supplementary test at this stage because of its technical complexity.

Antibodies, Monoclonal↗

PubMed1988

Marker discrepancy as a diagnostic criterion for lymphoid neoplasms.

Multimarker studies were conducted on 195 lymph node, 59 bone marrow, 44 peripheral blood, eight body fluid, and eight internal organ specimens. The markers were identified by fluorochrome-labeled antibodies quantified with flow cytometry. T-cell receptor gene rearrangements were used for the determination of T-cell clonality. These studies confirmed that CD 19 (B4, Leu 12) is highly sensitive for B-lymphoblastic leukemia, CD 7 (Leu 9) is highly sensitive for T-lymphoblastic leukemia, and CD 5 (Leu 1) is highly sensitive for chronic lymphocytic leukemia. When these markers were compared to antigens of the same cell lineage (e.g., CD 19 to CD 20 [Leu 16] or to surface immunoglobulin, CD 7 to CD 3 [Leu 4], and CD 5 to CD 3), a marked discrepancy between them was diagnostic of the corresponding tumor. T-cell marker discrepancy (CD3 vs. CD 7) was demonstrated in T-cell lymphomas, but it was also shown occasionally in polyclonal T-cell populations. On the other hand, a marked discrepancy between the percentages of a B-lineage (CD 19 or CD 20)-positive and a surface-immunoglobulin-positive population is a reliable phenotype for the diagnosis of a surface-immunoglobulin-negative B-cell lymphoma.

Antigens, Surface↗

PubMedDate not supplied

A sampling algorithm for segregation analysis.

Methods for detecting Quantitative Trait Loci (QTL) without markers have generally used iterative peeling algorithms for determining genotype probabilities. These algorithms have considerable shortcomings in complex pedigrees. A Monte Carlo Markov chain (MCMC) method which samples the pedigree of the whole population jointly is described. Simultaneous sampling of the pedigree was achieved by sampling descent graphs using the Metropolis-Hastings algorithm. A descent graph describes the inheritance state of each allele and provides pedigrees guaranteed to be consistent with Mendelian sampling. Sampling descent graphs overcomes most, if not all, of the limitations incurred by iterative peeling algorithms. The algorithm was able to find the QTL in most of the simulated populations. However, when the QTL was not modeled or found then its effect was ascribed to the polygenic component. No QTL were detected when they were not simulated.

Algorithms↗

PubMedDate not supplied

T-cell receptor expression in lymphoid neoplasms. A comparison of phenotypic expression and genotyping.

T-cell receptor antibodies (TCR alpha beta and TCR gamma delta) were used for a flow cytometric study of 114 specimens of lymphoid neoplasms and normal controls in order to find out whether or not the expression of TCR proteins differs in between normal and neoplastic tissues. It was found that TCR alpha beta population was predominant in all categories except T gamma lymphoproliferative disorder (TGLD), T-cell lymphoblastic leukemia (T-ALL), and natural killer-like T-cell lymphoma (NKTL), in which three of 18, one of three, and two of two specimens, respectively, showed a predominant TCR gamma delta population. Natural killer cell lymphoma (NKL) showed essentially absence of either TCR alpha beta or TCR gamma delta protein. Therefore, TCR antibodies can be selectively used in cases of TGLD, T-ALL, and NKTL to substantiate their diagnoses. Furthermore, the absence of TCR protein is characteristic of NKL and helps to distinguish it from NKTL. Without the TCR antibodies, TCR gene analysis is sometimes needed to separate these two entities. When comparing with genotyping, 11 of 12 cases with TCR beta gene rearrangement and one of two cases with TCR alpha gene rearrangement expressed TCR alpha beta protein. One of four cases with TCR gamma gene rearrangement and both cases with TCR delta gene rearrangement expressed TCR gamma delta protein. Thus, TCR antibody phenotyping can reliably predict TCR genotypes under most circumstances.

Diagnosis, Differential↗