Ano-genital human papillomavirus type 97 infection is detected in Canadian men but not women at risk or infected with the human immunodeficiency virus.

Background: Human papillomavirus type 97 (HPV97) DNA was detected in nearly 5% of anal samples collected from HIV-seropositive men living in Montreal, Canada. The rate of detection of HPV97 in the genital tract of Canadian women is unknown. Whether HPV97 is a local epidemic in HIV-seropositive men living in Montreal is also unknown.

Hybridization assay performed at ambient temperature for typing high-risk human papillomaviruses.

Background: Human papillomavirus (HPV) infection with oncogenic types is a prerequisite for cervical cancer development. HPV typing is required in the management of pre-cancerous lesions, epidemiological studies, and vaccination trials. None of the available HPV assays are satisfactory for routine diagnosis.

An in vitro selection scheme for oligonucleotide probes to discriminate between closely related DNA sequences.

Using an in vitro selection, we have obtained oligonucleotide probes with high discriminatory power against multiple, similar nucleic acid sequences, which is often required in diagnostic applications for simultaneous testing of such sequences. We have tested this approach, referred to as iterative hybridizations, by selecting probes against six 22-nt-long sequence variants representing human papillomavirus, (HPV). We have obtained probes that efficiently discriminate between HPV types that differ by 3-7 nt.

The value of clonality in the diagnosis and follow-up of patients with cutaneous T-cell infiltrates.

The diagnosis of early stages of cutaneous T-cell lymphoma (CTCL) is often difficult, especially for lesions that are at the borderline between reactive and neoplastic skin T-cell infiltrates. T-cell monoclonality in these lesions is considered by some to be an important prognostic factor of neoplastic evolution, whereas others claim that clonality can also be found in benign skin infiltrates and is therefore of limited diagnostic value. To address this controversy, the authors analyzed retrospectively eight patients with lymphocytic skin lesions who progressed to CTCL, and three patients with recurrent T-cell lymphocytic infiltrates who had not developed CTCL.

Frequent loss of heterozygosity at the DNA mismatch-repair loci hMLH1 and hMSH3 in sporadic breast cancer.

To study the involvement of DNA mismatch-repair genes in sporadic breast cancer, matched normal and tumoral DNA samples of 22 patients were analysed for genetic instability and loss of heterozygosity (LOH) with 42 microsatellites at or linked to hMLH1 (3p21), hMSH2 (2p16), hMSH3 (5q11-q13), hMSH6 (2p16), hPMS1 (2q32) and hPMS2 (7p22) loci. Chromosomal regions 3p21 and 5q11-q13 were found hemizygously deleted in 46% and 23% of patients respectively. Half of the patients deleted at hMLH1 were also deleted at hMSH3.

Allelic losses and DNA methylation at DNA mismatch repair loci in sporadic colorectal cancer.

Normal and tumor DNA samples of 35 patients with sporadic colorectal carcinoma were analyzed for microsatellite alterations at 12 markers linked to mismatch repair loci: hMLH1, hMSH2, hMSH3, hMSH6, hPMS1 and hPMS2. Remarkably, no correlation was observed between the replication error phenotype (RER+) and allelic losses at these loci. Hemizygous deletions, seen in 6/35 (17%) informative cases at hMLH1, 4/27 (15%) at hMSH2/hMSH6 and 6/34 (18%) at hMSH3, were rarely found in RER+ tumors.

Genomic loci susceptible to replication errors in cancer cells.

Microsatellite instability due to a deficiency in DNA mismatch repair is characteristic of a replication error (RER) phenotype. This widespread genomic instability is well documented in hereditary non-polyposis colon cancer (HNPCC) as well as subsets of sporadic carcinomas. Features of the RER phenotype such as the early appearance in tumour development and better prognosis of RER+ colorectal tumours render its examination important for cancer patients.

High resolution deletion mapping reveals frequent allelic losses at the DNA mismatch repair loci hMLH1 and hMSH3 in non-small cell lung cancer.

To study the involvement of DNA mismatch repair genes in non-small cell lung cancer, matched normal and tumoral DNA samples from 31 patients were analyzed for both LOH and microsatellite instability with 34 markers at or linked to hMLH1 (3p21), hMSH2 (2p16), hMSH3 (5q11-q13), hMSH6 (2p16), hPMS1 (2q32), and hPMS2 (7p22) loci. Chromosomal regions 3p21 and 5q11-q13 were found to be hemizygously deleted in 55% and 42% of the patients, respectively. Sixty five percent of the patients deleted at hMLH1 were also deleted at hMSH3.

Overall informativity, OI, in DNA polymorphisms revealed by inter-Alu PCR: detection of genomic rearrangements.

We studied two systems of multilocus markers revealed by PCR using primers directing amplification between Alu repeats in a tail-to-tail orientation. Genomic polymorphisms were detected as the presence or absence of the electrophoretic bands representing DNA fragments of a given length. A total of 104 such fragments segregating as Mendelian markers in a panel of eight CEPH families were analyzed by two-point linkage analysis.

U3 long terminal repeat-mediated induction of intracellular immunity by a murine retrovirus: a novel model of latency for retroviruses.

BL/VL3 radiation leukemia virus (RadLV) is a thymotropic, highly leukemogenic murine leukemia virus (MuLV) which is unable to replicate in vitro in mouse fibroblasts. We have previously reported that the U3 long terminal repeat region of its genome is responsible for this block (E. Rassart, Y.

B-cell lymphoma presenting as a midfacial necrotizing lesion.

A case of midfacial necrotizing lesion (midline nonhealing granuloma) is reported. Paraffin- and frozen-section immunocytochemistry suggested a tumor of B-cell lineage and was confirmed by Southern blot analysis that disclosed an immunoglobulin heavy chain gene rearrangement with no evidence of T-cell receptor genetic aberration. The tumor was of B-cell lineage despite the tumor site and the angiocentric pattern, which are typically seen with peripheral T cell lymphoma with this presentation.

DNA-binding proteins that interact with the long terminal repeat of radiation leukemia virus.

We used the electrophoretic mobility shift assay to identify the interactions of nuclear proteins with the long terminal repeat of leukemogenic, thymotropic BL/VL3 radiation leukemia virus (RadLV). In the promoter region, we identified a CCAAT box-binding protein (CBP) that has the same binding characteristics as the CCAAT box-binding protein that binds to the Moloney murine sarcoma virus promoter and most likely represents the CP1 factor. In the upstream enhancer region unique to BL/VL3, we detected several sequence-specific complexes, one with T-lymphocyte extracts but not with fibroblast extracts.

Molecular pathology of chronic myelogenous leukemia.

The presence of Philadelphia chromosome t(9:22) is a hallmark of 95% of clinical cases of chronic myelogenous leukemia (CML) as well as 20% of adult acute lymphoblastic leukemia (ALL) and 5% of acute myeloid leukemia (AML). The product of t(9;22) is a fusion protein BCR-ABL. The fusion proteins of CML, ALL and AML have increased tyrosine kinase activity and show a transforming potential in vitro and in animal models.