1,721,007 research outputs found
B Non-Hodgkin lymphoma in a haemophilia patient with idiopathic CD4+ T-lymphocytopenia.
No full textWe report here a case of an HIV-uninfected, anti-hepatitis C virus (HCV) positive haemophiliac, who was transfused with blood and intermediate purity factor VIII concentrates. Since 1988, a progressive decline in the CD4+ T-cell count was recorded, and in 1993 a B-cell non-Hodgkin's lymphoma (B-NHL) was diagnosed. The morphological appearance of the tumor with features of intermediate/mantle zone lymphoma, and the absence of EBV sequences within the tumor, ruled out the occurrence of a typical "opportunistic" lymphoma. However it is possible that the blood product therapy and its infectious complications may have played a role on immune function impairment
Chromosome damage induced in cord blood T-lymphocytes infected in vitro by HTLV-I.
No full textExperiments were carried out to investigate whether the human T-lymphotropic virus type I (HTLV-I), alone or in combination with a chemical mutagen such as mitomycin C (MMC), has the capacity to damage host chromosomes. Cord-blood T lymphocytes (CBL) were infected by co-cultivation with lethally irradiated HTLV-I-producing cells. Infected and immortalized CBL were then studied for frequencies of sister chromatid exchanges (SCE), chromosome breaks and micronuclei. HTLV-I-infected cells had statistically higher baseline SCE, chromosome aberrations and micronucleus values than the uninfected control CBL. While MMC treatment further augmented these values both in control and in infected lymphocytes, the latter did not show dose-related increases, most likely because of the more pronounced MMC-induced delaying effect on cell progression to mitosis. In view of similar previous observations in mouse lymphocytes carrying the Moloney murine leukemia virus, it is suggested that expression of a common retrovirus gene product, such as the pol endonuclease, might be responsible for the cytogenetic abnormalities observed. In addition to the IL-2 autocrine loop, the direct induction of chromosome damage by HTLV-I in target lymphocytes may be related to the pathogenesis of malignancies associated with HTLV-I infection
Association of p53 gene and protein alterations with metastases in colorectal cancer.
No full textIF: 4,269
Abstract: Using monoclonal antibody PAb 1801, p53 protein was detected in the neoplastic cells of 39 (46.9%) of 83 colorectal carcinomas studied. Patients with p53+ tumors showed a higher incidence of lymph node and liver metastases (p = 0.035); in patients whose tumors were located in the rectosigmoid, p53 expression also correlated with a more advanced stage according to Dukes' classification (p = 0.015) as well as nodal (p = 0.006) and liver (p = 0.019) metastases. Following amplification of exons 5 to 8 of the p53 gene by means of the polymerase chain reaction technique, single-strand conformation polymorphism analysis disclosed an anomalous migration pattern in 23 of the 39 p53+ tumors and in four of the 35 p53 - tumors analyzed. Sequence analysis showed G:C --> A:T transitions in 63.6%, G:C --> T:A and G:C --> C:G trans versions in 18.2%, deletions and insertions in 13.6%, and A:T --> G:C transitions in 4.6% of the cases. Loss of heterozygosity was studied in the DNA of 79 patients; allelic loss was found in 29 (49.1%) of the 59 informative patients. Loss of heterozygosity was correlated with p53 overexpression (p = 0.0002) as well as with the presence of mutations as detected by single strand conformation polymorphism analysis (p = 0.0024)
A CD30-POSITIVE T-CELL LINE ESTABLISHED FROM AN AGGRESSIVE ANAPLASTIC LARGE-CELL LYMPHOMA, ORIGINALLY DIAGNOSED AS HODGKINS-DISEASE
No full textTen months following the diagnosis of Hodgkin's disease (HD), a 46-year-old woman presented cutaneous and leukemic involvement by CD30+ anaplastic large cells, from which a continuously growing, exogenous growth factor-independent T cell line was established. The cultured cells are phenotypically and genotypically T cell in type, negative for EBV, HTLV-I and HTLV-II viral sequences, and release soluble CD30 into the supernatant. Karyotype analysis disclosed several chromosomal abnormalities, but none on chromosome 5q. The involvement of the short arm of chromosome 17 prompted us to investigate the TP53 gene by means of the polymerase chain reaction single-strand conformation polymorphism (PCR-SSCP) analysis, but no alterations were found in exons 5-8
New insights into human papillomavirus-associated head and neck squamous cell carcinoma
No full textHuman papillomavirus (hPV)-associated head and neck squamous cell carcinoma (hnSCC) is an entity with peculiar clinical and molecular characteristics, which mainly arises from the reticulated epithelium lining the crypts of the palatine tonsils and the base of the tongue. The only head and neck site with a definite etiological association between persistent high-risk (hr) hPV infection and development of SCC is the oropharynx. hPV-positive malignancies represent 5-20% of all hnSCCs and 40-90% of those arising from the oropharynx, with widely variable rates depending on the geographic area, population, relative prevalence of environment-related SCC and detection as-say. hPV-16 is by far the most common hr hPV genotype detected in oropharyngeal SCC (oPSCC), and the only definitely carcinogenic genotype for the head and neck region. Patients with hPV-induced oPSCC are more likely to be middle-aged white men, non-smokers, non-drinkers or mild to moderate drinkers, with higher socioeconomic status and better performance status than subjects with hPV-unrelat-ed SCC. hPV-induced hnSCCs are often described as non-keratinizing, poorly differentiated or basaloid carcinomas, and are diagnosed in earlier T-category with a trend for a more advanced n-category, with cystic degeneration, than the hPV-unrelated carcinomas. hPV positiv-ity is associated with better response to treatment and modality-independent survival benefit. Treatment selection in hPV-related oropha-ryngeal carcinoma is becoming a critical issue, and although there is no evidence from randomized, controlled trials to support a treatment de-escalation in hPV-positive SCC, some investigators argue that intensive combined modality strategies may represent an overtreatment
Absence of the cell cycle inhibitor p27Kip1 protein predicts poor outcome in patients with stage I-III colorectal cancer.
No full texti.f.: 3.82
p53 gene alterations and protein accumulation in colorectal cancer.
No full textI.F. 1.581
Abstract: Aim-To correlate immunohistochemical staining with single strand conformation polymorphism (SSCP) analysis of the p53 gene in colorectal cancer in order to understand how the findings provided by the two techniques complement each other in defining p53 functional status.Methods-Frozen tumour tissue from 94 patients with colorectal cancer was studied for p53 protein accumulation and gene mutations. Accumulation of p53 protein was detected by immunohistochemistry using PAb1801 and BP53-12-1 monoclonal antibodies. The findings were then compared with SSCP analysis of exons 5 to 8 of the p53 gene. All cases with a positive result by SSCP analysis were confirmed by sequencing.Results-Nuclear staining was observed in 51 (54.2%) cases. SSCP analysis of the DNA amplified by PCR revealed that the electrophoretic pattern had shifted in 30 cases; sequence analysis confirmed the occurrence of a mutation in 29 cases and of a polymorphism in one. In 27 cases both assays gave a positive result, and in 40 both were negative; therefore, concordance between PCR-SSCP and immunohistochemistry was seen in 72% of cases.Conclusion-The data indicate that positive immunostaining corresponds with the presence of a mutation in most, but not all, cases studied; other mechanisms could be responsible for stabilisation and accumulation of p53 protein in the nucleus. Nonsense mutations which do not confer stability on the protein will not be detected by immunohistochemistry and false negative results can also occur with SSCP analysis
HPV-16 E6 L83V variant in squamous cell carcinomas of the upper aerodigestive tract.
Get PDFPURPOSE: The aim of this prospective case series study was to determine the prevalence of HPV-DNA, analyze the E6 mRNA expression, identify intra-type variation in the E6 oncogene in upper aerodigestive tract (UADT) squamous cell carcinoma (SCC), and correlate the presence of HPV-DNA with several clinical parameters and outcome.
METHODS: Frozen samples of UADT-SCC were analyzed for the presence and characterization of HPV-DNA and RNA sequences by means of polymerase chain reaction (PCR), reverse transcriptase-PCR, and direct sequencing of amplified products.
RESULTS: HPV-DNA sequences were detected in 10% of the tumors, all of which were typed as HPV-16. Positivity for HPV-16 E6/E7 mRNA was observed in five of the eight HPV-positive tumors (62.5%). The HPV-16 E6 L83V variant was present in five cases. Multivariate analysis identified a history of absence of smoking (P = 0.009) as a predictor of HPV-positive tumor. No significant differences in overall and disease free survival curves were observed between patients with HPV-positive tumors and patients with tumors without detectable HPV-DNA.
CONCLUSION: Our findings support the etiological participation of HPV-16 in a subset of UADT-SCCs from patients lacking traditional risk factors. The potential prognostic significance of HPV-16 E6 L83V variant in HPV-16 positive UADT-SCCs should be more extensively investigated
Vulvar carcinoma in a 12-year-old girl with vertically acquired human immunodeficiency virus infection
No full textWe report the first case of a girl with vertically acquired human immunodeficiency virus (HIV) infection, who developed invasive squamous cell carcinoma of the vulva at 12 years of age. Lesions resembling bowenoid papulosis covered the perianal area as well. She underwent a nonmutilating surgical excision of the infiltrating lesion. More than 3 years later, her clinical condition is excellent, although dysplastic, noninfiltrating multifocal lesions persist. This case highlights the need to perform careful periodic genital examinations in all HIV-infected children and adolescents born to HIV-positive mother
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