Your browser doesn't support javascript.
loading
Show: 20 | 50 | 100
Results 1 - 2 de 2
Filter
Add more filters










Database
Language
Publication year range
1.
Genes Chromosomes Cancer ; 27(1): 11-6, 2000 Jan.
Article in English | MEDLINE | ID: mdl-10564581

ABSTRACT

We have studied 215 male patients (aged 45-97 years) whose sole cytogenetic abnormality was clonal loss of the Y chromosome in metaphase cells from unstimulated cultures. The patients comprised a control group with no evidence of hematologic disease and four disease case groups: 1) myelodysplastic syndrome (MDS), refractory anemia, refractory anemia with excess blasts (RAEB), RAEB in transformation, and chronic myelomonocytic leukemia; 2) acute myelogenous leukemia; 3) myeloproliferative disorder (MPD), chronic granulocytic leukemia, and polycythemia vera; and 4) B-cell lymphoma/leukemia. The frequency of cells with Y loss increased with age and was significantly greater in cases than in controls, but it was not correlated with survival or with prior therapy. The frequency of cases with a -Y clone was 6.3% of male karyotypes and represented 16.4% of all abnormal male cytogenetic reports. Much of the difference between cases and controls appears to be accounted for by a greater frequency of cases with > 75% Y loss. A value of 81% chromosome Y loss maximized the combined sensitivity (28%) and specificity (100%) for predicting disease status, but a 75% cutoff provided the best estimate of disease risk. Even in older males, if > 75% of metaphase cells are 45,X,-Y, they probably represent a disease-associated clonal population, and it is possible that the critical genetic change is not visible through the microscope. This observation is true for MDS, MPD, B-cell disease, and especially acute myelogenous leukemia. The prognostic association of Y chromosome loss for survival appears to be neutral or favorable. Genes Chromosomes Cancer 27:11-16, 2000.


Subject(s)
Chromosome Deletion , Hematologic Diseases/genetics , Y Chromosome/genetics , Aged , Aged, 80 and over , Aging/genetics , Aneuploidy , Hematologic Diseases/diagnosis , Hematologic Neoplasms/diagnosis , Hematologic Neoplasms/genetics , Humans , Karyotyping , Male , Middle Aged , Prognosis , Time Factors
2.
Int J Cancer ; 41(5): 727-31, 1988 May 15.
Article in English | MEDLINE | ID: mdl-2452795

ABSTRACT

Analbuminemic rats (NAR) are a mutant breed with an inherent inability to synthesize albumin. However, heterozygous rats born of a pair of NAR and Sprague-Dawley (SD) rats can synthesize albumin. Immunohistochemical staining for albumin shows that, although the majority of hepatocytes of SD x NAR F1 (female SD x male NAR) rats are positive for albumin, a small number of hepatocytes are negative. These albumin-negative hepatocytes are frequently found in the form of clusters which appear cytologically normal. When the rats were given a dietary regimen of 2-acetyl-aminofluorene (2-AAF), there was a significant increase in the number of albumin-negative hepatocytes. On the other hand, diethylnitrosamine (DEN) or 5-azacytidine did not increase the number of albumin-negative hepatocytes. 2-AAF and DEN also induced enzyme-altered hepatocytes but the albumin-negative hepatocytes were of a completely different class from the enzyme-altered hepatocytes. The results of this study indicate that some kind(s) of carcinogens induce mutated hepatocytes which are probably not involved in carcinogenesis.


Subject(s)
Albumins/metabolism , Carcinogens/pharmacology , Liver/metabolism , Serum Albumin/deficiency , 2-Acetylaminofluorene/pharmacology , Animals , Azacitidine/pharmacology , Cell Division , Diethylnitrosamine/pharmacology , Glutathione Transferase/metabolism , Histocytochemistry , Immunoenzyme Techniques , Liver/drug effects , Male , Placenta/enzymology , Rats , Rats, Inbred Strains , Rats, Mutant Strains
SELECTION OF CITATIONS
SEARCH DETAIL
...