PubMed Health⌕ Search

Biomedical subjects

T Raposa

Publications and source records attributed to T Raposa.

At least 19 recordsLinked to original sources
PubMed2001

Increased risk for cancer in multiple myeloma patients and their first-degree relatives.

Analyzing data of 125 multiple myeloma patients, the authors found a 40-fold increased tumor incidence among the patients and their first-degree relatives as compared to the average population. These tumors were the same as those usually found among Hungarians. There was no difference as to the patient's blood group antigens in the families of myeloma patients with or without other tumor. IgA-type disease was found to be relatively more frequent in the group of patients who had tumor besides myeloma. In a prospective study, authors could not find mutation of suppressor gene p53 in 14 patients and their 16 healthy first-degree relatives. This may indicate that there is no p53 suppressor gene alteration responsible for the high-risk condition for tumorgenesis in this population.

Aged↗
PubMed1999

The usefulness of in vivo gene expression investigations from peripheral white blood cells: a preliminary study.

Alterations of onco/tumour suppressor genes are involved in the formation of human hematological malignancies. Previously, in animal models, we demonstrated the applicability of in vivo gene expression investigations to monitor the effects of certain carcinogenic chemicals. In our present study we determined the expression of onco/suppressor genes from isolated peripheral white blood cells of patients with chronic myeloid leukaemia (CLL) and non-Hodgkin lymphoma (NHL). Gene expressions were determined by isolation of total RNA and slot blot hybridization with chemiluminescently labeled gene probes (Ha-ras, c-myc and p53) Expression levels were compared before and after treatment with a combined cytostatic protocol, containing cyclophosphamide, doxorubicin, vincristine and prednisolone (CHOP). Both the CLL and NHL group of patients exhibited significantly higher expression of the investigated genes than healthy controls. One month after the cytostatic treatment, we found considerably fewer individuals with overexpressed oncogenes than before the treatment. Our study proved that onco/tumour suppressor gene expressions could be used as biomarkers of certain hematological malignancies, and to monitor the therapeutical effect of cytostatic drugs.

Antineoplastic Combined Chemotherapy Protocols↗
PubMed1991

Comparative studies on genotoxic and carcinogenic effects of different cytostatic protocols. I. In vivo cytogenetic analyses in CBA mice.

In vivo rodent cytogenetics may provide an important basis for an animal model for the assessment of the carcinogenic potential of antitumor drugs in man. In this paper, genotoxic alterations (i.e. sister chromatid exchanges and micronuclei) caused by different cytostatic protocols in CBA/Ca mice are described. The strongest sister chromatid exchange inducing effects were shown by the ABVD (doxorubicin-dacarbazine-bleomycinvinblastine) group and combinations containing cyclophosphamide. Compounds which affect the mitotic spindle induced only micronuclei, but not sister chromatid exchanges.

Animals↗
PubMed1989

Cytochemical maturation index for the prognostication of adult acute nonlymphocytic leukaemia.

76 adult acute nonlymphocytic leukaemias (ANLL) were characterized by cytochemical markers and placed in a coordinate system. The position of each ANLL was determined on the basis of the peroxidase and nonspecific esterase reactivity of the blast cells. This classification numerically identifies the maturation tendency and heterogeneity of individual ANLL cases according to its position in the coordinate system. 49 ANLL patients were treated with TAD protocol and the response rate seemed to be in a conspicous correlation with the position of the individual ANLL cases in the modified arrangement. Cases exhibiting a strong peroxidase maturation, i.e. the cytochemical maturation index being 80% or more had a considerable higher complete remission rate and longer duration of remission than those with low (less than 80%) maturation index. Age profoundly influenced even this figure.

Adult↗
PubMed1988

Studies on the vasoocclusive crisis of sickle cell disease IV. Mechanism of action of pentoxifylline (Trental).

Pentoxifylline was shown to prevent sickling induced by deoxygenation of SS-genotype blood from sickle cell disease patients. It also prevents development of cell stiffness, based on decreased membrane fluidity. This effect is related to increased red cell ATP content, decreased potassium loss during sickling and decreased attachment of hemoglobin to the red cell membrane during sickling. There was no effect on osmotic fragility or mean corpuscular volume. There was some increase in pH of blood from patients in vasoocclusive crisis of sickle cell disease under the effect of pentoxifylline. The consideration is discussed that pentoxifylline may prevent vasoocclusive crisis, but may not abort an existing process.

Adenosine Triphosphate↗
PubMed1987

The relationship between sister chromatid exchange induction and leukemogenicity of different cytostatics.

The genotoxicity of frequently used cytostatic agents was characterized by the enumeration of the sister chromatid exchanges (SCEs) induced by them in vivo in phytohemagglutinin-stimulated peripheral blood lymphocytes. Fifty-nine cancer patients undergoing and off chemotherapy are included in this study. The aim was to identify cytostatics according to their ability to alter the SCE frequency. Cytostatics with strong SCE-inducing ability (melphalan, cyclophosphamide, cyclophosphamide + vincristine + 5-fluorouracil, cyclophosphamide + vincristine + procarbazid + prednisolone) usually exhibited a longlasting SCE elevation. Cytosine arabinoside, hydroxyurea, vincristine, 5-fluorouracil, tamoxifen, and azathioprine did not induce SCEs. These data were compared with the leukemogenic potential of the same drugs in order to validate the relevance of SCE studies in man to signal carcinogenic hazards. It was found that over 80% of all secondary leukemias (collected from the world literature from 1930 to 1980) were preceded by the administration of cytotoxic compounds inducing long-lasting SCE elevation in lymphocytes. Only 3% of all secondary leukemias can be attributed to drugs not inducing SCEs in vivo in PHA-stimulated lymphocytes. This indicates that the lesions important for SCEs and secondary leukemias to emerge bear close biological similarities. Thus SCE studies can be used in selecting therapeutical protocols or new cytostatics with less carcinogenic potential to man.

Acute Disease↗
PubMed1984

Characteristics of secondary acute nonlymphocytic leukemias. Cytological aspects (a review).

A register of 746 cases of secondary acute leukemias has been established by reviewing the literature from 1930-1980. Out of these 680 belong to acute nonlymphocytic leukemias, FAB M1-M6. Data have been subjected to a multiparameter analysis in term of previous therapy and subtype characteristics of acute nonlymphocytic leukemia (ANLL). There are indications that secondary ANLL are characterized by the preponderance of early acute myeloblastic leukemias if compared to de novo ones. Furthermore it has been shown that alkylating agents induced decidedly more acute myelomonocytic leukemias whereas irradiation tended to induce more acute myeloblastic leukemia. Since secondary acute leukemias represent a serious late consequence of alkylating agent and irradiation therapy it is high time to find new therapeutical modalities for lymphomas and to consider the withdrawal of alkylating agents from the therapy of autoimmune disorders.

Alkylating Agents↗
PubMed1981

Clastogenicity and sister chromatid exchange induction by ftorafur.

The main effect of Ftorafur at the chromosomal level is the induction of chromatid and chromosome breaks, which is some pronounced in neoplastic or transformed cells than in normal cells. Different cell lines used in the study exhibited both in vitro and in vivo varying sensitivity to Ftorafur. Ftorafur does not increase the frequency of SCE.

Animals↗
PubMed1978

Sister chromatid exchange studies for monitoring DNA damage and repair capacity after cytostatics in vitro and in lymphocytes of leukaemic patients under cytostatic therapy.

The effect of various cytostatic drugs was studied on the frequency of sister chromatid exchanges (SCEs) in vitro and in PHA-stimulated lymphocytes of leukaemic patients under cytostatic therapy. The lymphocyte system is a sensitive one for the detection of DNA damage after administration of cytostatic drugs in vitro. Mitomycin C, busulphan, vincristine, chlorambucil, cytosine arabinoside, cyclophosphamide and lycurim were tested. All except cyclophosphamide induced high frequencies of SCEs in the first mitosis after their administration. The experiments with PHA-stimulated lymphocytes in vivo from patients treated with cytostatics showed that cytosine arabinoside, in combination with thioguanine, did not induce higher frequencies of SCEs, whereas in patients who were treated with cyclophosphamide alone or in combination with other cytostatic drugs, there was a higher incidence of SCEs during treatment. About 10 days after the termination of the treatment the elevated freuqencies of SCEs returned to the initial level. After administration of some mutagens, especially alkylating agents in vivo, the lymphocyte system can be used to assess induced DNA repair by continuously monitoring for SCEs.

Antineoplastic Agents↗