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E L Prigogina

Publications and source records attributed to E L Prigogina.

At least 19 recordsLinked to original sources
PubMed1989

Chromosomal characteristics of malignant lymphoma.

Results of a cytogenetic and morphological study of 60 malignant lymphomas (ML) are presented. The most often observed chromosome abnormalities were rearrangements involving 14q32, 11q13, 11q21-23, 6q15, 6q21, 12p11-12, 17p11-12, and extra chromosomes 18, 3, 21 and 7. Translocations involving 14q32, leading to the appearance of marker 14q+, were noted in 41% of the tumors. Strict correlations between karyotype and morphology of ML were not seen. However, rearrangements of 11q were mostly found in low-grade tumors and markers 6q- in high-grade tumors. The absence of t(14;18), which is regarded to be the most common abnormality in ML, and an unusually high incidence of t(11;14) in our series confirm the uneven geographical distribution of ML with these translocations. Chromosome abnormalities in ML and acute lymphoblastic leukemia are compared.

Adolescent↗
PubMed1988

Nonrandom chromosomal abnormalities in acute lymphoblastic leukemia of childhood.

The leukemic cell karyotype was studied in 103 children with acute lymphoblastic leukemia. An abnormal chromosome pattern was revealed in 81 of 98 patients studied before treatment (82.6%) and in the five children studied in relapse. Aside from specific chromosomal abnormalities defined by the Third International Workshop on Chromosomes in Leukemia, other nonrandom rearrangements were observed, particularly del(14)(q11-13), del(12)(p11-12), and t(1;19)(q22-23;p13), often associated with partial trisomy for 1q. Patients with del(14) had tumorous lymph-nodes or other extramedullary tumors. The course of the disease in these children was rapid. Patients with markers such as Ph, 6q-,14q+, and with a t(4;11) had a low incidence of complete remission and short survival. The most favorable course of the disease was observed in the group of children with over 50 chromosomes in the leukemic cells.

Adolescent↗
PubMed1988

A new specific chromosomal rearrangement, t(11;20)(p15;q11), in myeloblastic leukemia with maturation.

The translocation t(11;20)(p15;q11) was found as the sole acquired clonal chromosome abnormality in two patients with acute myeloid leukemia. The bone marrow morphology in both cases corresponded to the M2 subtype of the French-American-British (FAB) classification. None of the patients achieved complete remission, and both died less than 6 months after diagnosis. This particular translocation has not previously been reported in acute nonlymphocytic leukemia.

Adolescent↗
PubMed1986

Chromosomes in acute nonlymphocytic leukemia.

The karyotype of leukemic cells was studied in 88 acute nonlymphocytic leukemia (ANLL) patients. Chromosome abnormalities were discovered in 78.4% of all patients and in 72.5% of the 69 patients studied before treatment. Characteristic abnormalities: translocations 8;21, 15;17, 9;22 or 6;9, rearrangements of 11q, gain of chromosomes 8 or 21, and loss or deletion of chromosomes 5 or 7 were detected in 56 of 69 patients with abnormal karyotypes. Translocation 8;21 was revealed in 27 patients; 20 of them had M2 FAB-form, four had M1, and three had M4. In patients with t(8;21) the incidence of complete remission was higher and the duration of first remission and survival longer than in patients with other abnormalities or with a normal karyotype.

Acute Disease↗
PubMed1985

Increased numbers of marrow basophils may be associated with a t(6;9) in ANLL.

We have characterized another subset of acute nonlymphocytic leukemia (ANLL) based on the cytogenetic and morphologic findings in a group of nine patients. Five patients had chromosomal analyses performed at the University of Chicago, two patients were studied at the All-Union Cancer Research Center in Moscow, and one patient each was studied at the University of Maryland and at Fairfax Hospital in Fairfax, Virginia. All nine patients had a reciprocal translocation involving the short arm of chromosome 6 and the long arm of chromosome 9 [t(6;9)(p23;q34)]. The patients, four males and five females, ranged in age from 5 to 51 years; the median age of 38 years is lower than that typically seen in ANLL. Only two of eight treated patients entered a complete remission. Classification of bone marrow morphology according to FAB Cooperative Group criteria revealed AML-M1 in one patient, AML-M2 in four, and AMMoL-M4 in three. One patient had refractory anemia with excess blasts (RAEB) which evolved to AML-M2. All bone marrow specimens showed severe myelodysplasia, with Auer rods present in seven of the nine cases. Of note was the particular prominence of bone marrow basophils (greater than 1%) in eight of the nine (89%) patients. Among 160 evaluable patients with ANLL de novo seen at the University of Chicago whose cells lacked a t(6;9), only five (3%) had greater than 1% basophils in the marrow aspirates. It is of interest that the breakpoint in 9q involves the same chromosomal band as that in the t(9;22) observed in chronic myelogenous leukemia (CML), in which increased basophils are a prominent feature. Thus, the association of the t(6;9) with increased bone marrow basophils in ANLL may provide additional insight into the chromosomal location of genes regulating the production and/or maturation of basophils.

Acute Disease↗
PubMed1983

Chromosomal rearrangements with a common breakpoint at 6p23 in five cases of myeloid leukemia.

Rearrangement of the short arm of chromosome 6 with a breakpoint at 6p23 was found in five patients with myeloid leukemia. Three of them had different morphological variants of AML (M2, M3, M4) and two blastic crisis of Ph1 negative and Ph1 positive CML. Identical translocation, t(6;9)(p23;q34), was revealed in two patients. One of them had AML (M2), the other blastic crisis of Ph1 negative CML. The blast cells of the last patient were morphologically similar to those in the M2 variant of AML. Translocation (6;9)(p23;q34) was also detected in two AML patients of Rowley and Potter (1976). The role of the breakpoint at 6p23 in myeloid malignancies needs further investigation.

Adolescent↗
PubMed1983

Chromosome abnormalities in chronic myeloid leukemia in children.

Banded chromosomes of leukemic cells were studied in 53 children with chronic myeloid leukemia (CML). Ph1 chromosome was found in 21 children, and the remaining 32 cases were Ph1 negative. Besides Ph1 translocation additional chromosomal abnormalities, including marker i(17q), were revealed in three of eight children studied in blastic crisis of Ph1 positive CML. Leukemic cells of most patients with Ph1 negative CML possessed normal karyotype. Clones with chromosomal abnormalities were found in 12 of 32 cases. Most characteristic were monosomy 7 (in four children) and trisomy 8 (in three). Abnormal karyotype may be a bad prognostic sign in Ph1 negative CML. The presented data confirm the difference in age of appearance, bone marrow pattern and clinical course between Ph1 positive ("adult") and Ph1 negative (juvenile) types of CML in children. Probable prenatal commencement of CML in babies and children in the first years of life is discussed.

Adolescent↗
PubMed1982

Similar chromosomal abnormalities in several retinoblastomas.

The study of banded chromosomes of nine sporadic unilateral retinoblastomas revealed near diploid karyotypes with multiple numerical and (or) structural abnormalities in all tumors. An identical marker i(6p) was noted in cells of the modal class of six retinoblastomas. Extra copies of the short arm of chromosome 6 were observed in seven tumors: +i(6p) in 6 and +6q-in one. Less regular but repeated findings were a loss of one sex chromosome, and markers 1p+ and 17q+. The structure of these markers was not identical in different tumors. Abnormalities of chromosome 13 were not observed in tumor cells, nor in blood lymphocytes stimulated by PHA.

Aneuploidy↗
PubMed1981

Correlations between the clinical course, characteristics of blast cells, and karyotype patterns in chronic myeloid leukemia.

Results of chromosome studies of blood and bone marrow cells from 101 patients with Ph1 positive chronic myeloid leukemia (CML) confirm the assumptions that clinical and morphologic manifestations of the disease correlate with karyotype peculiarities of leukemia cells. Several variants of the clinical course of CML may be distinguished. One is the variant with a short chronic phase and a comparatively long terminal phase. In blastic crisis the blast cells are peroxidase negative and do not possess cytoplasmic inclusions. Acute transformation occurs without any additional chromosome damage. The second, more common form is less severe because of longer chronic phase but it has a short and grave acute stage. The blast cells present definite signs of myeloid differentiation, they have basophilic or neutrophilic cytoplasmic granules and are peroxidase positive. Marker i(17q) often combined with trisomy 8 is a characteristic chromosome abnormality in the terminal stage of this variant. The third type has an extremely long chronic phase but ends in a rapidly progressing severe and resistant to therapy "lymphoid" blastic crisis. Blast cells have typical "lymphoid" morphology, they are peroxidase negative and contain granular PAS positive substance. Various additional chromosome changes appear in the terminal stage. Future studies of a larger series of patients may possibly reveal more CML variants.

Adolescent↗
PubMed1979

Chromosomes in acute leukemia.

The karyotype of leukemic cells of 78 acute leukemia patients (37 ANLL, 34ALL, and 7 of unknown type) was studied by means of G-banding. Chromosomal abnormalities were found in 50 patients (72%). Chromosomes 8,21,5,7,11, and 19 were preferentially involved in the abnormalities, both in ANLL and in ALL. A high incidence of the characteristic rearrangement t(8;21) was noted in AML: (in 6 of 22 AMP patients). An identical reciprocal translocation--t(4;11)--was seen in 4 out of 34 ALL patients.

Adolescent↗
PubMed1979

Chromosomal marker 20q- in cases of osteomyelosclerosis and CML.

Two male patients with myeloproliferative disorders (osteomyelosclerosis in one and CML in the other) were found to have a chromosomal marker 20q- in blood cells (unstimulated short time cultures). Marked erythropoietic disturbances were not revealed in these cases. The specificity of the 20q- marker for red cell disorders is discussed.

Aged↗
PubMed1978

Chromosome abnormalities and clinical and morphologic manifestations of chronic myeloid leukemia.

Forty cases of chronic myeloid leukemia (CML) were studied and subgroups of cases with similar chromosomal abnormalities in terminal stage were defined. Certain correlations were observed between the type of chromosomal changes, and clinical and morphologic manifestations of the disease: (1) It seems that, in cases without any karyotype changes other than translocation (9;22), the terminal stage is longer and milder than in cases with additional chromosomal abnormalities; (2) cases with marker i(17q) are clinically and morphologically rather uniform and are characterized by distinct signs of myeloid differentiation of blast cells, absent in other cases; (3) in cases with various atypical chromosomal abnormalities, the course of the terminal stage is the most rapid and grave. The blast cells differ from myeloblasts and resemble lymphoid elements.

Adolescent↗
PubMed1977

Karyotype peculiarities of malignant lymphomas.

Karyotypes of 30 malignant lymphomas were studied with the aid of G-banding. Frequent occurrence of rearranged chromosomes 14 and 11 was noted. In several tumors, identical acrocentric markers, appearing after translocation of the long arm of chromosome 11 on the long arm of chromosome 14, were revealed. Other common karyotype abnormalities in lymphomas were trisomy 3 and trisomy 18. The chromosomes preferentially involved in karyotype abnormalities of the malignant lymphomas are mostly not altered in other hemoblastoses.

Adolescent↗
PubMed1975

Marker chromosome 14q+ in two non-Burkitt lymphomas.

Marker chromosome 14q+, similar to the specific marker of the Burkitt lymphoma, was revealed in all malignant blood cells of a patient with generalized lymphosarcoma, in all lymph node cells, and in a part of the blood cells of a patient with chronic lymphocytic leukaemia. Possible causes of this similarity are discussed.

Chromosome Aberrations↗
PubMed1975

Certain patterns of karyotype evolution in chronic myelogeneous leukaemia. Chromosome abnormalities in CML.

The study of chromosome banding pattern of leukaemic cells in 15 patients with CML revealed t(9;22) in all cases. Similar additional chromosome abnormalities were observed in the terminal stage of the disease in 5 of 9 patients with aneuploid cell lines. The most frequent abnormalities were i(17q) and trisomy 8. The regularities of karyotype evolution in the terminal stage of CML are discussed.

Adult↗
PubMed1975

G banding in cytogenetic study of hemoblastoses.

G banding was used in the study of the karyotype of malignant cells in 10 patients: 5 with CML (3 in blastic crisis), 3 with AL and 2 with lymphosarcomas. In all cases of CML 22q-- (Ph1-chromosome) and 9q+ were present in leukemic cells. An i(17q) was observed in the karyotype of 2 out of 3 patients in blastic crisis of CML. In AL and lymphosarocmas small chromosome rearrangements were revealed and the origin of marker chromosomes could be established by the aid of G banding.

Acute Disease↗