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F Mitelman

Publications and source records attributed to F Mitelman.

At least 361 records · Page 20Linked to original sources
PubMed1987

Marker ring chromosome--a new cytogenetic abnormality characterizing lipogenic tumors?

We have analyzed three intramuscular lipomas, two atypical and one with ordinary benign histology, as part of a systematic study of the karyotypic characteristics of mesenchymal tumors. A large ring chromosome of uncertain origin, but possibly representing a rearranged chromosome #3, was found in all three tumors. Previous reports on the chromosome banding pattern in lipogenic neoplasms are restricted to only three cases, all liposarcomas. In one of these, a well differentiated liposarcoma, a ring chromosome was described that was remarkably similar in morphology to the aberration reported here. We conclude that this ring chromosome may constitute a characteristic cytogenetic marker for lipogenic tumors.

Adult↗
PubMed1987

Cytogenetic analyses in 89 patients with secondary hematologic disorders--results of a cooperative study.

Eighty-nine patients who developed a secondary hematologic disorder and were studied with chromosome analysis were collected from nine institutions. The results of the study confirmed previous findings, in particular, -5/5q-, -7/7q-, -17, and +21 were the most frequently encountered aberrations. Moreover, a t(1;7)(p11;p11) was reported in four cases and consistent chromosome abnormalities were observed in a small group of patients who had been treated only with surgery, but not with chemo- or radiotherapy for a previous tumor.

Acute Disease↗
PubMed1987

Prognostic implication of cytogenetic findings in 106 patients with non-Hodgkin lymphoma.

The cytogenetic findings in samples from 106 patients with non-Hodgkin lymphomas (NHL), histopathologically classified according to the Kiel classification, have been correlated with survival time. Clonal chromosomal abnormalities were found in 60 patients, and only normal karyotypes in ten. The chromosome analysis of the remaining samples failed. The failures did not differ in survival compared with the cytogenetically successful cases, indicating that this group is not a prognostic entity within NHL. The cytogenetic findings were classified in six ways in order to evaluate the prognostic value of the cytogenetic pattern. Multivariate analysis demonstrated that presence of clonal chromosome abnormalities and the number of aberrations both were important prognostic factors independent of histopathology, whereas, the modal chromosome number, presence of translocations, or unidentified marker chromosomes were not. Some characteristic chromosome abnormalities were correlated with survival time: Patients with a 1p+ marker or +7 had a significantly shorter survival time than patients with normal karyotypes only (NN). Patients with +3, +12, 6q-, i(17q), and t(14;18)(q32;q21) did not differ significantly from the NN group.

Chromosome Aberrations↗
PubMed1987

Normal bone marrow karyotype in acute leukemia or myelodysplasia following rheumatoid arthritis?

Cytogenetic analyses by means of trypsin-Giemsa banding technique were performed on bone marrow cells from a total of 12 patients--nine with acute nonlymphocytic leukemia and three with myelodysplastic syndrome--and a history of rheumatoid arthritis. Clonal chromosomal abnormalities were identified in two patients with previous exposure to petroleum products, and radiation therapy for a malignant tumor, respectively; one additional patient had a loss of the Y chromosome as the sole aberration. All the remaining nine patients had completely normal karyotypes. Seven patients had received treatment for rheumatoid arthritis with mutagenic drugs. Acute nonlymphocytic leukemia or myelodysplastic syndrome secondary to cytotoxic treatment for a previous malignancy display multiple, usually complex, structural and numerical chromosomal abnormalities in the majority of cases. The contrasting findings in the present patient series suggest other pathogenetic mechanisms in acute nonlymphocytic leukemia and myelodysplastic syndrome following rheumatoid arthritis.

Acute Disease↗
PubMed1987

Characteristic patterns of chromosome abnormalities in acute myeloid leukemia with Auer rods.

Two hundred and four cytogenetically investigated patients with acute myeloid leukemia (AML) were evaluated for the presence (AR+) or absence (AR-) of Auer rods. Chromosome analysis was successful in 187 patients (92%). Seventy-eight patients (38%) were AR+. Cytogenetic abnormalities were detected in 35 (49%) AR+ patients and in 66 (57%) AR- patients. The proportion of patients with complex karyotypic changes (more than two aberrations) was significantly higher in the AR- group (p less than 0.01). Also, unidentifiable marker chromosomes were significantly more frequent in the AR- group (p less than 0.01). Twenty-one of 23 AR+, but none of 46 AR- patients with structural changes, had involvement of 21q22, 17q11-12, or 11p13-15. In contrast, structural changes of 1p, 5q, 7q, 9q, 11q, or 22q were present in 31 AR- but in only two AR+ patients. Four patients had translocations involving 21q22 without rearrangements of 8q22. All were AR+, but only one displayed M2 morphology. We draw the conclusion that chromosomal changes affecting 21q22 might be primarily related to AR formation, whereas, changes of 8q22 produce the characteristic differentiation pattern leading to M2 morphology, consistently found in AML with t(8;21)(q22;q22). With regard to numerical abnormalities, -7 and +8 occurred about equally often in the two groups, whereas, +11 and -Y, especially when present as the sole aberrations, were predominantly found in AR+ patients. In contrast, -5 and +21 were exclusively found in AR- patients. The results indicate that AR+ AML is characterized by a relatively limited number of chromosomal abnormalities that are different from the aberrations found in AR- patients. This feature has not been emphasized in previous studies correlating hematologic and cytogenetic findings in AML.

Bone Marrow↗
PubMed1987

A case of myelodysplastic syndrome with high platelet counts and a t(3;8)(q26;q24).

A 62-year-old male patient with refractory anemia with excess of blasts had a t(3;8)(q26;q24) as an acquired chromosomal abnormality in the bone marrow. This aberration has not been previously reported as a sole anomaly in any type of neoplasm, including myelodysplastic or myeloproliferative disorders. The findings of disturbed thrombocytopoiesis with high platelet counts and micromegakaryocytes in the bone marrow support the idea that alteration of the transferrin receptor gene, localized to 3q26, may be of pathogenetic significance.

Anemia, Refractory, with Excess of Blasts↗
PubMed1987

Clonal chromosome abnormalities in two liposarcomas.

Two liposarcomas were analyzed with chromosome banding technique. The sole chromosomal abnormality in one of the tumors, a mixed type (myxoid and round cell) liposarcoma, was t(12;16)(q13;p11), a rearrangement previously reported to be associated with myxoid liposarcoma. The other tumor, a pleomorphic liposarcoma, displayed massive numerical rearrangements (modal chromosome number 94-112), and numerous, mostly unidentifiable, marker chromosomes. The following clonal structural aberrations were recognized: del(1)(p22), del(1)(q23), t(7;?)(p22;?), i(17q), and t(19;?)(q13;?).

Adult↗
PubMed1987

Relationship between cytogenetic findings and histopathology in non-Hodgkin lymphoma.

The cytogenetic findings in 70 patients with non-Hodgkin lymphoma have been correlated with tumor histopathology according to the Kiel classification. Certain chromosome aberrations displayed a nonrandom association with the grade of malignancy: 4 lymphomas out of 6 with 1p+, 5 out of 7 with del(6)(q15), 7 out of 11 with 14q+, and 5 out of 8 with +18 belonged to the high grade malignancy group, whereas 9 lymphomas out of 10 with t(14;18) were low grade malignant. Two aberration types were closely associated with specific histopathologic subtypes: t(14;18) occurred in 7 cases out of 10 in centroblastic/centrocytic (cb/cc) follicular lymphomas, and 5 cases out of 6 with i(17q) were cb or cb/cc. Although less striking, there was a tendency for del(6)(q15) to occur in cb or cb/cc lymphomas (4 cases out of 7), in contrast to only 1 case out of 5 with the more distal deletion del(6)(q21).

Adolescent↗
PubMed1987

Cytogenetic studies in Hodgkin's disease.

Cytogenetic analysis was attempted in 20 patients with Hodgkin's disease. No mitoses were found in 2 cases, normal metaphases in 7, and normal metaphases with nonclonal aberrations in 7. Of the 4 cases with clonal aberrations, one had +16 as the sole change, whereas the remaining tumors had multiple numerical and structural changes.

Adolescent↗
PubMed1987

New structural chromosomal rearrangements in congenital leukemia.

The karyotypic abnormalities and clinical data on three patients in whom acute leukemia was diagnosed within the first 6 months of life are presented. The four structural chromosomal rearrangements detected in the bone marrow from these patients, i.e., t(7;12)(q36;p13) and t(1;19)(q11;q11) in case 1, t(2;10;11;12)(q21q31;p13;q13;q24) in case 2, and t(11;19)(q23;p13) in case 3, have not previously been associated with congenital leukemia. Acquired chromosomal changes have until now been reported in only 31 leukemic infants in this age group. Of the total material, 18 patients had acute lymphoblastic leukemia and 16 had acute nonlymphocytic leukemia. The by far most frequently recorded cytogenetic aberration has been t(4q;11q), seen in 14 cases of lymphoblastic leukemia. Although t(4q;11q) has not been found in a single patient with acute nonlymphocytic leukemia, these leukemias have often had other rearrangements involving the same region of 11q. Hence, genetic material around 4q21 may be active in lymphocytic differentiation, whereas gene(s) in 11q23 may be important in the neoplastic process in a less cell-type specific manner and perhaps particularly vulnerable to neoplastic rearrangement in fetal life. The finding of four cases out of 34 with translocations between 11q23 and chromosome 19 indicates that this rearrangement might characterize a specific cytogenetic subgroup of leukemia in the very young.

Acute Disease↗
PubMed1986

Geographic heterogeneity of chromosome aberrations in hematologic disorders.

The incidence of characteristic nonrandom chromosome aberrations in malignant cells of unselected, consecutively studied, and previously untreated patients from various geographic regions has been surveyed. The results demonstrate significant geographic heterogeneity in the distribution of the specific aberrations considered among the four malignant disorders studied in a sufficient number to permit conclusions, viz., acute nonlymphocytic leukemia, chronic myeloid leukemia, polycythemia vera, and myelodysplastic syndrome.

Chromosome Aberrations↗
PubMed1986

Structural chromosome aberrations in a case of angioleiomyoma.

Chromosome analysis of cells from an angioleiomyoma revealed the karyotype 46,XX,del(6)(p21p23),del(21)(q21)/46,XX. The possible importance of these structural derangements is discussed within the framework of current knowledge on chromosome aberrations in benign neoplasms.

Adult↗
PubMed1986

Near-haploidy in a case of plasmocytoma.

Chromosome studies of a solitary plasmocytoma in the femoral bone revealed a near-haploid chromosome number of 31-32 with a loss of one homolog of each chromosome pair except #1, #7, #9, #15, #19-21, and the sex chromosomes (XY). The cytogenetic findings have been compared with 16 cases of near-haploid neoplasms from the literature studied using banding techniques. A common feature present in 13 of the 16 cases reported was found to be disomy 21; the only chromosomes consistently present in one copy in all neoplasms were #2, #3, #4, and #5.

Chromosome Aberrations↗
PubMed1986

Clustering of chromosomal breakpoints in neoplasia.

It is becoming increasingly difficult to assimilate in a meaningful fashion the wealth of new information regarding chromosomal changes in human cancer. Compilation and analysis of this data is essential if a clear picture of the incidence and specificity of cancer associated chromosome abnormalities is to be seen. This report provides an overview of our most recent and comprehensive analyses on chromosomal changes in 5345 neoplasms, providing further evidence for a clustering of chromosomal breakpoints in human neoplasia.

Chromosome Aberrations↗
PubMed1986

Reciprocal translocation t(3;12)(q27;q13) in lipoma.

A reciprocal translocation, t(3;12)(q27;q13), was found as the sole karyotypic abnormality in an intramuscular lipoma. The morphology of the derivative 3q+ was strongly reminiscent of the large ring marker we have previously described in three other lipomas, indicating a pathway through which the rings may have arisen. These data, combined with the previous preliminary report by Turc-Carel et al. of a similar t(3;12) in another lipoma strongly suggest that this rearrangement may be a characteristic cytogenetic marker in benign lipogenic tumors.

Chromosomes, Human, Pair 12↗
PubMed1986

Secondary chromosome aberrations in the acute leukemias.

Information was retrieved from a computer-based data bank about additional chromosome aberrations in patients with acute lymphatic or nonlymphatic leukemia (ALL or ANLL) and one of the following primary rearrangements: In ALL t(9;22), t(11;14), t(1;19), t(4;11), t(8;14), and del(6q); in ANLL t(9;22), t(6;9), t(8;21), t(15;17), t(9;11), inv(16), and del(20q). The distribution of secondary changes was nonrandom. Chromosomes #1, #7, #8, and #9 were frequently involved in both disease groups, albeit with some pointed differences regarding the types of rearrangements making up the majority of aberrations. Chromosome #6 was clearly more affected in ALL, whereas, loss of a sex chromosome was largely restricted to ANLL patients. Differences between specific subtypes were detectable in both ALL and ANLL. Sex chromosome loss occurred almost exclusively in patients with t(8;21), who also tended to have del(9q) and/or trisomy 8. On the other hand, patients with t(15;17) often had del(7q) or monosomy 7, trisomy 8, and del (9q) as part of their karyotypes. None of the patients with inv(16) had del(9q). Instead, structural aberrations of chromosomes #7, #16, and #19 were fairly numerous in this subgroup, as was trisomy 8. Structural changes of #1, particularly translocations and duplications, were especially frequent in ALL patients with primary rearrangements t(8;14) or del(6q). In both ALL and ANLL, patients with t(9;22) had similar additional changes, often +8, -7, and/or +Ph. The findings indicate that the initial cytogenetic change is an important factor in determining the nature of subsequent chromosomal abnormalities developing in the malignant clone.

Acute Disease↗
PubMed1986

High resolution banding analysis of the reciprocal translocation t(6;9) in acute nonlymphocytic leukemia.

The cytogenetic, hematologic, and clinical characteristics of a 13-year-old girl with acquired t(6;9)(p23;q34) and dysmyelopoietic syndrome developing into acute myelomonocytic leukemia are described, bringing the total number of patients with t(6;9) and hematologic disease described in the literature up to 19. The diagnosis has been acute myeloid leukemia in the great majority of these patients; only four have had acute myelomonocytic leukemia. High resolution analysis at the 550 band stage localized the breakpoints in chromosomes #6 and #9 to p23 and 9q34.3, respectively. Previous investigations employing high resolution cytogenetics have mapped the typical 9q breakage site in chronic myeloid leukemia to 9q34.1. In situ hybridization studies have demonstrated that the cellular oncogene c-abl remains on the derivative 9q+ chromosome in t(6;9), whereas it is moved to the Ph marker in t(9;22). Thus, the combined data indicate that c-abl is located between 9q34.1 and 9q34.3, i.e., in subband 9q34.2 or its immediate vicinity.

Acute Disease↗