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S Heim

Publications and source records attributed to S Heim.

At least 289 records · Page 16Linked to original sources
PubMed1988

Multiple structural chromosome rearrangements, including del(7q) and del(10q), in an adenocarcinoma of the prostate.

Cytogenetic analysis of a poorly differentiated adenocarcinoma of the prostate revealed the complex karyotype: 76-86,X, -Y, +X, +X, +del(X)(q24), +t(1;10) (p22;q24), -2, +der(2) t(1;2;?)(p32;q24p13;?), +der(2)t(1;2;?) (p32;dq24p13;?), +3, +3, +4, +5, +5, +6, +7, +del(7) (q22), -8, +der(8)t(8;?)(q24;?), + der(8)t(8;?)(q24;?), +9, +10, +10, +der(10)t (1;10)(q24;q22), +del (10)(q23), +11, +11, +12, +der(12)t(4;12)(q11;p11), +der(12)t(4;12) (q11;p11), +14, +der (15)t(1;15)(q21;p11), +t(16;?) (q21;?), +17, +18, +19, +19, +20, +20, +21, +22, +2-5 mar. The karyotype contains deletions of both 7q and 10q, abnormalities that also have been described previously in prostatic adenocarcinomas, and which hence may represent primary chromosomal rearrangements in this type of cancer.

Adenocarcinoma↗
PubMed1988

Normal frequency of chromosome breakage in lymphocytes from patients with musculoskeletal sarcoma.

Spontaneous chromosome aberrations were studied in lymphocytes from 23 untreated patients with musculoskeletal sarcoma and 27 controls. Among the sarcoma patients, the mean gap, break, and gap + break events per 100 metaphases were 0.9, 2.2, and 3.0, respectively. The corresponding values for the control group were 1.3, 1.6, and 2.8. The mean number of aberrant mitoses was 2.4% in the sarcoma group and 2.5% in the controls. None of the differences between patients and controls were statistically significant. Thus, we found no evidence of inherent chromosome instability in patients with malignant mesenchymal tumors.

Adolescent↗
PubMed1988

Isochromosomes i(8q) or i(9q) in three adenocarcinomas of the lung.

We have cytogenetically analyzed three primary adenocarcinomas of the lung. All tumors had chromosome numbers in the triploid region. The multiple structural aberrations included rearrangements of 3p, in two cases affecting the segment 3p14-23, where deletions are characteristically found in small cell lung carcinomas. Isochromosomes for 8q were present in two tumors and i(9q) in one tumor. In the few previously reported cytogenetic analyses of pulmonary adenocarcinomas, all of which examined metastases or cell lines, i(8q) was found in one case and i(9q) in two cases. These isochromosomes, therefore, represent previously unrecognized nonrandom changes in adenocarcinomas of the lung, and might constitute primary aberrations in this tumor type.

Adenocarcinoma↗
PubMed1988

Bands involved in primary chromosome rearrangements in sarcomas are not constitutionally liable to breakage in sarcoma patients.

The localization of breakpoints in spontaneous chromosome aberrations, i.e., chromatid and chromosome gaps, breaks, and exchanges, has been studied in cultured skin fibroblasts from 34 untreated patients with musculoskeletal sarcoma and 38 controls. A total of 325 aberrations in the sarcoma group and 251 in the control group could be assigned to particular bands. The distribution was non-random (P less than 0.001) in both groups. Twenty-one bands in the sarcoma group and 20 in the control group appeared as hot spots, with 11 represented in both groups. Only three hot spots, all of which were present among both patients and controls, coincided with bands involved in primary sarcoma-associated chromosome rearrangements. The results indicate that the chromosome breakage pattern of non-malignant cells is similar in sarcoma patients and controls. Hence, the occurrence of primary structural rearrangements in sarcomas cannot be accounted for by any constitutional proneness to chromosome breakage at these bands.

Adult↗
PubMed1988

Three major cytogenetic subgroups can be identified among chromosomally abnormal solitary lipomas.

We have investigated cytogenetically a total of 35 solitary lipomas, 10 of which have been reported previously. Of the 25 tumours presented herein for the first time, clonal chromosome aberrations were detected in 17. The remaining eight had normal karyotypes, although two of them had nonclonal aberrations in about one quarter of the cells. Based on the cytogenetic findings in all 35 lipomas, four major subgroups can be distinguished. These are characterized by: (I) hyperdiploid karyotypes including one or more supernumerary ring chromosomes (5 cases); (II) diploid karyotypes with mostly balanced rearrangements involving 12q13-14 (13 cases), including the rearrangement t(3;12) (q27-28;q13-14) in 4 cases; (III) hypodiploid or diploid karyotypes with other aberrations than ring chromosomes or rearrangements of 12q13-14 (8 cases); and (IV) normal karyotypes (9 cases).

Adult↗
PubMed1988

Rings, dicentrics, and telomeric association in histiocytomas.

We report clonal karyotypic abnormalities in six of 12 cytogenetically investigated malignant fibrous histiocytomas. Four of eight tumors of the pleomorphic subtype had complex clonal chromosome aberrations, including ring chromosomes, dicentric chromosomes, and/or telomeric associations. No common characteristic aberration could be distinguished. Two of four myxoid tumors had clonal changes: One had one to two ring chromosomes and an extra chromosome #2; another had a supernumerary ring chromosome as the sole abnormality.

Aged↗
PubMed1988

Unique karyotypic abnormalities in a squamous cell carcinoma of the larynx.

We have cytogenetically examined short-term cultures from a squamous cell carcinoma of the larynx, a type of carcinoma in which chromosome aberrations have hitherto not been reported. The tumor karyotype was 46,XY,inv(2)(p22q24),t(9;13)(q34;q12),t(11;18)(q23;q21). None of these abnormalities have been described in carcinomas before.

Aged↗
PubMed1988

Multiple unrelated clonal chromosome abnormalities in an in situ squamous cell carcinoma of the skin.

We have cytogenetically analyzed short-term cultures from an in situ squamous cell carcinoma of the skin (Bowen's disease). The following mosaic tumor karyotype was found: 46,XX, -1, +der(1)(pter----p22::q11----cen----p22:), -9, +der(9)t(1;9)(q11; p24)/46,XX,t(3;6) (q21;p21)/46,XX,t(5;14)(q13;q24),t(7;18)(q32;q11)/46,XX,t(8;11)(p22;q13) /46, XX,t(8;11) (p22;q13),t(15;17) (q13;q24)/46,XX,t(12;15)(q12;p11). None of the rearrangements correspond to previously known cancer-associated abnormalities. Two of the clones are obviously related, and it is reasonable to assume that the t(15;17) developed as an evolutionary change in a cell that already contained t(8;11)(p22;q13). Since five clones without cytogenetic similarities were found in this in situ skin carcinoma, we suggest that the tumor was of polyclonal origin. It is impossible to decide whether all, or indeed any, of the visible abnormalities constitute pathogenetically essential primary changes, or merely represent chromosomal markers of secondary importance in tumorigenesis.

Carcinoma in Situ↗
PubMed1988

Trisomy 5 and t(5;14)(q11;q32) as the sole abnormalities in two different clones from a centroblastic non-Hodgkin's lymphoma.

A 62-year-old previously healthy woman presented with a centroblastic non-Hodgkin's lymphoma in the thyroid. Chromosome analysis revealed two unrelated clones, 47,XX,+5 and 46,XX,-14,+der(14)t(5;14)(q11;q32). The two clones may reflect a polyclonal origin, or they may be the descendants of the same neoplastically rearranged cell. In the latter case, the clonal aberrations are either secondary to an event detectable only at the molecular level, or one of them is a primary cytogenetic event while the other arose through clonal evolution with loss of the primary aberration. The best candidate for the primary change would be trisomy 5. Trisomy 5 has previously been associated with lymphomas with diffuse, large, noncleaved morphology, a group within the Working Formulation largely equivalent to centroblastic lymphomas in the Kiel classification. Our findings thus support the notion that trisomy 5 may be associated with centroblastic/diffuse, large, noncleaved lymphomas.

Chromosome Banding↗
PubMed1988

Ring formation and structural rearrangements of chromosome 1 as secondary changes in uterine leiomyomas with t(12;14)(q14-15;q23-24).

Cytogenetic analysis of short-term cultures from two uterine leiomyomas revealed, in addition to the primary abnormality, the reciprocal translocation t(12;14)(q14-15;q23-24), secondary structural changes that in both cases included ring chromosomes and rearrangements of chromosome 1. One tumor had the karyotype 46,XX,r(1)(p34q32),ins(8;9)(q13;q13q22),t(12;14)(q14-15;q23- 24). Massive numerical rearrangements were found in the second leiomyoma, with chromosome numbers ranging from 47 to 92. In spite of this variability, two main cell populations could be discerned, one near-diploid, the other hypotetraploid, with most mitoses having chromosome numbers between 80 and 88. These findings were corroborated by flow cytometry, which revealed two peaks corresponding to DNA indexes of 0.97 and 1.77. The structural abnormalities t(1;1)(p31;q44) and t(12;14)(q14-15;q23-24) were present in all karyotypically abnormal cells, and one or more unidentified ring chromosomes were observed in most of the hypotetraploid mitoses. In no cells were double copies of the t(1;1) and t(12;14) rearrangements detected. The similarity between the secondary changes in the cases reported here suggests that clonal evolution in uterine leiomyoma is nonrandom.

Adult↗
PubMed1988

Multiple karyotypic rearrangements, including t(X;18)(p11;q11), in a fibrosarcoma.

The tumor stem line of a soft tissue fibrosarcoma, histologic malignancy grade III, had 43 chromosomes with several clonal chromosome aberrations, including the three balanced translocations t(X;18)(p11;q11), t(2;15)(p23;q26), and t(7;22)(q11;q13), two partly identifiable marker chromosomes, der(3)dic(3;?)(p11;?) and der(5), one small marker of unknown origin, and loss of one chromosome #11, #18, #19, and #21.

Adult↗
PubMed1988

Chromosome abnormalities in leiomyosarcomas.

Short-term cultures from seven soft tissue leiomyosarcomas were investigated cytogenetically. Sufficient mitoses for chromosome analysis were obtained in six cases, four of which had only normal karyotypes. In one tumor, an intramuscular leiomyosarcoma of the lower arm, a variety of nonclonal structural and numerical aberrations were found in two thirds of the metaphases. Another tumor, a subcutaneous leiomyosarcoma of the knee, had clonal abnormalities resulting in the karyotype 46,X,der(X)t(X;4)(:Xq26----cen----Xp22::4q23----4qter) , del(4)(q23)/47,X,der(X)t(X;4),del(4)(q23), + 20. Flow cytofluorometric measurements of the DNA content in the six leiomyosarcomas successfully karyotyped revealed diploid values in five tumors. The leiomyosarcoma displaying numerous nonclonal changes had two cytofluorometric peaks, 1.01 and 1.39, indicating that the metaphases available for cytogenetic study cannot have been fully representative of the tumor stemline.

Adult↗
PubMed1988

Complex chromosome rearrangements in an extraabdominal desmoid tumor.

Cytogenetic studies of an extraabdominal desmoid tumor revealed karyotypic abnormalities in 20 of 50 analyzed metaphases, with no less than 13 clonal marker chromosomes, 11 of which could be at least partially identified. The hypodiploid stemline karyotype was interpreted as: 43-45,XX,-1,-1, + der(1)(?::1p36----1q21::?) + der(1)t(1;?)(p11;?), + der(1) (1pter----1p31::1p11----1cen----1q32::?),- 3,del(3)(p12), + der(3)t[del(3)(p12);?](q25;?), + der(6) t(6;?)(q15;?),-8,-9,-9,-10, + der(10)t(10;?)(p13;?),-12, + der(12)(?::12q14----12q23::?), -13, -13,-15,-19,dic(21;22)(p13;q13),-21, + der(21)t(21;?)(p13;?),-22, + der(22)t(22;?)(q13;?), + 1-3mar/46,XX. This finding of clonal chromosome rearrangements strongly suggests that extraabdominal desmoid tumor is a neoplastic disease.

Adult↗
PubMed1988

A specific translocation, t(12;14)(q14-15;q23-24), characterizes a subgroup of uterine leiomyomas.

We have cytogenetically investigated short-term cultures initiated from 34 uterine leiomyomas, all of which were histologically completely benign. Clonal chromosome abnormalities were detected in five cases, a normal female complement in 22, whereas, in the remaining seven tumors no karyotype could be established. Apparently identical reciprocal translocations, t(12;14)(q14-15;q23-24), were found as the sole abnormality in four tumors. The fifth abnormal case contained a t(2;14)(p11;p11). We conclude that chromosome aberrations may be found in myomas of the uterus, and that t(12;14)(q14-15;q23-24) characterizes a subset of these tumors.

Chromosome Banding↗
PubMed1988

Multiple apparently unrelated clonal chromosome abnormalities in a squamous cell carcinoma of the tongue.

We have cytogenetically examined short-term cultures from a squamous cell carcinoma of the tongue, a tumor type in which chromosome aberrations hitherto have not been reported. No less than 12 pseudodiploid clones were detected, giving the tumor karyotype 46,X,der(X)t(X;1)(q26;p32),der(1)(Xqter----Xq26::1p32 ----cen----1q42:), del(13)(q11q21),t(15;?) (q26;?)/46,XX,t(1;?)(p34;?),inv(2)(p21q11)/46,XX,t(1;10)(p32;q24)/ 46,XX, + der(1)(12pter----12p11::1p11----cen----1q32:: 11q13----11q22::1q32----1q42:), del(11)(q13q22), -12, der(17)t(1;17) (q42;p13)/46,XX,inv(1)(p22q44)/47,XX,del(1)(q32),der(17)t(1; 17)(p22;q25), der(1)inv(1) (q25q44)t(1;17)(p22;q25),ins(14;7)(q11;q22q36), + 14/46,XX,t(1;4)(q23;q35)/46, XX,t(1;21) (q25;q22),t(2;10)(q31;q26),t(22;?)(q12;?)/46,XX,del(1)(q32)/46,XX, t(1;8)(q44;q21)/46,XX, t(2;21)(q11;p11)/46,XX,t(9;11)(q34;q13). The large number of apparently unrelated abnormalities leads us to suggest that the carcinoma may have been of multiclonal origin.

Aged↗