ISSN:1045-2257    

DOI:10.1002/gcc.2870020102

出版商:Wiley Subscription Services, Inc., A Wiley Company    

年代:1990

数据来源: WILEY

摘要:

AbstractUterine leiomyoma—a benign smooth muscle tumor—has recently been found to contain tumor‐specific chromosome aberrations. Although only normal karyotypes were detected in 50 to 80% of cytogenetically investigated tumors, 104 leiomyomas with karyotypic aberrations have already been reported. At least four cytogenetically abnormal subgroups have been identified thus far, characterized by rearrangements of 6p, del(7)(q21.2q31.2), +12, and t(12;14)(q14‐15;q23‐24). The remaining abnormal tumors have had various nonrecurrent anomalies. Secondary karyotypic rearrangements, sometimes including ring chromosomes, have been found in one‐third and reflect clonal evolution. Occasional leiomyomas have contained multiple numerical and structural rearrangements. Though benign, these cytogenetically grossly aberrant tumors often displayed more atypical histological features than are usually seen in leiomyoma. Multiple leiomyomas have been investigated from 69 patients, with detection of chromosome anomalies in at least two separate tumors from the same uterus in ten cases. In half of these patients unrelated aberrations were found in different leiomyomas from the same uterus. On other occasions the aberrations were identical, indicating that although some uterine leiomyomas originate independently, others may develop by intra‐myometrial spreading from a common neoplastic clone. Some common features are discernible between the karyotypic pictures of uterine leiomyoma and angioleiomyoma; rearrangements of 6p, 13q, and 21q have been described in both tumor types. The cytogenetic similarities so far detected between leiomyoma and the malignant muscle tumors—leiomyosarcoma and rhabdomyosarcoma—are few and may be fortuitous. The cytogenetic profiles of leiomyoma and lipoma are strikingly similar; both tumor types have nonrandom rearrangements of 12q13‐15, t(12;14) in leiomyoma and t(3;12) in lipoma, as well as variant rearrangements of the same 12q segment. Both also have cytogenetic subgroups characterized by changes in 6p and ring chromosomes. Finally, karyotypic similarities exist also between leiomyoma and pleomorphic adenoma of the salivary gland, which includes a subset of tumors with anomalies of 12q13‐15, and with myxoid liposarcoma, which has t(12;16)(q13;p11) as a tumor

ISSN:1045-2257    

DOI:10.1002/gcc.2870020103

出版商:Wiley Subscription Services, Inc., A Wiley Company    

年代:1990

数据来源: WILEY

摘要:

AbstractA 68‐year‐old man presented with t(4;11)(q21;q23). B‐lineage acute lymphoblastic leukemia (ALL) which was negative for C‐ALL antigen and TdT. Clonal evolution to five different, but related karyotypes, in which chromosomal material distal either to 1q11 or 1q21 was translocated to the terminal regions of 4q‐, 11q, 16q, and 19p resulted in partial or total trisomy of 1q. The patient, having achieved a short remission, died 14 weeks after diagnosis. Five reports of jumping translocations in hematological malignancies, four with B‐lineage malignancy, are reviewed. One (four cases) or both (one case) of the same 1q breakpoints were consistently found and 11q and 16q were repeatedly involved. Such cases, having multiple subclones with trisomy 1q, may form a distinct subg

ISSN:1045-2257    

DOI:10.1002/gcc.2870020104

出版商:Wiley Subscription Services, Inc., A Wiley Company    

年代:1990

数据来源: WILEY

摘要:

AbstractCytogenetic studies on fresh human breast cancers revealed that homogeneously staining regions (HSRs), which are assumed to represent DNA amplification, are observed in almost half of the cases. To search for a possible relationship between HSRs and proto‐oncogene amplification, 16 proto‐oncogenes, includingERBB2, were studied by Southern blot analysis in four tumors with two or three HSRs, and in three tumors without HSRs. Only four proto‐oncogenes were found to be amplified in at least one tumor each:HSTandINT2(x3),MYC(x2–3), andFES(x>10). The large sizes of the HSRs, which each corresponded to several percent of the haploid genome, were hardly compatible with the low rate of amplification, except forFESand then only if a large adjacent segment was co‐amplified. This incomplete correlation was demonstrated by in situ hybridization, using biotinylated probes, which showed fluorescent spots on only one HSR forFESin one tumor and forINT2in another one. Our results indicate that most of the large amplifications corresponding to HSRs do not involve the proto‐oncogenes usually studied in breast cancer. The large amplification ofFES, detected in one tumor, may be c

ISSN:1045-2257    

DOI:10.1002/gcc.2870020105

出版商:Wiley Subscription Services, Inc., A Wiley Company    

年代:1990

数据来源: WILEY

摘要:

AbstractAlthough several independent series of non‐Hodgkin's lymphomas (NHLs) have been subjected to cytogenetic studies or analyses of lineages by assaying for clonal immunophenotypes and clonal rearrangements affecting immunoglobulin (IG) and T‐cell receptor (TCR) genes, no published reports exist of series of non‐B‐cell NHLs on which cytogenetic, immunohistochemical, andIGandTCRgene rearrangement studies have been undertaken together. Among 434 NHLs ascertained prospectively between January 1984 and December 1988 at the Memorial Sloan‐Kettering Cancer Center, 278 cases with clonal chromosome abnormalities were identified. Of the latter, 20 were non‐B‐cell NHLs, which in turn comprised 15 peripheral T‐cell lymphomas (PTCLs) and 5 lymphomas of uncertain lineage (LULs). The LULs either were bigenotypic, had discordant immunophenotype and immunogenotype, or showed no evidence of B‐cell, T‐cell, or histiocytic derivation. Of the 15 PTCLs, eight expressed the Ki‐1 antigen and four of these had translocations involving the band 5q35 [t(5q35)]. Of the five LULs, four expressed the Ki‐1 antigen and one of these had a translocations involving band 5q35. Previous studies have associated t(5q35) with Ki‐1 positive NHLs characterized histologically by a pleomorphic diffuse large cell morphology. In our series of 12 Ki‐positive non‐B‐cell NHLs, five (42%) had a 5q35 translocation. They were histologically indistinguishable from the subset without the translocation. The frequent lineage uncertainty exhibited by Ki‐1 positive NHLs of similar histology and cytogenetic abnormalities suggests their derivation from an

ISSN:1045-2257    

DOI:10.1002/gcc.2870020106

出版商:Wiley Subscription Services, Inc., A Wiley Company    

年代:1990

数据来源: WILEY

摘要:

AbstractA reciprocal translocation between chromosomes 15 and 16 has been detected in seven murine plasmacytomas induced by a combination of pristane and Abelson virus. Six of the tumors were induced in a new, unconventional experimental system based on transfer of uninfected or Abelson virus infected bone marrow and spleen cells, respectively, into pristane treated mice. All six tumors were of donor type. The seventh tumor appeared in a conventional pristane + Abelson virus treated mouse. This tumor was unusual in carrying both the 15;16 variant translocation and the typical 12;15 translocation, in the same tumor cells. In the new 15;16 variant, the breakpoint of chromosome 15 was at the interphase of the D2/3 sub‐bands, as in mouse plasmacytomas with the previously well‐known typical 12;15 and variant 6;15 translocations. The breakpoint on chromosome 16 was mapped to band 16B1, corresponding to the presumed cytogenetic site of the lg‐lambda gene. In three of the seven tumors with the 15;16 translocation, the derivative chromosome 15 had undergone a duplication, a feature that has not been previously encountered in the MPC‐associated 12;15 and 6;15 translocation carriers. The reciprocal derivative chromosome 16 was lost from one of the seven tumors. We postulate that the 15;16 translocation results in juxtaposition of themycgene to lambda sequences, probably in a similar orientation as previously described for the variant 6;15 transl

ISSN:1045-2257    

DOI:10.1002/gcc.2870020107

出版商:Wiley Subscription Services, Inc., A Wiley Company    

年代:1990

数据来源: WILEY

摘要:

AbstractThe frequency and distribution of rare and common chromosomal fragile sites in metaphases derived from peripheral lymphocytes were compared in 26 patients with malignant solid tumours and 24 normal controls. In order to avoid bias in evaluation, the identity of each individual as patient or control was disclosed only after the study was completed. Rare heritable folic acid inducible fragile sites were found in five patients (2q13; 6p23; 8q22; 16p12) and two controls (8q22). Common fragile sites were present in 21 of 26 patients and in 19 of 24 controls. These differences are statistically not significant in the Fisher test. We conclude that the expression of fragile sites does not indicate a predisposition for solid tumours.

ISSN:1045-2257    

DOI:10.1002/gcc.2870020108

出版商:Wiley Subscription Services, Inc., A Wiley Company    

年代:1990

数据来源: WILEY

摘要:

AbstractClonal karyotypic abnormalities were detected in 7 of 42 cytogenetically analyzed benign ovarian tumors. An adenofibroma had –X and a mucinous cystadenoma had t(1;11)(q25;q23) as the sole abnormality. Trisomy 12 was found in the remaining five tumors. It was the only change in two fibromas and a serous cystadenoma; the fourth tumor, a mucinous cystadenoma, had one clone with + 12 and one with + 12 and + 10, and the fifth tumor, a fibrothecoma, had +4, +9, +12. The finding of trisomy 12 in five of seven karyotypically aberrant tumors suggests that this aberration characterizes a hitherto unrecognized cytogenetic subgroup of benign ovarian neoplasm

ISSN:1045-2257    

DOI:10.1002/gcc.2870020109

出版商:Wiley Subscription Services, Inc., A Wiley Company    

年代:1990

数据来源: WILEY

摘要:

AbstractThe present case, together with other reports reviewed herein, defines a new subtype of therapy‐related acute myeloid leukemia (t‐AML). This variant of t‐AML is characterized by a short interval from initial drug therapy to bone marrow dysfunction and monocytic morphology without trilineage dysplasia. Unlike classic t‐AML, which frequently has abnormalities of chromosomes 5 and/or 7, this new subtype is characterized by rearrangements involving band q23 of chromosome 11, most commonly a 9;11 translocation. The majority of patients with this subtype of t‐AML had prior cytotoxic therapy with topoisomerase II‐reactive drugs including anthracyclines, epipodophyllotoxins, or actinomycin D, combined with either an alkylating agent or cisplatin. This association of prior therapy which includes topoisomerase II‐reactive agents and a rapidly appearing t‐AML involving the monocytic line and chromosome 11 requires a

ISSN:1045-2257    

DOI:10.1002/gcc.2870020110

出版商:Wiley Subscription Services, Inc., A Wiley Company    

年代:1990

数据来源: WILEY

摘要:

AbstractThe DNA probe p82H was used to visualize centromeric DNA in micronuclei (MN) of human cells. Slides prepared from cultures treated by the aneugen (causing aneuploidy) colcemid showed significantly more MN with centromeric signals than those treated by the clastogen (causing chromosome breakage) bleomycin. These results indicate that in situ hybridization with the alphoid p82H DNA probe is a suitable method with which to distinguish between MN containing whole chromosomes and acentric fragments, and hence allows one to discriminate between the clastogenic and aneugenic effects in MN formation.

ISSN:1045-2257    

DOI:10.1002/gcc.2870020111

出版商:Wiley Subscription Services, Inc., A Wiley Company    

年代:1990

数据来源: WILEY