摘要:

AbstractClonal abnormalities of the long arm of chromosome 13 were detected in 9 of 54 patients with Burkitt lymphoma‐leukemia. All abnormalities involved band 13q34, in three patients as t(1;13). The 13q34 abnormalities are thus the second most frequent secondary chromosomal abnormalities, after those of chromosome 1, in these lymphoid proliferation

ISSN:1045-2257    

DOI:10.1002/gcc.2870010202

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

年代:1989

数据来源: WILEY

摘要:

AbstractCell lines differing in their malignant potential have been derived from the murine BW5147 T‐cell lymphosarcoma. To evalute the involvement of chromosomal aberrations in tumor progression within this model, we have analyzed the karyotypes and the in vitro invasiveness of 13 related nonmetastatic and metastatic variants. Giemsa banding revealed the presence of several marker chromosomes, one of which was of particular importance. Depending on the cell line, four variants of this marker I were found: Marker Ia corresponds to two translocated chromosomes 3, marker Ib is a deleted Ia marker, marker Ic is a Ib translocated to a small unidentified chromosome fragment, and marker Id is a further deleted Ib marker. The Ia and Id markers were characteristic for the noninvasive, nonmetastatic lines, whereas the Ib and Ic markers predominated in the invasive, metastatic variants. The results suggest that metastasis‐enhancing genes are located between the D and F1 band of mouse chromosome 3 and that metastasis‐suppressing genes are located between the F1 and H band of the same chrom

ISSN:1045-2257    

DOI:10.1002/gcc.2870010203

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

年代:1989

数据来源: WILEY

摘要:

AbstractCytogenetic investigation of short‐term cultures from a bizarre leiomyoma of the uterus, a tumor type not hitherto karyotypically characterized, revealed two abnormal clones with multiple complex rearrangements. Three‐fourths of the aberrant cells were hypodiploid with the composite karyotype 38–44, XX,−6,−7,−10,−11,+20,−22, r(1), der(2) (:2p23→cen→2q13::1q21→1qter), der(2)t(2;9)(p21;q13), t(5;?)(q35;?), t(5;?),(q35;?), + der(5)t(5;15)(q11;q15), der(8)t(8;11)(q24;q13), t(15;?)(p12;?), der(16)t(12;16)(q13;p13),+r,+mar. The remaining abnormal mitoses were hypotetraploid, with chromosome numbers ranging from 74 to 86. These massively rearranged cells showed the same markers that were found in the hypodiploid clone, but in duplicate, indicating that this clone had arisen through polyploidization of hypodiploid cells. Flow cytometry reveale

ISSN:1045-2257    

DOI:10.1002/gcc.2870010204

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

年代:1989

数据来源: WILEY

摘要:

AbstractThe proliferative potential index (PPI), which is the proportion of all G1 cells which are in late G1, has been shown to reflect disease state in patients with acute leukaemia. We have determined PPI in paired blood and marrow samples from children with acute lymphoblastic leukaemia (ALL) at different stages of the disease, and found a close correlation between blood and marrow PPI irrespective of disease stage. Therefore blood PPI can replace marrow PPI for monitoring disease control in ALL.

ISSN:1045-2257    

DOI:10.1002/gcc.2870010205

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

年代:1989

数据来源: WILEY

摘要:

AbstractWe have prepared karyotypes from 22 primitive neuroectodermal tumors (PNETs) from pediatric patients ranging in age from 10 months to 16 years. Twenty‐one cases were newly diagnosed, primary, posterior fossa tumors. One case was a recurrent tumor in a patient previously treated with radiation. Cytogenetic results were obtained from direct preparations and/or short‐term (1–10 day) culture. Three tumors had apparently normal karyotypes. Nineteen tumors demonstrated numerical and/or structural abnormalities. The most frequent structural chromosomal changes were deletions and nonreciprocal translocations. Four tumors contained double minutes. Several chromosomes appear to be nonrandomly involved in PNETs. These include chromosomes 5, 6, 11, 16, 17, and a sex chromosome. The most consistent change, however, was an i(17q), present in one‐third (8/22) of the cases. Strikingly, in three of these eight tumors, the i(17q) was the only structural abnormality observed. An i(17q) is not specific for pediatric PNETs, as it is also seen in leukemias and other solid tumors. However, in PNETs it may be primary change related to tumor development and/or progression. Clinically, there was no correlation of the cytogenetic findings with histologic features of the tumors, size of the tumor, extent of metastasis, or surgical re

ISSN:1045-2257    

DOI:10.1002/gcc.2870010206

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

年代:1989

数据来源: WILEY

摘要:

AbstractCytogenetic analysis was performed on short‐term cultures of primary tumor tissue obtained from five patients with pleural malignant mesothelioma. Clonal karyotypic abnormalities were detected in four patients, none of whom had received cytotoxic therapy prior to karyotypic evaluation. Recurring chromosomal changes included partial deletions of 1p and 3p, and monosomy of 18, 19, and 22. We also reviewed data on 24 previously reported pretreatment patients and determined that alterations of chromosomes 1, 3, and 22 are frequently associated with malignant mesothelioma. Partial loss of chromosome 1 due to deletions or other rearrangements most frequently involve bands 1p11‐pter with the shortest region of overlap (SRO) occurring at 1p21–p22 in our patients. Deletions and other structural changes of chromosome 3 usually involve the region 3p14‐p25. The SRO of 3p deletions appeared to be at band 3p21. Monosomy 22 represents the most consistent specific whole chromosome loss seen in malignant mesothelioma, being observed in 11 of 28 cases summarized. In addition, structural changes of 22q have been observed in three patients, and a breakpoint at 22q11 was reported in each case. Taken collectively, these data suggest that a cascade of events involving alterations of genes on more than one specific chromosome may play a critical role in the development of malignant mesothelioma. The pattern of recurring chromosomal loss, particularly of 1p, 3p, and 22q, indicates that these regions should be targeted for future molecular investigations into the possible involvement of suppressor genes in this mal

ISSN:1045-2257    

DOI:10.1002/gcc.2870010207

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

年代:1989

数据来源: WILEY

摘要:

AbstractThe gene for the human platelet‐derived growth factor (PDGF) A type receptor was assigned to the proximal long arm of chromosome 4 by using in situ hybridization. Of 141 labeled metaphase cells, 74 had grains over chromosome 4, with a distinct peak at bands q11q–q12. The presence of the gene on chromosome 4 was also confirmed by hybridization to chromosome specific libraries. This places thePDGFAreceptor gene in the same region of chromosome 4 as theKIToncogene, another member of thePDGFgrowth factor receptor subfamily. The two other members of this gene family, thePDGFBreceptor and the colony stimulating factor‐1 (CSF1) receptor, are closely linked on the distal half of the long arm of chromos

ISSN:1045-2257    

DOI:10.1002/gcc.2870010208

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

年代:1989

数据来源: WILEY

摘要:

AbstractAt least 70% of human neuroblastomas display cytogenetically visible aberrations in the short arm of chromosome 1. We have used a panel of probes detecting polymorphic DNA loci, most of which were derived from a library of microdissected distal 1p chromosome fragments, to compare the hybridization pattern of DNA on nine different tumors and the corresponding normal tissue. In eight of the neuroblastomas allelic loss was observed with at least two probes. The deletions were of different size. Since a consensus deletion in all eight tumors included the segment 1p36.1–2, we conclude that genetic information related to neuroblastoma tumorigenesis is located within this approximately 10 megabase segment. Previous studies have revealed the amplification ofMYCNin neuroblastomas. Our study did not provide evidence for a correlation betweenMYCNamplification and the 1p deletion, suggesting that the two genetic alterations result from molecular mechanisms that are not directly related to each othe

ISSN:1045-2257    

DOI:10.1002/gcc.2870010209

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

年代:1989

数据来源: WILEY

摘要:

AbstractCytogenetic analysis of short‐term cultures from 11 moderately to poorly differentiated ovarian seropapillary cystadenocarcinomas revealed clonal chromosomal abnormalities in nine tumors. Two bands were involved in structural rearrangements in more than half of the tumors. The band most frequently affected was 19p13; rearrangements giving rise to a 19p+ marker chromosome were found in seven tumors, and in four of them the 19p+ markers appeared to be identical. Structural rearrangements resulting in loss of 11p13‐11pter material were found in six tum

ISSN:1045-2257    

DOI:10.1002/gcc.2870010210

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

年代:1989

数据来源: WILEY

摘要:

AbstractThe Philadelphia chromosome is present in more than 95% of chronic myelogenous leukemia patients and in up to 25% of patients with acute lymphocytic leukemia. The major consequence of the aberration is the fusion of theABLandBCRgenes. The position of the breakpoint on chromosome 22 determines which species of the potential three fused mRNAs and proteins will be synthesized. We have used the polymerase chain reaction (PCR) to detect these mRNAs in 53 patients and cell lines and found that around 20% contain simultaneously twoBCR‐ABLmRNAs, presumably due to a process of alternative splicing. The results also indicate that most patients in lymphocytic blast crisis of CML contain the mRNA in whichbcrexon 2 is linked toABLexon II. Finally, we identified, cloned, and characterized aBCR‐related sequence that originated from m

ISSN:1045-2257    

DOI:10.1002/gcc.2870010211

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

年代:1989

数据来源: WILEY