摘要:

AbstractA workshop held by the „Groupe Français de Cytogénétique Hématologique”︁ has identified a t( 10; 11)(p13–14;q14–21) in four acute lymphoblastic leukemias of T‐cell lineage. The immunophenotypes were consistent with immature thymocytes. This translocation is therefore a new candidate for a recurrent translocation in early T‐cell leukemia. A similar translocation has been reported as a rare change in early pre‐B lymphoid leukemias and also in myeloid leukemias. It is not known whether the similar cytogenetic changes involve different molecular breakpoints or whether the same rearrangement affects a multipotential stem cell capable of lymphoid and myel

ISSN:1045-2257    

DOI:10.1002/gcc.2870030602

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

年代:1991

数据来源: WILEY

摘要:

AbstractCytogenetic analysis was performed on samples from ten patients diagnosed with aneurysmal bone cyst. Six of the patients were male and four were female, with ages ranging from 7 to 24 years. Results were obtained in eight of the cases; all were karyotypically normal.

ISSN:1045-2257    

DOI:10.1002/gcc.2870030603

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

年代:1991

数据来源: WILEY

摘要:

AbstractSix squamous cell carcinomas of the vulva (SCV) were karyotyped in short‐term culture and in early passages as established cell lines. Each tumor was cytogenetically distinct, contained multiple chromosome rearrangements, and was karyotypically stable in culture. Heterogeneity within individual tumors was manifested by the presence of more than one clonal population, but the clones within each tumor were closely related to one another. Seven consistent chromosome abnormalities found in five of the six tumors were: losses of 3p 14‐cen, 8pter‐p 11, 22q 13.1 ‐q 13.2, and the short arm of the inactive X; chromosome gains involving 3q25‐qter and 11 q21; and rearrangement breakpoints at 5cen‐q 12. Ten additional chromosome changes were observed in four of the six SCVs, and together, 22 changes occurred in at least three of the tumors. Two specific losses, 10q23‐q25 and 18q22‐q23, were present in all four tumors that exhibited biologically aggressive behavior in vivo, but these losses were not found in the tumors of the two long‐term survivors. These findings indicate that: 1) SCVs are genetically complex, but homogeneous; 2) loss of 18q22‐q23 and loss of 10q23‐q25 may be associated with a poor prognosis; and 3) development and progression of SCV appear to result from cumulative effects of altered gene dosage at mult

ISSN:1045-2257    

DOI:10.1002/gcc.2870030604

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

年代:1991

数据来源: WILEY

摘要:

AbstractWe have examined interactions among intratumor subpopulations during the rejection of immunogenic variants of a murine mammary carcinoma (SPI) and in the outgrowth of tumorigenic “revertant” subsets. Analysis of subclones isolated during the early phase of rejection of one immunogenic variant revealed extensive cellular heterogeneity of tumor‐forming ability and class I major histocompatibility complex (MHC) expression. Two main categories of subclones were identified. One set expressed high levels of class I MHC (MHCH) and grew poorly or not at all in normal syngeneic mice. The second set of clones expressed generally low levels of class I MHC (MHCL) and exhibited progressive growth in vivo, similar to the parent tumor. The steady‐state mRNA levels for class I MHC and β2‐microglobulin were constitutively elevated in MHCHclones compared to MHCLclones or the parent tumor. However, in vivo tumorigenic outgrowths from immunogenic variants always expressed the MHCHphenotype. A cytogenetic analysis was carried out to determine the clonal origin and lineage relationship of in vivo selected tumor outgrowths. Surprisingly, tumor outgrowths from mixtures of karyotypically distinct MHCHand MHCLsubclones were derived from one lineage within the MHCHsubset, despite the fact that MHCHsubclones exhibited slower growth in vivo than MHCLsubsets when analyzed individually. These results suggest that in polyclonal populations the various subsets sometimes interact in a way that overrides the influence of immunogenic and MHC phenotypes of individual

ISSN:1045-2257    

DOI:10.1002/gcc.2870030605

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

年代:1991

数据来源: WILEY

摘要:

AbstractGene amplification and related alterations in gene dosage were analyzed in a series of 34 cell lines derived from different human head and neck squamous cell carcinomas (SCCHN).INT2gene amplification was observed in 62%,MYCgene amplification in 24%, andEGFRgene amplification in 21 % of the cell lines. There was a strong correlation betweenEGFRgene amplification and increased copies of theERBB2gene on chromosome 17, suggesting a synergistic selection for these two genes either during cancer progression or in culture. Two abnormalities showed a significant correlation with clinical course:MYCgene amplification showed an inverse correlation with tumor recurrence (r = ‐ 0.44, p = 0.01), and a small increase inMYCLgene copies on chromosome I correlated with the presence of metastases (r = 0.61, p = 0.001). This alteredMYCLgene dosage might represent a chromosome translocation rather than true gene amplification. In addition to gene amplification, 79% of the cell lines had increased copies of chromosome 8. Comparison of the cell lines with several of the corresponding primary tumors demonstrated that most gene amplifications were already present in the primary tumors, although some appeared de novo in cell culture. These studies indicate that gene amplification, especially ofINT2, is a prominent abnormality in head and neck squamous cell cancer. Aneuploidy and chromosomal lesions other than gene amplification were also found to alter the dosage of several oncogenes specificall

ISSN:1045-2257    

DOI:10.1002/gcc.2870030606

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

年代:1991

数据来源: WILEY

摘要:

AbstractThree patients with leukemia and one with a myeloproliferative disorder carried an interstitial deletion of chromosome 13, del(13)(q12q14), in leukemic cells. Proximal and distal breakpoints of the deleted segment were characterized by using DMA restriction fragment length polymorphisms of chromosome 13 supplemented by quantitative densitometry of hybridization signals to determine the copy number of individual loci. Both proximal and distal breakpoints varied between patients, and it is unlikely that a significant hybrid gene was formed by rejoining at the breakpoint junctions. The retinoblastoma gene was encompassed by the deleted segment in all four patients.

ISSN:1045-2257    

DOI:10.1002/gcc.2870030607

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

年代:1991

数据来源: WILEY

摘要:

AbstractHSB‐2 is a cell line derived from a patient who had T‐cell acute lymphoblastic leukemia (T‐cell ALL) with a t( 1;7)(p34;q34). We used a genomic probe from the T‐cell receptor beta (TCRB) locus (7q34) to identify DNA rearrangements in HSB‐2. Two rearranged Bg/11 DNA fragments were cloned, and one of these clones was shown to contain the translocation breakpoint on the derivative chromosome 1 [der(1)]. We used a probe derived from this clone to isolate an unrearranged phage clone encompassing the breakpoint at 1 p34. The restriction map of this clone was compared to the published maps of known protooncogenes located at 1 p32–34. By restriction mapping, Southern blot analysis, and DNA sequencing we showed that the translocation breakpoint on chromosome 1 is located within the first intron of the LCK gene. The LCK gene codes for p56lck, a member of the SRC family of cytoplasmic tyrosine protein kinases. There are two classes of LCK transcripts (type 1 and type 11), each expressed from a distinct promoter, and each having a unique 5′ untranslated region (UTR); the protein coding regions of the two classes are identical. The breakpoint in the t( 1;7) separates the two LCK promoters and juxtaposes the constant region of the TCRB locus with the proximal promoter and with the protein‐coding region of the LCK gene on the de

ISSN:1045-2257    

DOI:10.1002/gcc.2870030608

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

年代:1991

数据来源: WILEY

摘要:

AbstractWe examined tissue extracted from 19 gastric, 7 pancreatic, and 23 colorectal carcinoma specimens to determine the comparative incidence of allele loss on chromosomes 5, 17, and 18 and that ofKRAS2point mutations. Chromosome 5 allele loss occurred at the same frequency in all three gastrointestinal tumors (approximately 30%), whereas chromosome 17 and 18 allele losses were seen at a significantly lower frequency in gastric (20%) and pancreatic (0%) malignancies than in colorectal cancer (57%). Point mutations inKRAS2were seen in 83% of pancreatic and 52% of colon cancers, but not in gastric cancer specimens. In pancreatic tumors, these mutations were always found in the second nucleotide of codon 12. In colorectal cancer, the distribution was more variable, involving the second nucleotide of codon 13 and both the first and second nucleotides of codon 12. These results suggest that inactivation of the adenomatous polyposis coli gene on chromosome 5 may be an initiating step for carcinomas of the stomach and pancreas as well as of the colon, but that the genes involved in tumor progression events may be tissue‐ or tumor‐speci

ISSN:1045-2257    

DOI:10.1002/gcc.2870030609

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

年代:1991

数据来源: WILEY

摘要:

AbstractWe describe the cytogenetic findings in short‐term cultures from 40 malignant gliomas, all of which had at least one clone with a simple numerical chromosome aberration. More than one aberrant clone was found in 17 tumors. The most frequent changes were loss of a gonosome (sole aberration in 38 clones), trisomy 7 (sole aberration in four clones), and combinations thereof (the aberrations + 7 and — X or — Y were found together as the only changes in four clones). Clones with solitary trisomies for other autosomes—3, 5, 6, and 18—were seen in five tumors. Clones with structural rearrangements were found in nine tumors. The bands most commonly involved were I p36, 7p22, 9p22, 17p 13, and 19q 13. An extra copy of chromosome 7 was seen as part of a structurally abnormal clone in five tumors. In one case, trisomy 7 and even tetrasomy 7 were found in clones with simple numerical changes, but not in the clone with structural rearrangements. Likewise, the clonal loss of a gonosome was in six tumors, with structural abnormalities not present in the structurally aberrant clones; on the other hand, in two clones with structural aberrations a sex chromosome had been lost. The combined findings indicate that loss of a sex chromosome and trisomy 7 should not be seen as tumor‐specific aberrations in gliomas. Instead, both glioma parenchyma cells and nonneoplastic cells in brain tumors may have a propensity to acquire extra copies of chromosome 7 and to los

ISSN:1045-2257    

DOI:10.1002/gcc.2870030610

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

年代:1991

数据来源: WILEY

摘要:

AbstractIn three cases of alveolar rhabdomyosarcoma with variant translocations, two tumors contained an identical translocation, t(1;13)(p36.1;q14); the third tumor contained a t(8;13)(p21;q14). All three patients were 2 years old, markedly younger than the median age for patients with t(2; 13)‐positive alveolar rhabdomyosarcoma. The alteration of genetic material on chromosome 13 may be of primary importance in the development of alveolar rhabdomyosarcom

ISSN:1045-2257    

DOI:10.1002/gcc.2870030611

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

年代:1991

数据来源: WILEY