Isolation and chromosomal assignment of 100 highly informative human simple sequence repeat polymorphisms

Hudson, Thomas J.; Engelstein, Marcy; Lee, Matthias K.; Ho, Elizabeth C.; Rubenfield, Marc; Adams, Christopher; Housman, David E.; Dracopoli, Nicholas C.

doi:10.1016/0888-7543(92)90133-d

Cited by 223 publications

(73 citation statements)

References 18 publications

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“…Moreover, to obtain further veri®cation that the cell lines recovered after fusion and selection in G418-hygromicin medium were actually hybrids of the parental cell lines, we used pairs of PCR primers that span highly polymorphic sequences on speci®c chromosomes (23,24). Primer pairs were ®rst screened to identify those that yelded size polymorphisms in the different cell lines; then genomic DNA, isolated from each of the hybrid cell lines and from the parental cells, was ampli®ed by PCR with these pairs of primers.…”

Section: Cytogenetic Characterizationmentioning

confidence: 99%

The highly malignant phenotype of anaplastic thyroid carcinoma cell lines is recessive

Martelli

Miano

Battaglia

et al. 2000

European Journal of Endocrinology

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Objective: The aim of our studies was to determine whether the phenotype of the anaplastic thyroid carcinomas is dominant or recessive. In fact, it is hypothesized, on the basis of epidemiological and pathological data, that undifferentiated thyroid carcinomas are derived from differentiated tumours through a mechanism of tumour progression. Design: Cell hybrids have been generated by cell fusion of anaplastic thyroid carcinoma cell lines, which show a highly malignant phenotype, to cell lines deriving from differentiated thyroid carcinoma, which show a non-tumorigenic or a poorly tumorigenic phenotype. All of the parental cell lines showed impaired p53 gene function. Results: The cell hybrids contained alleles from the parental cell lines. All of the cell hybrids showed a lower growth rate compared with the parental undifferentiated carcinoma cell lines and were unable to grow in soft agar and to induce tumours after injection into athymic mice. Conclusion: Taken together, these ®ndings suggest that the highly malignant phenotype of the anaplastic thyroid carcinoma is achieved by the impairment of gene functions that negatively regulate cell growth, rather than by the activation of dominant oncogenes.

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Section: Cytogenetic Characterizationmentioning

confidence: 99%

The highly malignant phenotype of anaplastic thyroid carcinoma cell lines is recessive

Martelli

Miano

Battaglia

et al. 2000

European Journal of Endocrinology

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“…Each analysis was performed at least twice to ensure reproducible detection of AI (another independent PCR ampli®cation, gel separation, and quanti®cation). In an attempt to distinguish allelic gain from LOH, comparative multiplex PCR (Cairns et al, 1994) was performed with microsatellite marker D4S244 or D21S222 (Hudson et al, 1992), located in unaltered chromosomal regions (Watanabe et al, 1995), as internal controls.…”

Section: Detection Of Allelic Imbalancementioning

confidence: 99%

PTEN/MMAC1/TEP1 involvement in primary prostate cancers

et al. 1998

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“…Each analysis was performed at least twice to ensure reproducible detection of AI (repeat independent PCR ampli®cation, gel separation, and quanti®cation). In an attempt to distinguish allelic gain from LOH, comparative multiplex PCR (Cairns et al, 1994) was performed with the microsatellite marker D4S244 or D21S222 (Hudson et al, 1992) located in unaltered chromosomal regions (Watanabe et al, 1995), as internal controls.…”

Section: Dna Analysismentioning

confidence: 99%

Molecular analysis of the FHIT gene in human prostate cancer

et al. 1998

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A variety of studies suggest that the FHIT gene, which encompasses the fragile site at 3p14.2, is a candidate tumor suppressor gene in several forms of human cancer. To determine whether the FHIT gene is altered in prostate carcinomas, we examined 15 prostate tumors, four normal prostate tissue specimens and RNA from a pool of 62 normal human prostate tissues (Clontech) for the integrity of FHIT transcripts, using a robust singlestage PCR and a nested PCR method. In each case a major FHIT-speci®c full-length product was observed. Additional aberrantly sized products, which were more numerous in the nested PCR strategy, were present at a far lower level than the full-length transcripts in 14 of 15 tumors, three of four normal human prostate tissues and in the pooled normal prostate RNA. Sequence analysis revealed that these aberrant products corresponded to alternatively spliced FHIT transcripts, which were neither more numerous nor more prominent in the tumors than in the normal prostate specimens. Deletion at the FHIT locus was also evaluated by using three intragenic polymorphic markers (D13S1481, D3S1300, and D3S1234). Allelic loss was observed in two tumors, but these genomic alterations did not correspond to the aberrant FHIT transcripts. DNA analysis, furthermore, suggested that the tumor heterogeneity was not a likely explanation for presence of normal and alternatively spliced FHIT transcripts in the prostate tumors. In conclusion, we detected neither frequent loss of heterozygosity nor tumor speci®c transcripts of the FHIT gene in human prostate cancer.

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Isolation and chromosomal assignment of 100 highly informative human simple sequence repeat polymorphisms

Cited by 223 publications

References 18 publications

The highly malignant phenotype of anaplastic thyroid carcinoma cell lines is recessive

The highly malignant phenotype of anaplastic thyroid carcinoma cell lines is recessive

PTEN/MMAC1/TEP1 involvement in primary prostate cancers

Molecular analysis of the FHIT gene in human prostate cancer

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