Refined mapping of eight cosmid markers on human chromosome 22

Kurahashi, Hiroki; Akagi, Kenzo; Yana, Ikuo; Melot, Thomas; Delattre, Olivier; Thomas, Gilles; Okada, Shintaro; Takai, S; Nishisho, Isamu

doi:10.1007/bf01876844

Cited by 2 publications

(1 citation statement)

References 12 publications

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“…correlation was not statistically significant ( p 0.068, Fisher's cHKA-212 and cHKA-110, recently isolated cosmid markers exact test). Association between LOH within the SRO and were finely mapped with a panel of somatic-cell hybrids LOH at D18S5 was not statistically significant ( p 0.944, (Kurahashi et a/., 1994). In addition, probe YNZ22 (D17S30) Fisher's exact test).…”

Section: Dna Probesmentioning

confidence: 96%

Frequent loss of heterozygosity at telomeric loci on 22q in sporadic colorectal cancers

Yana

Kurahashi

Nakamori

et al. 1995

Intl Journal of Cancer

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To date, several tumor-suppressor genes responsible for the tumorigenesis of colorectal cancer have been identified. However, studies of loss of heterozygosity (LOH) have suggested several chromosomal regions which may contain additional tumor-suppressor genes for colorectal cancer. To determine the extent and variation of allelic loss on 22q, on which LOH has been frequently observed, a total of 68 sporadic colorectal cancers was examined for LOH on the chromosome arm by means of 16 polymorphic DNA markers. LOH was observed in 28 tumors (41%), of which 9 showed LOH at all informative loci. The remaining 19 tumors showed variable patterns of partial loss on 22q, delimiting the smallest region of overlap (SRO) between D22S90 and D22S94. Moreover, LOH within the SRO correlated with a progression in terms of Dukes' stages. These results suggest that an additional tumor-suppressor gene for colorectal cancer may exist on 22q distally to the NF2 locus and that inactivation of the gene may possibly play a role in the progression or metastasis of colorectal cancers.

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Section: Dna Probesmentioning

confidence: 96%

Frequent loss of heterozygosity at telomeric loci on 22q in sporadic colorectal cancers

Yana

Kurahashi

Nakamori

et al. 1995

Intl Journal of Cancer

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Deletion mapping of the long arm of chromosome 22 in human meningiomas

Akagi

Kurahashi

Arita

et al. 1995

Intl Journal of Cancer

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Cytogenetic and molecular genetic analyses have shown that a tumor-suppressor gene for human meningioma is located on the long arm of chromosome 22. Recently, somatic mutations of the NF2 gene have been identified in sporadic meningiomas. However, tumorigenesis of certain cases of meningioma cannot be fully explained by inactivation of the NF2 gene alone. Thus, to obtain some indication as to the existence of another tumor-suppressor gene, it seemed important to re-examine the loss of heterozygosity (LOH) on 22q in sporadic meningioma. A total of 46 sporadic meningiomas was examined for LOH at 20 loci on 22q. LOH was observed in 29 tumors (63%), of which 13 (28%) showed different patterns of a partial loss of 22q. However, the NF2 locus was retained in one tumor that lost a more distal part of 22q. Moreover, 27 of the 28 tumors which showed LOH at the NF2 locus also lost alleles at more telomeric loci. These results raise the possibility that another tumor-suppressor gene for meningioma may exist on 22q and that its localization may be distal to the D22S102 locus.

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Refined mapping of eight cosmid markers on human chromosome 22

Cited by 2 publications

References 12 publications

Frequent loss of heterozygosity at telomeric loci on 22q in sporadic colorectal cancers

Frequent loss of heterozygosity at telomeric loci on 22q in sporadic colorectal cancers

Deletion mapping of the long arm of chromosome 22 in human meningiomas

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