Cytogenetic characteristics of oral squamous cell carcinomas in Fanconi anemia

被引：7

作者：

Hermsen M.A.J.A. ^{[1
]}

Xie Y. ^{[2
]}

Rooimans M.A. ^{[2
]}

Meijer G.A. ^{[1
]}

Baak J.P.A. ^{[1
]}

Plukker J.Th.M. ^{[3
]}

Arwert F. ^{[2
]}

Joenje H. ^{[2
]}

机构：

[1] Department of Pathology, Free University, Medical Center, Amsterdam

[2] Department of Clinical Genetics and Human Genetics, Free University, Medical Center, Amsterdam

[3] Department of Oncological Surgery, University Hospital, Groningen

来源：

Familial Cancer | 2001年 / 1卷 / 1期

关键词：

Carcinogenesis; Comparative genomic hybridization; DNA cross-linking agents; Fanconi anemia; Squamous cell carcinoma;

D O I：

10.1023/A:1011528310346

中图分类号：

学科分类号：

摘要：

Fanconi anemia (FA) is an autosomal recessive syndrome with a marked predisposition to malignancies, in particular acute myeloid leukemia and squamous cell carcinoma of the oral cavity. We examined oral squamous cell carcinoma tissue from two FA patients (FA-A and FA-C) by comparative genomic hybridization. Both tumors, which were negative for human papilloma as well as Epstein-Barr viral sequences, showed multiple alterations with a high proportion of whole-arm chromosomal gains and losses. This combination of features as well as the sites involved in chromosomal breakage are very similar to what is typically observed in non-FA oral tumors. These results suggest that the process leading to early occurrence of oral cancer in FA patients follows a similar pathway as in non-FA cancer patients, which would support a caretaker function for FA genes in the protection against oral carcinogenesis. Since FA patients are uniquely hypersensitive to DNA cross-linking agents, while oral cancer in the general population is thought to be environmentally induced, these results also suggest that environmental DNA cross-linkers may be causally involved in oral carcinogenesis.

引用

页码：39 / 43

页数：4

共 20 条

[1]

Auerbach A.D., Buchwald M., Joenje H., Fanconi anemia, The Genetic Basis of Human Cancer, pp. 317-332, (1998)

[2]

Young N.S., Alter B.P., Aplastic Anemia Acquired and Inherited, pp. 275-324, (1994)

[3]

Vokes E.E., Head and neck cancer, N Engl J Med, 328, pp. 184-193, (1993)

[4]

Koo W.H., Knight L.A., Ang P.T., Fanconi's anaemia and recurrent squamous cell carcinoma of the oral cavity: A case report, Ann Acad Med Singapore, 25, pp. 289-292, (1996)

[5]

Kinzler K.W., Vogelstein B., Cancer-susceptibility genes. Gatekeepers and caretakers, Nature, 386, pp. 761-763, (1997)

[6]

Joenje H., Oostra A.B., Wijker M., Et al., Evidence for at least 8 Fanconi anemia genes, Am J Hum Genet, 61, pp. 940-944, (1997)

[7]

Strathdee C.A., Gavish H., Shannon W., Et al., Cloning of cDNAs for Fanconi's anaemia by functional complementation, Nature, 356, (1992)

[8]

Lo Ten Foe J.R., Rooimans M.A., Bosnoyan-Collins L., Et al., Expression cloning of a cDNA for the major Fanconi anemia gene, FAA, Nature Genet, 14, pp. 320-323, (1996)

[9]

De Winter J.P., Waisfisz Q., Rooimans M.A., Et al., The Fanconi anaemia group G gene FANCG is identical with XRCC9, Nature Genet, 20, pp. 281-283, (1998)

[10]

Snijder P.J., Cromme F.V., Van den Brule A.J., Et al., Prevalence and expression of human papillomavirus in tonsillar carcinomas, indicating a possible viral etiology, Int J Cancer, 51, pp. 845-850, (1992)

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