Acquired chromosome changes in cholesteatoma

Acquired chromosome changes in cholesteatoma

Abstracts CHROMOSOMAL 189 ABERRATIONS CA~CINO~S or IN FOUR SQUAMOUS CELL THE ORA~ CAVITY B r a u n S. ~, G u n a w a n B. , Schmitz H. 2, FU...

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Abstracts

CHROMOSOMAL

189

ABERRATIONS

CA~CINO~S or

IN

FOUR

SQUAMOUS

CELL

THE ORA~ CAVITY

B r a u n S. ~, G u n a w a n B. , Schmitz H. 2, FUzesi L. 1 IInstitute of Pathology, RWTH A a c h e n 2 D e p a r t m e n t of Oral Surgery, R W T H A a c h e n Pauwelsstr. 30, 52057 Aachen, G e r m a n y

FISH A N A L Y S I S OF DERIVATIVE CHROMOSOME#3 IN T U M O R I G E N I C KERATINOCYTE LINE. Dyer KA, Tedford KL, Behler C, and McDougall JK. Fred Hutchinson Cancer Research Center, Cancer Biology Group CI-015, 1124 Columbia Street, Seattle, WA 98104.

We report on four cases of squamous cell c a r c i n o m a s of the oral cavity. These p r i m a r y untreated squamous cell carcinomas of four p a t i e n t s who had u n d e r g o n e t u m o r resection and subsequent conservative or radical neck d i s s e c t i o n were a n a l y z e d by m e a n s of classical cytogenetics. Our cases generally showed a m o s a i c cytogenetic p a t t e r n of m u l t i p l e aberrant cell clones involving several chromosomes. Until recently, o n l y a few cases of squamous cell carcinomas have been reported in the literature. These cases also v e r y frequently consisted of cell clones with different cytogenetical abnormalities, underlining the m u l t i f a c t o r i a l e t i o l o g y of oral squamous cell carcinomas.

A whole chromosome probe to an aberrant #3 chromosome was made by linker-adapter PCR a m p l i f i c a t i o n of selected flow-sorted libraries from the FEP-1811 cell line. H y b r i d i z a t i o n of the probe to normal peripheral blood lymphocytes revealed localization to not only the entire #3 chromosome, but also 13q21-qter and 21q22. Hybridization of this probe and painting probes from normal #3,13 and 21 chromosomes to FEP-1811 metaphases confirmed that the der(3) is a complex rearrangement of 3, 13, and 21. The FEP-1811 cell line is a model system developed by this lab to study anogenital malignancies. The line is derived from primary human k e r a t i n o c y t e s which have been immortalized by transfection with human papilloma virus type 18 and become progressively tumorigenic. At late passage, these cells are capable of producing squamous cell carcinomas. Stabilization of rearrangements within the #3 chromosome occurs as the line proceeds to tumorigenicity.

ACQUIRED CHROMOSOMECHANGESIN CHOLESTEATOMA Lo Curto F (1), Maserati E (1), Castelnuovo P (2), Lanza L (2) - (1) Biologia Generale e Genetica Medica ; (2)Cli nica O t o r i n o l a r i n g o i a t r i c a . UniversitA di Pavia, C P 217 I 27100 Pavia, I t a l y .

CYTOGENETIC STUDY OF A SPORADIC INSULINOMA. Lucia Roque, Maria Jo~.o Bugalho, Luis Sobrinho, Josd Mendes Almeida and Jorge Soares. Instituto Portugu~s de Oncologia, 1093 Lisboa Codex, Portugal.

L i t t l e is known about the biology of cholesteatoma and no cytogenetic data are available. We attempted chromosome analyses in 30 cases of cholesteatoma, but 7 biopsies f a i l e d to grow because of bacterial contamination due to middle ear i n f e c t i o n s , while no growth took place in 12. We observed only normal karyotypes in 6 of the I I i n f o r mative cases, while anomalies were present in the other f i v e , both in single c e l l s or as clonal changes. The clonal anomalies observed were trisomies 7, 8, and 20, loss of the Y, and a deletion of the short arms of a no. 4. In 4 cases the heterochromatic regions of nos. I , 9, and 16 showed a stretched appearance in a high proport i o n of c e l l s . In all cases the karyotype of blood stimulated lymphocytes was normal.

Chromosomal analysis of a sporadic insulinoma performed after shortterm in vitro culture revealed a t(1;9)(p13;p22) as the sole chromosomal abnormality in 4 of the 35 cells analyzed. To our knowledge this is the first cytogenetic study in a sporadic insulinoma. Cytogenetic aberrations with breakpoints at chromosomes lp13 and 9p22 regions are frequently observed in distinct types of tumors. Two cancer related genes have been mapped in the former region: the neuroblastoma ms viral homolog (N-ras) and the Kirsten-ras-revertant 1 gene (K-rev 1). Rearrangements of K-rev 1 have already been described in a case of benign insulinoma by blot hybridization. The observation in the case described herein of a translocation with a breakpoint at lp13 raises the possibility that K-rev 1 is disrupted and further suggests that rearrangements of this gene might be involved in the pathogenesis of insulinomas.