
CHROMOSOMAL ABNORMALITIES IN
ENDOMETRIAL AND OVARIAN CARCINOMAS PazarbaÕi A1,*, Kasap M1, Demirhan O1, Vardar MA2,
Suleymanova-Karahan D1, Doran F3 *Corresponding Author: *Corresponding Author: Ayfer PazarbaÕi, Ph.D., Department of Medical Biology and
Genetics, University of Çukurova, School of Medicine, 01330 Balcali, Adana, Turkey; Tel.:
+90-322-338-70-68; Fax: +90-322-338-65-72; E-mail: payfer@cu.edu.tr page: 61
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RESULTS
Of the 38 tumor samples, 15 were excluded from the study because of bacterial contamination, detachment, or the presence of necrotic tissue. Karyotypic patterns were analyzed in 12 endometrial carcinomas and 11 ovarian carcinomas. All samples were from invasive epithelial tumors and characterized histologically as follows: of the endometrial tumors, four were at grade III, seven at grade II and one at grade I, while of the ovarian tumors, one was at grade III, five at grade II and five at grade I. The patients did not all show the same stage of cancer progression and there was no relationship between the complexity of chromosome constitution and the cancer progression. Structural alterations present in more than one cell were termed clonal alterations. Thirteen patients had clonal chromosomal abnormalities, eight had non clonal abnormalities, and two cases had normal karyotypes. Most specimens exhibited complex karyotypes with many numerical and structural changes (Table 1). Numerical changes were seen in six cases: case O5 had karyotype 54,XX with numerical changes at chromosomes 9, 10, 12, 14, 15 and 20. Aneuploidy was observed in case E5. Cases O11, E1, E6 and E7 showed near-triploid, tetraploid and polyploid modal numbers with heterogenous structural abnormalities. Eleven showed a variety of structural abnormalities and five had only one structural abnormality. Deletions, translocations, inversions, gaps or breaks, acentric fragments, double minutes, radials and endoreduplications were observed in varying proportions. Translocations were found in four cases. Case E1 had t(19;22)(q13;p13) and t(21;22)(p13;q13), while case E2 had t(14;21)(q11; q11), case O5 had t(3;7)(q;q) and case O4 had t(1;22)(qter;p). Two cases (13 cells of E6 and five cells of O11) had double minutes and one case with tri radial and quadriradials (seven cells of E6) (Table 1).
The cancer breakpoints and fragile sites observed are shown in Table 2. Chromosomes 3, 5, 1, 12, 17 and 2 (cited according to their frequency) were most frequently involved in structural abnormalities (Table 3 and 4 and Figure 1). Structural rearrangements acquired on chromosomes 2, 4, 7, 8, 9, 10, 11, 13, 15, 17, 18 and X in ovarian cancers and on chromosomes 14, 19, 20 and 22 in endo metrial cancers.
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