Detection of numerical abnormalities of chromosome 9 and p16/CDKN2A gene alterations in ovarian cancer with fish analysis.

BACKGROUND: The molecular events leading to the development of ovarian cancer are not well-established. Defects of the retinoblastoma protein (pRb)/cyclin-D1/p16 pathway have been shown to play a critical role in the development of human malignancies. In particular, the p16/cyclin-dependent kinase inhibitor 2A (CDKN2A) gene located on chromosomal region 9p21 frequently is altered in several types of cancer. MATERIALS AND METHODS: To investigate both the presence of numerical abnormalities of chromosome 9 and p16 gene alterations in ovarian cancer, we studied 28 cases by the fluorescence in situ hybridization (FISH) technique using a DNA p16 probe and an a-satellite probe specific for chromosome 9. RESULTS: Numerical abnormalities of chromosome 9 were found in all studied cases. Polysomy 9 was detected in 10 cases while monosomy 9 in seven cases. In 11 cases, there were two cell populations, one with polysomy 9 and the other with monosomy 9. In all cases, the p16 gene deletion was observed. Among them, 25 cases presented deletion of p16 gene in 21.43%-86.3% of the examined cells. Three cases carried deletion of the p16 gene in a lower proportion (12.04%-19.49%). In five cases with p16 gene deletion, homozygous deletion was detected. CONCLUSION: Numerical aberrations of chromosome 9 and p16 gene deletion are common findings in ovarian cancer. Data suggest that the p16 gene, located in the short arms of chromosome 9, may play a role in ovarian carcinogenesis. In addition, polysomy 9 could lead to activation of a number of oncogenes, thus participating in the neoplastic process in the ovaries.

Isochromosome 5p, a novel recurrent abnormality in breast cancer: is it a common abnormality in cancer?

BACKGROUND: The detection of recurring genetic changes in breast cancer can be extremely difficult. The tumors display very complex structural chromosomal rearrangements the origin of which are often very difficult to establish. The identification of recurrent chromosomal changes is a useful strategy for understanding tumorigenesis and specific chromosomal associations. Isochromosome i(5p) is a frequent finding in several types of cancer but it has been rarely described in breast cancer. The aim of the present study was to investigate the presence of i(5p) in primary breast tumors. MATERIALS AND METHODS: Sixteen cases of breast cancer were cytogenetically studied by direct culture of cancerous cells and G-banding technique. We focused on structural aberrations of chromosome 5 in order to identify the presence of i(5p) in breast cancer. RESULTS: All the cases presented complex chromosomal changes with hyperploidization and various unidentified marker chromosomes being the prominent finding. Among 16 cases studied 6 cases presented an i(5p). No other structural abnormalities of chromosome 5 could be identified. CONCLUSION: The presence of i(5p) in breast tumors suggests that this chromosomal abnormality plays an important role in the development of breast cancer. Isochromosome 5p needs to be further molecularly analyzed as a candidate region for the isolation of genes related to carcinogenesis. Moreover, the fact that i(5p) has been described in several different tumor types suggests that there are no fundamental tissue-specific differences in the genetic mechanisms leading to tumorigenesis.

Numerical abnormalities of chromosome 9 and p16CDKN2A gene deletion detected by FISH in non-small cell lung cancer.

BACKGROUND: Lung cancer is one of the most common types of cancer worldwide and its pathogenesis is closely associated with various environmental exposures and gene alterations. The identification of genetic changes is a useful strategy toward understanding tumourigenesis and specific genetic associations. Since the tumor suppressor gene p16 located at 9p21 chromosomal region might have an important role in lung carcinogenesis, the aim of the present study was to investigate p16 gene alterations and numerical aberrations of chromosome 9 in non-small cell lung cancer. MATERIALS AND METHODS: Nineteen cases of non-small cell lung cancer (11 squamous cell carcinomas, 6 adenocarcinomas and 2 large cell carcinomas) were investigated by fluorescence in situ hybridization (FISH) technique using a DNA p16 probe and alpha-satellite probe specific for chromosome 9. RESULTS: Polysomy 9 was found in 13 cases (6/11 squamous cell carcinomas, 5/6 adenocarcinomas and 2/2 large cell carcinomas). p16 gene alterations were found in 16 cases. Among them, deletion of p16 gene was found in 15 cases (8/11 squamous cell carcinomas, 5/6 adenocarcinomas and 2/2 large cell carcinomas). In six cases with p16 gene deletion, homozygous deletion was observed. CONCLUSION: Numerical aberrations of chromosome 9 and p16 gene deletion are common findings in all subtypes of non-small cell lung cancer. Despite suggesting the p16 gene in the 9p chromosomal region plays a role in lung carcinogenesis, the presence of other oncogenes reflected by polysomy 9 participating in the neoplastic process cannot be excluded. Data of the present study also suggest, that there might not be a fundamental relationship between genetic changes and histological subtype of non-small cell lung cancer.

Simple structural chromosomal abnormalities in advanced stage of ovarian cancer.

BACKGROUND: Ovarian cancer represents the leading cause of death among patients with gynaecological cancer. The identification of chromosomal abnormalities is a useful strategy toward understanding tumourigenesis and specific chromosomal associations. Since single chromosomal changes might be primary events implicated in the initiation of the neoplastic process, the aim of the present study was to investigate the presence of simple structural chromosomal changes in ovarian cancer. MATERIALS AND METHODS: Reviewing on ascetic effusions samples cytogenetically studied by direct culture of tumour cells and a G-banding technique, two ovarian cancer cases were found which presented simple structural chromosomal abnormalities. RESULTS: The first case presented an abnormal clone of cells with an acquired pericentric inversion of chromosome 9, inv(9)(p11q13), as a sole anomaly. The second case presented simple chromosomal changes with involvement of the Xq23 chromosomal region, while a translocation t(X;11)(q23;q23) was also defined. CONCLUSIONS: The significance of the acquired pericentric inversion 9 in the development of the neoplastic process remains unknown. The chromosomal regions Xq23 and 11q23 need to be further investigated in association with clinicopathological parameters in ovarian cancer. The documentation of more ovarian cancer cases with simple chromosomal abnormalities is considered of major importance facilitating the identification of candidate genes involved in the neoplastic process. Improving the molecular understanding of ovarian cancer development and progression could facilitate the detection of specific tumour subtypes.

Janus kinase 2 mutations in Philadelphia negative chronic myeloproliferative disorders: clinical implications.

The chronic myeloproliferative disorders (CMPD) are a group of clinically related diseases characterized by clonal hematopoiesis with increased proliferation of one or more myeloid cell lineages. The identification of JAK2 mutations (JAK2V617F and JAK2 exon 12) in patients with CMPD is of great significance in the understanding of the molecular mechanisms underlined the pathogenesis of the disease contributing also to clinical management of patients. However, the precise pathogenetic contribution of JAK2 mutation is far from being fully elucidated and it is currently under intense investigation. Testing of JAK2 mutations has made the diagnosis of CMPD more precise than ever before, while genotype-phenotype associations have been identified. Furthermore, the discovery of JAK2 mutations facilitated the development of new targeted therapies and clinical trials are currently ongoing.

Is there an association with constitutional structural chromosomal abnormalities and hematologic neoplastic process? A short review.

The occasional observation of constitutional chromosomal abnormalities in patients with a malignant disease has led to a number of studies on their potential role in cancer development. Investigations of families with hereditary cancers and constitutional chromosomal abnormalities have been key observations leading to the molecular identification of specific genes implicated in tumorigenesis. Large studies have been reported on the incidence of constitutional chromosomal aberrations in patients with hematologic malignancies, but they could not confirm an increased risk for hematologic malignancy among carriers of structural chromosomal changes. However, it is of particular interest that constitutional structural aberrations with breakpoints similar to leukemia-associated specific breakpoints have been reported in patients with hematologic malignancies. Because of insufficient data, it remains still unclear if these aberrations represent random events or are associated with malignancy. There has been a substantial discussion about mechanisms involved in constitutional structural chromosomal changes in the literature. The documentation of more patients with constitutional structural chromosomal changes could be of major importance. Most importantly, the molecular investigation of chromosomal regions involved in rearrangements could give useful information on the genetic events underlying constitutional anomalies, contributing to isolation of genes important in the development of the neoplastic process. Regarding constitutional anomalies in patients with hematologic disorders, a survey of the cytogenetic data of our cytogenetics unit is herein also presented.

Cytogenetic and molecular aspects of gastric cancer: clinical implications.

Gastric cancer is of major importance world-wide being the second most common cause of cancer-related death in the world. According to Lauren's histological classification gastric cancer is divided in two groups, the better differentiated intestinal carcinomas and the poorly differentiated diffuse-type cancers. The genetic changes underlying the initiation and progression of gastric cancer are not well defined. Gastric carcinogenesis is a multistep process involving a number of genetic and epigenetic factors. Although it has been proposed that different genetic pathways exist for differentiated and undifferentiated carcinomas, the two histological subtypes of gastric cancer share some common genetic alterations. Currently, tumor histology and pathologic stage are the major prognostic variables used in the clinical practice for gastric cancer patients. However, it is known that tumors with similar morphology may differ in biological aggressiveness, prognosis and response to treatment. Molecular genetic analysis of gastric cancer revealed a number of associations of certain genetic changes with pathological features, tumor biological behavior and prognosis of gastric cancer patients, suggesting that these genetic abnormalities might play an important role in gastric tumorigenesis. Increasing evidence suggests that the molecular genetic changes could be helpful in the clinical setting, contributing to prognosis and management of patients. Regarding epigenetic events in gastric tumorigenesis, a number of methylating markers have been proposed for risk assessment, prognostic evaluation and as therapeutic targets. However, further research is required in order to systematically investigate the genetic changes in gastric cancer estimating also their usefulness in the clinical practice. A good understanding of the genetic changes underlying gastric carcinogenesis may provide new perspectives for prognosis and screening of high risk individuals. Some of the genetic alterations could definitely improve tumor classification and management of gastric cancer patients. Also, based on molecular data identified in gastric cancer novel therapeutics might help to improve the treatment of this disease.

Single chromosomal abnormalities in Philadelphia-negative chronic myeloproliferative disorders.

BACKGROUND: In Philadelphia-negative chronic myeloproliferative disorders (CMPD), increased proliferation with effective maturation of the myeloid lineage is present, while peripheral leukocytosis, thrombocytosis or elevated red blood cell mass are found. This group of disorders includes polycythemia vera (PV), essential thrombocythemia (ET) and idiopathic myelofibrosis (IMF). Furthermore, cases that cannot be clearly defined are regarded as unclassified CMPD. In Philadelphia-negative CMPD, recurrent cytogenetic abnormalities occur, but no specific abnormality has been defined to date. Chromosomal abnormalities detected in a neoplastic disease as a sole anomaly are of major importance, possibly constituting primary changes implicated in the initiation or progression of the neoplastic process. The aim of this study was to investigate the frequency and the type of single chromosomal changes in Philadelphia-negative CMPD patients. MATERIALS AND METHODS: By conventional cytogenetics, 245 Philadelphia-negative CMPD cases at diagnosis were investigated for the frequency and the type of single chromosomal aberrations. RESULTS: Seventeen patients presented single chromosomal changes. These aberrations were, according to frequency, +8 (in 3 PV cases, 2 IMF and 2 unclassified myeloproliferative diseases), +13 in 3 cases (IMF, ET and unclassified myeloproliferative disease), monosomy 10 in 2 PV cases, monosomy 14 in one ET patient, +3, -4 and del(11)(q13) in 1 unclassified myeloproliferative disease each and monosomy 7 in 1 IMF case. CONCLUSION: It is unclear whether these abnormalities found at the time of diagnosis play a role in CMPD. However, since an isolated chromosomal abnormality may be implicated in the initiation of the neoplastic process, the documentation of more cases of CMPD with single abnormalities at the time of diagnosis would facilitate the identification of candidate genes involved in the neoplastic process.

Preferential involvement of chromosome 11 as add(11)(p15) in ovarian cancer: is it a common cytogenetic abnormality in cancer?

Ovarian cancer represents the leading cause of death among patients with gynecological cancer. The genetic changes underlying the development and progression of ovarian cancer are not well defined. Identification of chromosomal aberrations is a useful strategy toward understanding tumorigenesis and specific chromosomal associations. Studying 15 ovarian cancer cases by conventional cytogenetic techniques, we previously reported that 11p15 was the most consistent chromosomal breakpoint involved. The aim of the present study was to investigate the presence of structural changes of chromosome 11 in ovarian cancer. Ten cases of ovarian cancer were cytogenetically studied by direct culture of tumour cells and G-banding technique. Eight cases presented structural aberrations of chromosome 11 with 11p15 involved as add(11)(p15) in all 8 cases and 11q23 involved as add(11)(q23) in 3 cases. Findings of the present study further support the possible role of chromosomal abnormalities add(11)(p15) and add(11)(q23) in ovarian cancer. These aberrations may result either in loss of genetic material from 11p and 11q, respectively, or in specific genes alterations. It is necessary, these chromosomal regions to be further investigated at molecular and clinical level. Improving the molecular understanding of ovarian cancer development and progression could facilitate the detection of specific tumor subtypes and contribute also to novel strategies for the management of ovarian cancer patients.

Cytogenetic and molecular aspects of Philadelphia negative chronic myeloproliferative disorders: clinical implications.

Chronic myeloproliferative disorders (CMPD) are clonal disorders of the hematopoietic stem cell. The myeloid lineage shows increased proliferation with effective maturation, while peripheral leukocytosis, thrombocytosis or elevated red blood cell mass are found. In Philadelphia negative CMPD recurrent cytogenetic abnormalities occur, but no specific abnormality has been defined to date. The spectrum of cytogenetic aberrations is heterogeneous ranging from numerical gains and losses to structural changes including unbalanced translocations. The most common chromosomal abnormalities are 20q-, 13q-, 12p-, +8, +9, partial duplication of 1q, balanced translocations involving 8p11 and gains in 9p. Cytogenetic analysis of CMPD by conventional or molecular techniques has an important role in establishing the diagnosis of a malignant disease, adding also more information for disease outcome. Molecular studies may detect the possible role of candidate genes implicated in the neoplastic process, addressing new molecular target therapies. FIP1L1/PDGFRalpha rearrangements, as well as alterations of PDGFRbeta or FGFR1 gene have been found to be associated with specific types of CMPD. Recently, a novel somatic mutation, JAK2V617F, has been reported in most of the polycthemia vera (PV) patients, as well as in a lower percentage in essential thrombocythemia (ET) or idiopathic myelofibrosis (IMF) patients. This finding represents the most important advance in understanding of the molecular mechanisms underlined the pathogenesis of CMPD, contributing to the classification and management of patients.

Prenatal diagnosis of a cervical teratoma with a cytogenetic study.

We describe a cervical teratoma revealed in the prenatal period that was studied cytogenetically. We were recently confronted with the case of a fetal solid neck mass suggestive of a teratoma. After termination of pregnancy the tumor was studied cytogenetically. This is the first case in the recent literature where a clone of cells with an additional chromosome marker has been detected. Cytogenetic study of the fetal blood in addition to cytogenetic study of the tumor after the termination of pregnancy showed the karyotypes 46,XY and 46,XY/47,XY + m, respectively. Fetal cervical teratoma is a rare condition. Genetic investigation in the case should be considered in order to reveal chromosome rearrangements.

Gain of an isochromosome 5p: a rare recurrent abnormality in acute myeloid leukemia.

Chromosomal abnormalities characterize the biological behavior of acute myeloid leukemia (AML), also facilitating the identification of genes responsible for its development and/or progression. Isochromosome 5p, i(5p), represents a rare chromosomal abnormality described, to date, in only a few AML cases. In almost all the cases reported, the i(5p) was accompanied by other abnormalities. Here, a new case of AML, evolved from a myelodysplastic syndrome (MDS) with a clonal trisomy 8, is reported. The case presented the following karyotype: 46, XY[15]/47, XY, +8[4]/47,XY, +1(5) (p10)[3]/ 48,XY,+i(5)(p10)+8[3]. To our knowledge, this is the first reported case of AML to present a clone with an isolated i(5p). The cytogenetic findings supported the hypothesis that i(5p) may represent a primary abnormality, which characterizes a small subset of AML cases.

Cytogenetic findings in untreated patients with essential thrombocythemia.

Essential thrombocythemia (ET) is a chronic myeloid disorder that is characterized by persistent thrombocytosis, thrombohemorrhagic symptoms and a low risk of transformation to leukemia. Chromosomal abnormalities in ET are very rare and most of the patients studied were either in leukemic transformation or they had received treatment with cytotoxic agents. The number of cases studied at the time of diagnosis is very limited. In the present study, 67 cases with ET, at the time of diagnosis, were cytogenetically studied by a G-banding technique. Among them, only four presented chromosomal abnormalities. In two cases, a del(5)(q13q33) was identified, accompanied by trisomy 20 in one case, while, in the other case, monosomy 17 and a small marker chromosome were additionally found. In each of the remaining two abnormal cases, clonal isolated trisomy 13 or monosomy 14 were found, respectively. Since these chromosomal abnormalities were found at the time of diagnosis, they might be related to the neoplastic process. The documentation of more cases of chromosomal abnormalities in ET at the time of diagnosis may facilitate the identification of candidate genes involved in the neoplastic process.

Is aneusomy of chromosome 9 alone a valid biomarker for urinary bladder cancer screening?

BACKGROUND: Detection of genetically-changed tumor cells in the urine is one of the new approaches for the screening of bladder carcinomas. In a previous study, numerical aberrations of chromosome 9 were found in 85.18% of bladder tumors studied by the fluorescence in situ hybridization (FISH) technique. The purpose of the present study was to investigate whether chromosome 9 aneusomy alone is a valid, cost effective, biomarker for bladder cancer screening. MATERIALS AND METHODS: Twenty-seven voided urine specimens obtained from 22 bladder cancer patients, either at initial diagnosis or at the follow-up, were analyzed by the FISH technique with the centromeric probe specific for chromosome 9. RESULTS: In all except 2 out of the 13 specimens with a histological confirmation of cancer, FISH analysis showed aneusomy 9 (sensitivity 84.61%). Among 6 cases with a negative cystoscopy but a positive FISH analysis, 3 recurred within the following 2 months, while 2 no-recurrent patients continued to show positive FISH findings after 6 months. One patient was considered to be false-positive. Four cases with a negative cystoscopy showed disomy 9 and 2 of them recurred. CONCLUSION: Aneusomy 9 has a high sensitivity (84.61%) for the detection of bladder cancer. Patients with a negative cystoscopy but with aneusomy 9 should be kept under close clinical surveillance for potential disease recurrence. However, negative FISH results might not be a negative predictor for disease recurrence. Our results encourage further studies with a large number of patients and a long-term follow-up with concurrent FISH analysis.

Sex chromosome abnormalities in bladder cancer: Y polysomies are linked to PT1-grade III transitional cell carcinoma.

BACKGROUND: Bladder cancer is a heterogeneous group of tumors from both the biological and clinical points of view. Conventional cytogenetics and molecular genetic techniques have shown non-random aberrations in bladder cancer, while certain chromosomal changes have been found to be highly correlated with tumor grade or stage. The aim of this study was to evaluate, by fluorescence in situ hybridization (FISH), the numerical aberrations of chromosomes X and Y in bladder cancer, comparing the incidence of nuclei with aneusomies in different grades or histological stages of the tumors. MATERIALS AND METHODS: The FISH technique, using DNA probes specific for chromosomes X and Y, was applied to 35 male bladder tumor specimens directly processed for cytogenetic study. RESULTS: Polysomies of chromosome X were observed in 25 out of the 35 cases examined (71.43%), while numerical aberrations of chromosome Y were observed in 22 out of the 35 cases (62.86%). Of those cases with numerical aberrations of chromosome Y, 13 had polysomy (37.14%), while in 9 cases, loss of Y was observed (25.71%). Statistical analysis showed that numerical aberrations on chromosomes X or Y were not linked to histological stage, while a probable correlation was observed between aneusomies X or Y and tumor grade. Comparing the results of PT1-grade III tumors with those of PT1-grade II, statistical analysis showed that aneusomies Y and, especially, polysomy Y were correlated with PT1-grade III tumors, p = 0.023 and p = 0.010, respectively. An uncertain correlation between polysomy X and PT1-grade III tumors was found, p = 0.070. CONCLUSION: Our results may suggest that the genetic instability associated with PT1-grade III tumors may account for the considerable potential for aggression of these tumors. However, to draw definite conclusions, a large number of cases must be studied.

Cytogenetic findings in adult greek myelodysplastic syndrome patients: predominance of single trisomy 8.

Myelodysplastic syndrome (MDS) is a clonal disorder of the pluripotent hematopoietic stem cells which is characterized by ineffective and dysplastic hematopoiesis. The pathogenesis of MDS is not well defined and it appears that multiple genetic changes are involved. Several studies have shown that certain chromosomal abnormalities may be influenced by environmental factors, while differences in the incidence of certain aberrations in different areas have also been reported. The aim of this study was to investigate the frequency and the type of chromosomal changes in Greek primary MDS patients. Single chromosomal abnormalities were focused on as possibly being primary changes implicated in the initiation of the neoplastic process. Using conventional cytogenetics, 239 MDS patients were studied and 63 cases were found with an abnormal karyotype (26.36%). Among the cytogenetically abnormal cases, 46 patients presented single chromosomal abnormalities (73.1%). These aberrations were according to frequency +8 (28.57), del(5q), -7/del(7q) and +14 (6.35 each), i(17q) and del(11(q13) (4.76 each), +11, -Y, i(1q), del(8q), del(18p) and t(X;11) (1.59% each). In conclusion, the incidence of chromosomal abnormalities in Greek MDS patients was lower than that reported in the literature. The most common single anomaly was trisomy 8, while a relatively high incidence of an isolated +14 was also observed. Notably, this is the first time an isolated i(1q) has been described in the literature.

Mutational and methylation analysis of the cyclin-dependent kinase 4 inhibitor (p16INK4A) gene in chronic lymphocytic leukemia.

OBJECTIVES: Chronic lymphocytic leukemia (CLL) comprises a heterogeneous group of at least two types of disease entities characterized by distinctive clinical, immunophenotypical and genetic features. The molecular mechanisms underlying the pathogenesis and the histological transformation of CLL are not well known. The INK4A/p16, a cyclin dependent kinase inhibitor has been considered as a tumor suppressor gene. Inactivation of this gene by homozygous deletions, mutations and hypermethylation occurs in a variety of human neoplasms. The aim of the present study was to determine the frequency of p16 gene deletions and mutations as well as the methylation status of the same gene in CLL patients. METHODS: We examined 34 samples from CLL patients by Southern Blotting, Single-Strand Conformation Polymorphism (SSCP), DNA sequencing and Methylation-Specific PCR. RESULTS: Southern Blot analysis revealed non-rearranged bands in 33/34 cases. Homozygous deletions were not observed in any case. In 1/34 case a rearranged band was detected with EcoRI enzyme. The PCR-SSCP analysis of exons 1 and 3 revealed normal pattern of migration in all cases examined. The analysis of exon 2 revealed abnormal migration pattern in 2/34 cases (5.8%). Sequencing of these cases revealed the presence of the ALA148THR polymorphism. Methylation analysis of p16 gene promoter revealed hypermethylation of CpG islands in 6/34 cases (17.6%). CONCLUSION: These results indicate that genetic alterations of p16 gene are rare events in patients with CLL. The clarification of the role of p16 gene promoter methylation in the pathogenesis and evolution of CLL needs further investigation.

Perinuclear antineutrophil cytoplasmic antibody myeloperoxidase-positive vasculitis in association with ulcerative colitis.

We describe a patient with ulcerative colitis (UC) who developed small vessel vasculitis. Perinuclear antineutrophil cytoplasmic antibody myeloperoxidase (p-ANCA-MPO) positivity was detected along with a highly elevated titer of anticardiolipin antibodies. A total proctocolectomy was undertaken and the patient, more than 5 years later, remains in very good condition. The possible causative association between the UC, the p-ANCA-MPO-positive small vessel vasculitis, and the anticardiolipin antibodies is discussed.

Non-random structural chromosomal changes in ovarian cancer: i(5p) a novel recurrent abnormality.

Ovarian cancer represents the leading cause of death among patients with gynecological cancer. The genetic changes underlying the initiation and progression of ovarian cancer have not been well defined. However, non-random structural chromosomal changes have been identified with common chromosomal breakpoints. We have studied cytogenetically 15 cases of ovarian adenocarcinomas by a direct culture of cancer cells and a G-banding technique investigating the presence of recurrent structural aberrations with common chromosomal breakpoints. Among very complex structural rearrangements found, we could recognize recurrent structural aberrations involving according to frequency chromosomal regions 3p13-14, 11p15, 19q13, 3q21, 11q23, 11q10, 1p13, 1p36, and 17q24-25. Isochromosomes i(5p), i(17q), i(8q) and i(11q) were also observed. Isochromosome i(5p), rarely reported in ovarian cancer was found in seven cases suggesting that it may be a novel recurrent abnormality. Translocations t(1;11), t(3;19), t(3;17), t(7;11) and t(11;17) were also identified. Conventional cytogenetics continues to be valuable detecting the presence of non-random chromosomal breakpoints and facilitating the identification of genes implicated in tumorigenesis.