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Query: UMLS:C1140680 (ovarian cancer)
 28,141 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Eight families with two or more first-degree relatives affected with ovarian carcinoma were identified among a series of 138 consecutive ovarian cancer patients. History of breast cancer was reported in six of the eight families. Five of 19 patients with familial cancer developed ovarian cancer as a second primary tumor following breast carcinoma, whereas only 6/130 sporadic cases had a previous history of breast cancer. No significant difference was detected in clinical and pathological features between sporadic and familial cases. However, in three high-risk families ovarian cancer tended to develop at a younger age compared with other familial cases and with sporadic occurrences, and nulliparity was less frequent in the familial group. These observations emphasize the need to take into account multiple factors-in addition to positive family history-for the evaluation of genetic predisposition to ovarian carcinoma.
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PMID:Analysis of 138 consecutive ovarian cancer patients: incidence and characteristics of familial cases. 225 75

Genealogies for the Mexican-American city of Laredo, Texas, have been assembled by computer from individual civil and church records of birth, marriage, and death. Documentation is available on vital events in the lives of over 300,000 individuals, about 80% of the city population from 1870-1981. These data were collected to determine the degree to which death from cancer is more clustered in families than would be expected by chance alone; methods specific to this data base have been developed to accomplish this task. A statistically significant excess of familial cancer was observed overall when all cancer sites were pooled, but no evidence was observed for excess familial risk at single sites except for breast cancer and perhaps for ovarian cancer. The excess of breast cancer risk is comparable to that observed in other populations. A few site-combinations manifest excess familial risk, most notably those involving and dominated by breast cancer and certain digestive system sites. We do not confirm the degree of familiarity observed elsewhere for cancers of the lung, colorectum, stomach, or other sites in this generally low-risk population. Even where we find evidence of excess risk, the degree of excess is small and the number of multiply affected families too small to test etiologic models by segregation analysis. The absence of excess familial risk does not appear to be due to inadequate numbers of cases, since breast cancer is familial with no more occurrences in Laredo than other sites. These results differ to some extent from those found in a similar study of Utah Mormons, but it is unclear whether this is because of differences in risk patterns or statistical properties of the analytic methods used in the two studies.
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PMID:Familial aggregation of cancer in Laredo, Texas: a generally low-risk Mexican-American population. 371 Jan 37

In 118 patients with common epithelial ovarian tumors (carcinomas and tumors of borderline malignancy) treated at Tsukuba University Hospital and Tsukuba-Gakuen Hospital, family histories of ovarian and breast cancer were obtained from medical records or in interviews, and familial aggregation of these cancers was examined. 1. A positive family history was found in 10 patients (8.5%). The high incidences of familial ovarian cancer and ovarian cancer in patients who were previously affected with breast cancer were statistically significant. 2. Patients with serous adenocarcinoma showed a significantly greater rate of positive family history than those with mucinous adenocarcinoma. 3. No significant correlation was seen between the clinical stage and a positive family history. 4. Every patient except one with a positive family history had onset of ovarian cancer after menopause. The age at onset for familial ovarian cancer cases was younger than that for the patients' relatives who were affected previously. 5. There were 14 healthy women considered to be at high risk for ovarian cancer among 5 familial ovarian and 2 familial ovarian and breast cancer aggregations. These preliminary findings suggest that screening for early ovarian cancer should be conducted in high risk relatives of familial cancer patients and women affected with breast cancer previously. More detailed studies are needed to define the occurrence of familial or hereditary ovarian and breast cancers in Japan.
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PMID:[Analysis of familial aggregation of ovarian and breast cancer in patients with ovarian cancer]. 759 99

Prophylactic oophorectomy is presently the only effective method of ovarian cancer prevention. This study reviews current data on how prophylactic oophorectomy (PO) should be used in different risk groups. It is estimated that 7% of ovarian cancer patients have positive family history, of which 3-9% may end up having hereditary cancer syndromes. Women in direct genetic lineage of family cancer syndromes may have up to 50% lifetime risk of ovarian cancer. Because of such a high risk, PO is indicated for women with familial cancer syndromes after childbearing or the age of 35-40 at the latest. Most women with positive family history of ovarian cancer do not have one of the recognized hereditary cancer syndromes. However, women with one or two affected relatives do have an increased lifetime risk of ovarian cancer from a baseline of 1.6 to 5-7%. This risk is not high enough to warrant PO recommendation for a large number of women. After being properly informed and the patient still desires surgical prevention (i.e., cancer phobia), PO then becomes an indicated procedure. In women without family history of ovarian cancer, the role of PO remains controversial. The decision of PO as a concurrent procedure to other indicated gynecologic surgeries should depend on the individual patient and her ability to comply with lifelong estrogen replacement therapy.
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PMID:The role of prophylactic oophorectomy in cancer prevention. 783 8

Familial cancer clusters provide a unique opportunity to elucidate the molecular mechanisms central to the development of malignancy. We have identified four families in which 11 members developed epithelial ovarian cancer. The clinical course of disease in these individuals with familial ovarian cancer appears to be very different from that of patients with nonfamilial ovarian cancer. In order to compare these disease states, 34 cases matched for age at diagnosis (57 years), tumor histology (all adenocarcinomas), and a preponderance of advanced grade and FIGO stage of disease were selected. Patients with familial ovarian cancer exhibited a 67% 5-year survival in comparison with a 17% 5-year survival in the nonfamilial ovarian cancer cases. Preliminary studies indicate a lack of overexpression of the HER-2/neu oncogene in the familial cancer members' tumors. This may correlate with the indolent character of their disease. Abnormal p53 tumor suppressor gene expression was noted in four of six cancers tested. We also found germ line p53 mutations in three of the four families, but neither the germ line or tumor p53 prevalence was 100%. This is the first report of germ line p53 mutations associated with familial ovarian cancer and indicates that this gene may play a role in the development of some familial ovarian cancers.
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PMID:Familial ovarian cancer. 790 48

Women with a family history of ovarian cancer are at increased risk of ovarian cancer. Prophylactic oophorectomy (PO) remains the only effective method of ovarian cancer prevention. This study reviewed current data on the significance of family history and how prophylactic oophorectomy should be used in different risk groups. Approximately 7% of ovarian cancer patients have a positive family history of whom 3-9% may eventually manifest certain hereditary cancer syndromes. Women in direct genetic lineage of family cancer syndromes have up to a 50% lifetime risk of ovarian cancer. Because of the high risk, PO is indicated for women with familial cancer syndromes after childbearing or between the ages of 35-40 at the latest. The majority of women with a positive family history of ovarian cancer do not have one of the recognized syndromes. Women with one or two affected relatives have an increased lifetime risk of ovarian cancer from a baseline of 1.6 to 5-7%. This risk is not high enough to warrant PO for a large number of women. After being properly informed, the patient still chooses surgical prevention, she then receives PO. For women without a family history of ovarian cancer, the role of PO remains controversial. Assuming an annual incidence of 22,000 new cases of ovarian cancer, it is estimated that at least 1000 may be prevented if PO is diligently practiced during hysterectomy. Despite ovarian and breast cancer prevention, PO would lead to shorter life expectancy if estrogen therapy compliance were less than perfect. Thus, the decision on PO as a concurrent procedure should depend on the individual patient and her ability to comply with lifelong estrogen therapy.
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PMID:Ovarian carcinoma. A review of the significance of familial risk factors and the role of prophylactic oophorectomy in cancer prevention. 803 32

The isolation of genes that predispose to familial disease is an important goal in cancer research. The identification of such genes "opens up" the possibility of genetic diagnosis in families so that individuals who are at risk of cancer through inheriting a predisposing mutation can be identified. Genes that are involved in familial cancer syndromes may also be important in the pathogenesis of sporadic forms of the disease, which are often more common. In the search for genes that predispose to familial breast and ovarian cancer much recent progress has been made. A locus on the long arm of chromosome 17, in the interval 17q12-21, has been identified by genetic linkage, and appears to be responsible for disease in approximately 40% of breast cancer families and most families that contain breast and ovarian cancer. The region containing this locus, which has been called BRCA1, has been narrowed to a 3-4 cM interval defined by THRA1, the thyroid hormone receptor locus alpha, and D17S183, an anonymous microsatellite polymorphism. Loci other than BRCA1 that have been identified appear not only to predispose to breast and/or ovarian tumors, but to tumors at other sites too. A new locus has been identified on chromosome 2 which is linked to hereditary non-polyposis colorectal cancer (HNPCC). Families with HNPCC are also at risk of endometrial cancer and tumors of the ovary, amongst other cancer sites. Finally, mutations in the p53 gene are inherited in families with Li-Fraumeni syndrome, a rare cancer syndrome predisposing to breast tumors, sarcomas, leukemia and other cancers. Li-Fraumeni syndrome is also the only inherited cancer syndrome that predisposes at least in part to breast cancer where the actual predisposing gene is known. For the other cancer syndromes, the cloning of the predisposing genes is eagerly awaited.
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PMID:Predisposing genes in breast and ovarian cancer: an overview. 811 68

A predisposing gene (BRCA-1) for breast and ovarian cancer has been located on chromosomal region 17q12-21. According to Knudson's hypothesis if this gene is a tumor suppressor gene, allelic losses would be found in tumors occurring in families with cancer aggregations. We studied 25 samples of both benign lesions and malignant tumors, from breast cancer site-specific families and other familial cancer aggregations. Allelic losses seem to be more frequent in tumors from breast site-specific families but also include the predisposing locus in other syndromes, suggesting a role of BRCA-1 in such families. Finding of allele losses near this locus in benign lesions suggests that such alterations may represent a first step in breast carcinogenesis. It is noteworthy that allele losses involve larger chromosome fragments in malignant tumors than in benign lesions where BRCA-1 is not lost, suggesting a similar mechanism for genomic deletion in the tumorigenesis of the colon and of the breast.
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PMID:Detection of allelic losses on 17q12-q21 chromosomal region in benign lesions and malignant tumors occurring in a familial context. 829 Feb 55

Germline mutations within evolutionary conserved exons of the p53 gene predispose to tumor development in several familial cancer syndromes. We now report identification of a novel p53 mutation affecting the splice acceptor site of exon 6 in the germline DNA of a family with hereditary breast-ovarian cancer. This splice-site mutation, which results in omission of exon 6 and creates a frame-shift and premature stop codon in transcripts from the mutant allele, was found in seven family members--four of whom have developed breast, ovarian or choroid plexus tumors before age 35. Our finding suggests the need to examine the entire p53 gene for splice-site, frame-shift, and nonsense (as well as missense) mutations in families with early-onset hereditary breast and breast-ovarian cancers not linked to the BRCA1 gene on chromosome 17q. We propose that the term 'p53 familial cancer syndrome' be applied to clusters of tumors in families with documented germline p53 mutations, regardless of the histopathologic findings or pattern of tumor development.
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PMID:Splice-site mutation of the p53 gene in a family with hereditary breast-ovarian cancer. 830 8

Greggi and Kerlikowske have worked out that a woman has a 1.4% chance of developing ovarian cancer during her life. When cancer of the ovary is found, 5 to 10% of these cases have a familial form of this pathology. Thus there are some hereditary forms of cancer of the ovary and Lynch has demonstrated that there are three types of hereditary associations with ovarian neoplastic pathology: specific familial cancer of the ovary, cancer of the ovary associated with endometrial cancer and with non-polypoidal cancer of the caecum and rectum, cancer of the ovary associated with cancer of the breast. The clinical material we are presenting here is of the first type of association and we are reporting the study of a family in which 6 members in two generations had cancer of the ovary and of whom one had cancer of the breast as well. Familial cancer of the ovary shows different characteristics coming on as it does earlier (ten years earlier) and with a shorter length of survival (1.8 as against 5 years). The risk of the next generation having ovarian neoplastic pathology is clear because there is a 50% chance in a patient who has a history of cancer of the ovary in at least two first degree relatives. For most daughters when this type of familial cancer is found it is justifiable to carry out prophylactic oophorectomy from the age of 35 year onwards. Particular supervision should be carried out for patients who are members of a family where 2 index cases have been found within 20-35 years.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Familial cancer of the ovary. A family with 6 index cases]. 830 1


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