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PubMed1998

Iatrogenic risks of endometrial carcinoma after treatment for breast cancer in a large French case-control study. Fédération Nationale des Centres de Lutte Contre le Cancer (FNCLCC).

Since tamoxifen is widely used in breast cancer treatment and has been proposed for the prevention of breast cancer, its endometrial iatrogenic effects must be carefully examined. We have investigated the association between endometrial cancer and tamoxifen use or other treatments in women treated for breast cancer in a case-control study. Cases of endometrial cancer diagnosed after breast cancer (n = 135) and 467 controls matched for age, year of diagnosis of breast cancer and hospital and survival time with an intact uterus were included. Women who had received tamoxifen were significantly more likely to have endometrial cancer diagnosed than those who had not (crude relative risk = 4.9, p = 0.0001). Univariate and adjusted analyses showed that the risk increased with the length of treatment (p = 0.0001) or the cumulative dose of tamoxifen received (p = 0.0001), irrespective of the daily dose. Women who had undergone pelvic radiotherapy also had a higher risk (crude relative risk = 7.8, p = 0.0001). After adjusting for confounding factors, the risk was higher for tamoxifen users (p = 0.0012), treatment for more than 3 years (all p < 0.03) and pelvic radiotherapy (p = 0.012). Women who had endometrial cancer and had received tamoxifen had more advanced disease and poorer prognosis than those with endometrial cancer who had not received this treatment. Our results suggest a causal role of tamoxifen in endometrial cancer, particularly when used as currently proposed for breast cancer prevention. Pelvic radiotherapy may be an additional iatrogenic factor for women with breast cancer. Endometrial cancers diagnosed in women treated with tamoxifen have poorer prognosis. Women who receive tamoxifen for breast cancer should be offered gynaecological surveillance during and after treatment. A long-term evaluation of the risk-benefit ratio of tamoxifen as a preventive treatment for breast cancer is clearly warranted.

Adenocarcinoma↗

PubMed1998

Familial breast cancer in the family-cancer database.

We use the population-based Family-Cancer Database from Sweden to study familial breast cancer. The size of the population and the nation-wide registration of cancer offer unique possibilities for epidemiological studies of familial cancer, including complete and unbiased identification of cases in the probands and in their relatives, and complete and unbiased identification of the family relationships. Using the Database, we wanted to answer the following questions: (i) proportion of familial breast cancer among all breast cancers; (ii) familial relative risks in breast cancer alone or in combination with another cancer, defined either through the mother or the daughter; (iii) modification of familial risk by age; and (iv) effects of paternal breast cancer alone or in combination with maternal breast cancer. The proportion of familial female breast cancer among all breast cancers before 54 years of age in Sweden was 8.7%. The familial relative risk was about 1.8, but is likely to decrease to about 1.5 in the ageing population. The higher familial relative risks were evident in young women, being 4.0 when both the mothers and their daughters were diagnosed at ages <40 years. Paternal breast cancer, in combination with maternal breast cancer, caused a large (but not statistically significant) risk in the daughters. In mothers and daughters, ovarian but not colon cancer was increased in combination with breast cancer.

Adult↗

PubMed1996

Association between family history of cancer and breast cancer defined by estrogen and progesterone receptor status.

There are recent data to suggest that risk factors for breast cancer may differ according to whether the tumor expresses detectable levels of the estrogen receptor (ER) and progesterone receptor (PR). While a family history of breast cancer is one of the most consistent predictors of the disease, we recently reported a modest inverse association with ER+PR- tumors. However, the definition of a family history of cancer did not consider second-degree relatives or cancer sites that may be etiologically related. The current report presents additional data analysis from the Iowa Women's Health Study, a prospective population-based cohort study conducted among 41,837 postmenopausal women. At baseline in 1986, respondents provided information on family history of cancers of the breast, ovaries, or uterus/endometrium in their mothers, sisters, daughters, maternal and paternal grandmothers, and maternal and paternal aunts. Data on family history of prostate cancer in fathers and brothers and age at onset of breast cancer in mothers and sisters were collected in 1992. Cohort members were followed for cancer incidence through the statewide tumor registry. After 7 years and more than 235,000 person-years of follow-up, 939 incident cases of breast cancer were identified. Information was obtained from the tumor registry on ER (+/-) and PR (+/-) status for 610 cases (65.0%). A family history of breast cancer in first-degree relatives was associated with increased risk (relative risk [PR] = 1.4; 95% confidence interval [CI]: 1.1-1.6) for all receptor-defined subtypes of breast cancer except ER+PR- tumors (RR = 0.7; 95% CI: 0.3-1.4). These results were unchanged when data on second-degree relatives were included. When the onset of breast cancer in relatives occurred at or before the age of 45 years, increased risks were evident only for ER-PR+ and ER-PR- tumors (RR = 2.3 and 3.3, respectively). Conversely, when relatives were affected with breast cancer after the age of 45 years, increased risks were most apparent for ER+PR+ and ER-PR+ tumors (RR = 1.3 and 3.2, respectively). A family history of prostate cancer in first-degree relatives was associated with a 1.2-fold increased risk of breast cancer (95% CI: 0.98-1.50), largely a reflection of the association with ER-PR- tumors (RR = 1.5; 95% CI: 0.8-3.0). The small numbers of cases in some categories and the corresponding wide CIs preclude definitive conclusions, but these data are at least suggestive that joint stratification of breast tumors on ER and PR status may be useful in partitioning breast cancer families into more homogeneous subsets.

Adult↗

PubMed1999

Increased cancer risk among relatives of nonsmoking lung cancer cases.

Lung cancer has been shown to aggregate in families of nonsmoking lung cancer cases with an earlier age at onset. The current study evaluates whether relatives of nonsmoking lung cancer cases are at increased risk of cancers at sites other than lung. Families were identified through 257 population-based, nonsmoking lung cancer cases and 277 population-based, nonsmoking controls residing in metropolitan Detroit. Data were collected for 2,252 relatives of cases and 2,408 relatives of controls. First-degree relatives of nonsmoking lung cancer cases were at 1.52-fold (95% CI, 1.02-2.27) increased risk of cancer of the digestive system after adjustment for each relative's age, race, sex, and smoking status. Relative risk estimates also were elevated, but not significantly, for tobacco-related cancers (RR = 1.39) and breast cancer (RR = 1.72). Among first-degree relatives of younger probands (age 40-59), risk was non-significantly increased 72% (95% CI 0.95-3.10) for all cancers combined and 3.14-fold for cancers of the digestive system (95% CI 0.76-12.9). Nonsmoking relatives of cases were at increased risk of all cancer sites combined (RR = 1.32; 95% CI 1.003-1.73), cancers other than lung (RR = 1.37; 95% CI 1.03-1.82), and digestive system cancers (RR = 2.01; 95% CI 1.20-3.37). These findings of moderate familial aggregation for cancers of the lung, digestive system, breast, and tobacco-related sites suggest that common susceptibility genes may act to increase risk for a variety of cancers in families.

Adult↗

PubMed1993

Localized prostate cancer. Relationship of tumor volume to clinical significance for treatment of prostate cancer.

BACKGROUND: Using the Surveillance, Epidemiology, and End Results Program of the National Cancer Institute and American total mortality rates, the authors calculated the probability at birth of having a diagnosis of prostate cancer within a man's life to be 8.8% and then subtracted the incidence of microscopic Stage A cancers too small to ever be clinically significant. This gave a final probability of 8%. METHODS: Prostates were examined after 139 consecutive unselected cystoprostatectomies from patients with bladder cancers in whom it was unknown whether they had prostate cancer. Prostate cancer was found in 55 patients (40%); the volume of the largest cancer in each specimen was determined using histologic morphometry. The authors identified the 8% of these 139 cytoprostatectomy specimens with the largest volume of prostate cancer. RESULTS: The largest 11 of the 55 cancers represented 7.9% of the total 139 samples. These cancers ranged in volume from 0.5-6.1 ml, representing only 20% of all patients with prostate cancer. CONCLUSIONS: If the strong evidence is accepted that cancer progression is proportional to cancer volume, it was concluded that prostate cancers larger than 0.5 ml appear to correspond to the 8% of men who will be diagnosed with a clinically significant carcinoma, as derived previously. Conversely, those 80% of prostate cancers smaller than 0.5 ml probably are not likely to reach a clinically significant size in view of the long doubling time of this cancer.

Adult↗

PubMed2000

Cancer incidence in Abidjan, Ivory Coast: first results from the cancer registry, 1995-1997.

BACKGROUND: There are few data concerning cancer incidence rates in contemporary West Africa. The first data from the cancer registry of Abidjan, the capital of Ivory Coast, for the period 1995-1997 are reported in the current study. METHODS: The cancer registry attempts to record data on all new cases of cancer diagnosed in the city of Abidjan, including cases without histologic confirmation of diagnosis. RESULTS: Two thousand eight hundred fifteen new cancer cases were registered in 3 years, corresponding to age-standardized (world population) incidence rates of 83.7 per 100,000 in men and 98. 6 per 100,000 in women. As reported elsewhere in West Africa, the principal cancers in men were liver cancer (15%) and prostate cancer (15.8%), with modest rates of non-Hodgkin lymphoma (10.5%) and gastric cancer (4.5%). In women, breast cancer was the most frequent tumor (25.7%), followed by cervical cancer (24.0%) and non-Hodgkin lymphoma (7.3%). In contrast to other registry data from West Africa, Kaposi sarcoma occurs with moderate frequency (7.7% of cases reported in men and 2.1% in women). In the pediatric age group, relatively high incidence rates were found for Burkitt lymphoma. CONCLUSIONS: Although there most likely is some underascertainment of cases, so that the actual incidence rates may be underestimated, the cancer profile should be a fair reflection of the true situation. In addition to tumors that are well known to be common in sub-Saharan Africa, such as cancers of the liver and cervix, this urban population shows some features of "Westernization" of cancer patterns, in particular the relatively high rates of breast cancer and prostate cancer. The effects of the acquired immunodeficiency syndrome epidemic are reflected in the moderate rates of Kaposi sarcoma reported.

Adolescent↗

PubMed2000

Tamoxifen for relapse of ovarian cancer.

BACKGROUND: Tamoxifen is an important drug for treating breast cancer. Ovarian cancer cells are known to possess receptors for hormones and may thus also respond to tamoxifen. OBJECTIVES: Tamoxifen is used to treat breast cancer in women whose tumours have oestrogen receptors. Since ovarian cancers also commonly have oestrogen receptors, it has been suggested that tamoxifen may be of some benefit. The objective of this review was to assess the effects of tamoxifen in women with relapsed ovarian cancer. SEARCH STRATEGY: We searched the Cochrane Gynaecological Cancer Group trials register and references from relevant articles. We also contacted researchers and drug companies. SELECTION CRITERIA: Randomised and non-randomised studies of tamoxifen in women with ovarian cancer who have not responded to conventional chemotherapy. Only trials involving 10 or more patients were included. DATA COLLECTION AND ANALYSIS: One reviewer assessed eligibility and extracted data from non-randomised studies. Two reviewers were to have independently assessed the quality and extracted data from any randomised trials found. MAIN RESULTS: Eleven non-randomised series, one non-randomised phase two study and one randomised trial were included. Only observational data from women treated with tamoxifen are reported. Fifty-nine of 568 women (10.4%) treated with tamoxifen achieved an objective response to treatment. However this varied from 0% to 56% in different studies. Stable disease, for variable periods of four weeks or more, was observed in 109 of 356 (30.6%) women from eight studies. There were not enough data to assess duration of response, survival, or the palliative effect of tamoxifen on symptom control or quality of life. REVIEWER'S CONCLUSIONS: There is some evidence from observational studies that tamoxifen may produce a response in a modest proportion of women with relapsed ovarian cancer. However, there are no reliable data from randomised controlled trials.

Antineoplastic Agents, Hormonal↗

PubMed2006

Annual report to the nation on the status of cancer, 1975-2003, featuring cancer among U.S. Hispanic/Latino populations.

BACKGROUND: The American Cancer Society, Centers for Disease Control and Prevention, National Cancer Institute, and North American Association of Central Cancer Registries collaborate annually to provide U.S. cancer information, this year featuring the first comprehensive compilation of cancer information for U.S. Latinos. METHODS: Cancer incidence was obtained from 90% of the Hispanic/Latino and 82% of the U.S. populations. Cancer deaths were obtained for the entire U.S. population. Cancer screening, risk factor, incidence, and mortality data were compiled for Latino and non-Latino adults and children (incidence only). Long-term (1975-2003) and fixed-interval (1995-2003) trends and comparative analyses by disease stage, urbanicity, and area poverty were evaluated. RESULTS: The long-term trend in overall cancer death rates, declining since the early 1990s, continued through 2003 for all races and both sexes combined. However, female lung cancer incidence rates increased from 1975 to 2003, decelerating since 1991 and breast cancer incidence rates stabilized from 2001 to 2003. Latinos had lower incidence rates in 1999-2003 for most cancers, but higher rates for stomach, liver, cervix, and myeloma (females) than did non-Latino white populations. Latino children have higher incidence of leukemia, retinoblastoma, osteosarcoma, and germ-cell tumors than do non-Latino white children. For several common cancers, Latinos were less likely than non-Latinos to be diagnosed at localized stages. CONCLUSIONS: The lower cancer rates observed in Latino immigrants could be sustained by maintenance of healthy behaviors. Some infection-related cancers in Latinos could be controlled by evidence-based interventions. Affordable, culturally sensitive, linguistically appropriate, and timely access to cancer information, prevention, screening, and treatment are important in Latino outreach and community networks.

Adolescent↗

PubMed2002

Association between BRCA1 and BRCA2 mutations and cancer phenotype in Spanish breast/ovarian cancer families: implications for genetic testing.

Index cases from a clinically relevant cohort of 102 Spanish families with at least 3 cases of breast and/or ovarian cancer (at least 1 case diagnosed before age 50) in the same lineage were screened for germline mutations in the entire coding sequence and intron boundaries of the breast cancer susceptibility genes BRCA1 and BRCA2. Overall, the prevalence of mutations was 43% in female breast/ovarian cancer families, 15% in female breast cancer families and 100% in male breast cancer families. Three recurrent mutations (185delAG, 589delCT and A1708E) explained 63% of BRCA1-related families. Early age at diagnosis of breast cancer, ovarian cancer, bilateral breast cancer, concomitant breast/ovarian cancer in a single patient and prostate cancer but not unilateral breast cancer were associated with BRCA1 and BRCA2 mutations. Male breast cancer was associated with BRCA2 mutations. The presence of male breast cancer was the only cancer phenotype that distinguished BRCA2- from BRCA1-related families. We have developed a logistic regression model for predicting the probability of harbouring a mutation in either BRCA1 or BRCA2 as a function of the cancer phenotype present in the family. The predictive positive and negative values of this model were 77.4% and 79%, respectively (probability cutoff of 30%). The findings of our work may be a useful tool for increasing the cost-effectiveness of genetic testing in familial cancer clinics.

Age of Onset↗

PubMed1986

Cancer incidence in Murcia, Spain, in 1982: first results from a population-based cancer registry.

This report presents the first findings of the Murcia Cancer Registry, a population-based cancer registry set up in May 1981 in the Murcia region of southeast Spain (955,487 inhabitants). Descriptive epidemiological methods have been applied to study cancer incidence in 1982. The validity of cancer registration has been assessed for both completeness and accuracy. Altogether 1,987 cases were registered in 1982, the crude (all-ages) annual incidence rates per 100,000 being 238 in males and 179 in females. Excluding nonmelanoma skin cancer, which seems to be incompletely registered, age-standardized rates for Murcia are very similar to those of other registries in Spain in males, but lower in females. The risk was higher in males than in females for all sites and for the great majority of specific sites, especially larynx, oesophagus and bladder. The age-standardized rate for cancer of the larynx was 26 times higher in men than in women. Lung cancer was the most common cancer in males: the risk was 8 times that in females. Lung cancer rates were higher, in both males and females, than in other Spanish registries. Cancer of the larynx was the second most common site in males when either truncated rates (35-64 years) or cumulative incidence rates up to 64 years of age were used. The age-standardized rate (18 per 100,000) supports previous studies suggesting that the risk for this cancer in Spain and other Mediterranean countries is very high. The lung/larynx rate ratio in men was two. Cancer of the breast is the most common cancer among women, as in other registries in Spain and in most other countries. The age-standardized rate (29.4 per 100,000) is lower than breast cancer rates elsewhere in Spain. This difference may be partly explained by incompleteness of ascertainment in Murcia. The incidence rate for cancer of the cervix uteri was 4.9 per 100,000, excluding carcinoma in situ. Despite the limitations of the data, cervical cancer incidence in Murcia is likely to be similar to that in other regions of Spain.

Adolescent↗

PubMed2001

Epidemiologic differences between women with colorectal cancer and women with ovarian cancer.

BACKGROUND AND OBJECTIVES: The difference between the epidemiologic features of women with colorectal cancer and those with ovarian cancer has not been thoroughly studied. The aim of this study is to review the epidemiologic features of women with colorectal cancer and compare them with those of women with ovarian cancer. METHODS: The epidemiologic features of 705 women with colorectal cancer were compared with those of 503 women with primary epithelial ovarian cancer. Both groups included all women with the confirmed respective histologic diagnoses admitted to Roswell Park Cancer Institute between 1982 and 1996 who returned a voluntary self-administered epidemiologic questionnaire. RESULTS: Women with ovarian cancer were significantly younger, had higher education and income, had fewer children, and were more likely to have never been married and nulligravid than those with colorectal cancer. There was a significant difference in the contraceptive history between both groups among women > or = 45 years of age. More women with ovarian cancer had a family history of ovarian cancer and more women with colorectal cancer had a family history of colorectal cancer. CONCLUSIONS: The epidemiologic features of women with colorectal cancer are different from those with ovarian cancer. The difference between both groups might indicate difference in the environmental or genetic etiology of both cancers.

Colorectal Neoplasms↗

PubMed1998

Colorectal and extracolonic cancer variations in MLH1/MSH2 hereditary nonpolyposis colorectal cancer kindreds and the general population.

PURPOSE: This clinical case review aimed to identify phenotypic variations in colorectal and extracolonic cancer expression between hereditary nonpolyposis colorectal cancer (HNPCC) families with MLH1 and MSH2 germline mutations and the general population. METHODS: Colorectal cancer onset and site distribution were compared among 67 members of MLH1 kindreds, 45 members of MSH2 kindreds, and 1,189 patients from the general population. Synchronous and metachronous cancer rates, tumor stage, extracolonic cancer incidence, and survival were also compared. RESULTS: Mean ages of colorectal cancer onset were 44, 46, and 69 years for MLH1, MSH2, and the general population, respectively (P < 0.001). More proximal and fewer distal colon cancers were noted in HNPCC than the general population (P < 0.001, P = 0.04). Site distribution showed disparity of rectal cancers (8 percent MLH1 vs. 28 percent MSH2; P = 0.01) based on genotypes. Overall, synchronous colorectal cancer rates were 7.4, 6.7, and 2.4 percent for MLH1, MSH2, and the general population, respectively (P = 0.016). Annual metachronous colorectal cancer rates were 2.1, 1.7, and 0.33 percent for MLH1, MSH2, and the general population, respectively (P = 0.041). Colorectal cancer stage presentation was lower in HNPCC than the general population (P = 0.0028). Extracolonic cancers were noted in 33 percent of MSH2 patients, compared with 12 percent of MLH1 patients and 7.3 percent of the general population with colorectal cancers (P < 0.001). Combined MLH1 and MSH2 ten-year survival was 68.7 percent compared with 47.8 percent for the general population (P = 0.009 stage stratified, hazard ratio 0.57). CONCLUSION: The presence of rectal cancer should not preclude the diagnosis of HNPCC, because the incidence of rectal cancer in MSH2 was comparable with that in the general population. Phenotypic variations, including the preponderance of extracolonic cancers in MSH2 patients, did not result in survival differences between genotypic subgroups. These phenotypic features of HNPCC genotypes may have clinical significance in the design of specific screening, surveillance, and follow-up for affected individuals.

Adaptor Proteins, Signal Transducing↗

PubMed1987

The Melbourne Colorectal Cancer Study. Characterization of patients with a family history of colorectal cancer.

The characteristics of 702 colorectal cancer patients are described in relation to the presence of absence of a family history of colorectal cancer in near relatives. No statistically significant associations were found between those with a family history of colorectal cancer and age at detection, sex, country of birth, religion, number of cancers (single, synchronous, or metachronous), previously removed benign colorectal polyps, and adenomatous polyps found in the resection specimen. The family history rate of colorectal cancer for colon cancer cases was statistically significantly higher than for rectal cancer cases (chi 2(1) = 3.8, P = .05) and there was a gradient of decreasing risk from colon to rectum. The family history rate of colorectal cancer in parents of those who were less than 50 years old was twice that of those 50 or older (P = .07), consistent with the view that earlier age of onset is a characteristic of those with a family history of colorectal cancer. There was a statistically significantly higher family history rate of colorectal cancer in respondents who knew of the disease compared with those who did not (chi 2(1) = 5.5, P less than .05). It is unclear if this effect represents recall bias or self-selection bias. In contrast, the rates for a family history of heart disease and stroke were similar, irrespective of the respondent's knowledge of their colorectal cancer status. Thus in the Melbourne study, the family history rate of colorectal cancer was higher in colon cancer than in rectal cancer, there was a decreasing gradient of risk from colon to rectum, and a tendency for earlier age of onset of colorectal cancer in those with a history of this cancer in a parent.

Age Factors↗

PubMed2004

Novel germline mutations in breast cancer susceptibility genes BRCA1, BRCA2 and p53 gene in breast cancer patients from India.

Mutations in breast cancer susceptibility genes, BRCA1 and BRCA2 account for more than 80% of hereditary breast and ovarian cancers. p53 tumor suppressor gene that controls cellular growth and differentiation is also known to be mutated in more than 50% of human cancers including breast cancer. We have carried out a study on BRCA1 and BRCA2 along with p53 gene mutations in both sporadic as well as familial breast cancer patients from India where breast cancer is fast emerging as a major cancer among premenopausal urban women. We examined 124 untreated primary breast cancer patients comprising 100 sporadic and 24 familial cases including 56 age-matched healthy controls for the presence of BRCA1, BRCA2 and the p53 gene mutations using PCR-SSCP and direct nucleotide sequencing. Certain frequently mutated exons such as 2, 5, 11, 13 and 20 of BRCA1, exons 2, 9, 11 (for 6174delT), 18 and 20 of BRCA2 and 4-9 exons of p53 gene were analyzed in sporadic breast cancer while all 22 coding exons of BRCA1 including its flanking intronic regions along with above mentioned exons of BRCA2 and p53 gene were analyzed in familial breast cancer patients. We identified six patients (25%) with BRCA1 mutation of which three were found to be of novel type one in exon 16 (4956insG) and two in exon 7 (Lys110Thr) (Ser114Pro) out of 24 familial breast cancer patients studied from two different geographic regions/populations of India. Two sisters from a single family (12.5%) out of eight families from Goa with Portuguese colonial origin showed presence of founder Ashkenazi Jewish BRCA1 mutation (185delAG) along with (IVS7 561-34T>C; IVS18 5271 + 66G > A). While from New Delhi, four (25%) of 16 breast cancer families showed BRCA1 mutations; a frame shift protein truncating (4956insG), a transition nonsense (Gln1395Stop) and two amino acid substitutions (Lys110Thr) and (Ser114Pro). Only one (4%) p53 mutation (Val97Ile) in its exon 4 along with BRCA1 mutation (4956insG) could be detected. No major sequence variation in BRCA2 gene was observed except for G203A at 5' UTR of exon 2, a common population polymorphism in two Goan patients who also showed silent nucleotide change for amino acid serine at codon 1436 of BRCA1 gene. None of the 100 sporadic breast cancer patients revealed any protein truncating or deleterious BRCA1 or BRCA2 gene mutation. Interestingly, three (3%) p53 mutations in its exon 5 were detected in sporadic breast cancer patients. Although three novel BRCA1 mutations including a founder Ashkenazi Jewish BRCA1 mutation were recorded in Indian women with familial breast cancer, the overall prevalence of BRCA gene mutations in Indian women with a family history of breast cancer appears to be low.

Adult↗

PubMed1995

Loss of heterozygosity on chromosome 17q11-21 in cancers of women who have both breast and ovarian cancer.

OBJECTIVE: Our purpose was to determine the frequency of allele loss in the region of the BRCA1 gene in cancers of women who have both breast and ovarian cancer. STUDY DESIGN: Four polymorphic microsatellite markers on chromosome 17q11-21 were examined by the polymerase chain reaction in deoxyribonucleic acid from paraffin blocks of normal tissues, breast cancers, and ovarian cancers in 24 women who had primary cancers in both sites. RESULTS: Loss of heterozygosity was seen in one or more markers on chromosome 17q11-21 in 46% of breast cancers and 78% of ovarian cancers. In 38% of cases allele loss was seen in both cancers, and in all these cases the same allele was lost in both cancers. Significantly younger ages at diagnosis of both breast and ovarian cancer were noted among cases with allele loss in both cancers compared with cases in which allele loss was found only in the ovarian cancer (p < 0.05). CONCLUSIONS: Because cases in which 17q11-21 allele loss was seen in both cancers had a young age of onset and the same allele was always deleted in both cancers, hereditary alterations in BRCA1 may play a role in this subset. The older age of onset in cases in which allele loss was seen only in the ovarian cancer suggests that the development of these cancers is not related to an inherited defect in BRCA1.

Alleles↗

PubMed2006

Cancer incidence in first-degree relatives of a population-based set of cases of early-onset breast cancer.

Reliable determination of familial risks for cancer is important for clinical counselling, cancer prevention and understanding cancer aetiology. Family-based gene identification efforts may be targeted if the risks are well characterised and the mode of inheritance is identified. Early-onset breast cancer in a family member is a risk indicator for cancer among first-degree relatives; however, the familial risk pattern has not been assessed fully in population-based incidence studies. We estimated the risks for cancers of the breast, ovary and other sites among the first-degree relatives of 8868 patients in whom breast cancer was diagnosed before they reached the age of 50 years (diagnosed during the period 1943-1999). Population registers and parish records were used to identify 31,235 first-degree relatives, who were followed up to 31 December 2002 for occurrence of cancer by linkage to the Danish Cancer Registry. The observed incidence rates were compared with national rates adjusted for age, sex and calendar period. Overall, 39% of the 674 cases of breast cancer and 43% of the 143 cases of ovarian cancer among relatives were associated with a diagnosis of early-onset breast cancer in a family member. Among relatives under 50 years of age, the proportions were 56% and 58%, respectively, and among relatives 50 years or above the proportions were approximately 30% and 10%. In addition, a slightly but significantly increased risk for cancer of the cervix uteri was observed among relatives, and among those under 50 years of age, we found significantly increased risks for cancers of the colon and gall-bladder. In conclusion, the excess risk for breast cancer in first-degree relatives is large and remains sizable in the subgroup of female relatives aged 50 years or older, and that mutations in BRCA1/2 seem to explain only half of breast cancer cases attributable to family history.

Adolescent↗

PubMed2005

Incidentally detected prostate cancer in cystoprostatectomies: pathological and morphometric comparison with clinically detected cancer in totally embedded specimens.

There are limited data regarding the pathological features of incidentally detected prostate cancer. Examination of cystoprostatectomy specimens obtained during bladder cancer treatment affords a unique opportunity to examine incidentally detected prostate cancer and determine its relationship with clinically detected prostate cancer obtained during radical prostatectomy. We compared the pathological findings of incidentally detected prostate cancer in 132 consecutive cystoprostatectomy specimens from patients treated for bladder cancer with a consecutive series of 228 radical prostatectomy specimens from patients treated for prostate cancer. All specimens were totally embedded and whole-mounted. Karyometry was evaluated in select subsets of patients from the study groups. Incidentally detected cancer was found in 42% of cystoprostatectomy specimens, and the cancers were of lower Gleason score and lower pathological stage with fewer positive surgical margins than in clinically detected cancers in age-matched radical prostatectomies. High-grade prostatic intraepithelial neoplasia (PIN) was present in 82% of radical prostatectomy specimens, in 70% of cystoprostatectomies with incidentally detected prostate cancer, and in 54% of cystoprostatectomies without prostate cancer. Mean nuclear and nucleolar area was lower in incidentally detected cancer and PIN when compared with clinically detected cancer and PIN, respectively, similar to the results with proliferative indices. We conclude that incidentally detected cancer is less aggressive than clinically detected cancer.

Humans↗

PubMed2006

Radiation-associated endometrial cancers are prognostically unfavorable tumors: a clinicopathologic comparison with 527 sporadic endometrial cancers.

INTRODUCTION: Previous reports have suggested that patients who have undergone pelvic radiation for cervical cancer are at risk for developing poorly differentiated endometrial cancers with poor prognoses. MATERIALS AND METHODS: We conducted a retrospective chart and histologic review of patients from Memorial Sloan-Kettering Cancer Center and MD Anderson Cancer Center diagnosed with endometrial cancer after radiation therapy (RT) for cervical cancer from 1976 to 2000. The comparison group comprised MSKCC endometrial cancer patients whose tumors were not radiation associated ("sporadic cancers"). RESULTS: We identified 23 patients who developed endometrial carcinoma or carcinomasarcoma after RT for cervical carcinoma and 527 sporadic endometrial cancer patients. When radiation-associated endometrial cancers (RAECs) were compared with sporadic cancers, significant differences were noted with regard to stage, grade and histologic subtype distribution. In the RAEC group, there were 16 (70%) stages III and IV cancers compared with 101 (19%) in the sporadic group (P<0.001). There were 20 (87%) grade 3 cancers in the RAEC group versus 161 (31%) in the sporadic group (P<0.001). There were 16 (70%) high-risk histologic subtypes (serous, clear cell, carcinosarcoma, undifferentiated) in the RAEC group versus 79 (15%) in the sporadic group (P<0.001). Median survival in the RAEC group was 24 months versus not reached in the sporadic group (P<0.001). Radiation remained a significant factor for poor prognosis in a stratified analysis, in which we compared sporadic and RAEC cancers controlled for age, histology, grade and stage. However, radiation lost significance in a multivariate analysis, in which stage- and grade-matched cancers from both groups were compared. DISCUSSION: The clinicopathologic characteristics of RAECs, which include a preponderance of high-stage, high-grade and high-risk histologic subtypes, indicate that these tumors differ from sporadic endometrial carcinomas. However, patients with RAECs do not appear to have a significantly worse prognosis when compared with patients with high-stage and high-grade sporadic cancers.

Adenocarcinoma, Clear Cell↗