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PubMed1996

Risk of cancer in relatives of testicular cancer patients.

The incidence of cancer at sites other than the testis has been investigated in the families of 797 Norwegian and 178 Swedish patients diagnosed with testicular cancer during 1981-91. In the families of the Norwegian patients, the total number of cancers in the relatives was significantly lower than the expected number derived from national incidence rates [observed number of cancers 250, expected number of cancers 281.92, standardised incidence ratio (SIR) 0.89, 95% confidence interval (CI) 0.78-1.00]. This finding can be accounted for almost entirely by the finding of fewer than expected prostate and gastrointestinal cancers in the parents of cases. The other common cancers were found at slightly lower than or near the expected levels in the relatives. In the Swedish cohort, which accounts for less than 20% of cases, the observed number of cancers was very close to the expected number. Fourteen fathers of cases had prostate cancer compared with 27.57 prostate cancers expected, giving a SIR of 0.51 (P=0.006). Mothers had more lung cancers (ten cases observed, SIR=2.11, P=0.04) and cancers of the endometrium than expected (13 cases observed, SIR=1.73, P=0.09). These findings may be interpreted as support for theories proposing hormonal dysfunction as causing testicular cancer. Fifty-four gastrointestinal cancers were observed in the parents compared with 68.48 expected (SIR=0.78, P=0.082). Furthermore, testicular cancer was not found to be associated with the known dominantly inherited cancer syndromes [Familial breast (-ovarian) cancer, hereditary no-polyposis colon cancer]. However, one patient belonged to a Li-Fraumeni family, raising the possibility that testicular cancer may be an infrequent component of this rare cancer syndrome. This study supports the hypothesis that families of testicular cancer patients are not prone to cancer.

Cohort Studies↗

PubMed1997

Early gastric cancer mimicking advanced gastric cancer.

The clinicopathological features of 37 early gastric cancers mimicking advanced gastric cancer were reviewed retrospectively, and were compared with 596 other early gastric cancers and 126 mp gastric cancers, defined as gastric cancer invading the muscularis propria of the stomach. A greater tumour size (P < 0.005), submucosal invasion (P < 0.005), lymph node and lymph vessel invasion (P < 0.005) and vascular invasion (P < 0.025) were found more frequently in early gastric cancers mimicking advanced gastric cancers than in other early gastric cancers. There were no significant differences in the clinicopathological findings between early gastric cancers mimicking advanced gastric cancers and mp gastric cancers. Patients with early gastric cancers mimicking advanced gastric cancers showed a lower survival rate than patients with other early gastric cancers, but a higher survival than those with mp gastric cancers. The macroscopic appearance of an advanced gastric cancer was an indicator of massive submucosal invasion and lymph node metastasis in early gastric cancer. As early gastric cancers mimicking advanced gastric cancers showed similar clinicopathological findings to mp gastric cancers, these cancers should be treated as mp gastric cancers.

Female↗

PubMed1994

Familial clustering of breast and prostate cancers and risk of postmenopausal breast cancer.

BACKGROUND: Previous studies have suggested that cancers of the breast and prostate cluster in families and that the presence of both diseases in a family may be associated with increased risk of breast cancer. PURPOSE: Our purpose was to evaluate whether 1) prostate cancer aggregates in families with postmenopausal breast cancer, 2) families with cancers of the breast and prostate are the same ones as families with cancers of the breast and ovary, and 3) a family history of prostate cancer is associated with increased risk of postmenopausal breast cancer. METHODS: We analyzed data from a large prospective cohort study of Iowa women that were (at baseline) aged 55-69 years in 1986. At the third follow-up survey in 1992, self-reported data on family history of breast, ovarian, and prostate cancers in parents and siblings were provided by 30,883 women. Additional information was collected to ascertain whether the age-of-onset of breast cancer in mothers or sisters was before or after the age of 45 years. Cancer occurrence was documented using the State Health Registry of Iowa. RESULTS: History of prostate cancer in their father or a brother was reported by 3384 (11.0%) of the women, and a total of 4090 women (13.2%) reported breast cancer in their mother or a sister. A positive family history of both cancers was reported by 556 women, significantly (two-sided P < .001) greater than the 457 women expected if the family histories were independent. The aggregation of breast, prostate, and ovarian cancers was reported by 22 participants, greater than the 2.7 expected (two-sided P < .0001). During 6 years of follow-up, 578 breast cancers were identified in the cohort at risk. Compared with women without a family history of either cancer, women with a family history of breast cancer had a relative risk (RR) of 1.37 (95% confidence interval [CI] = 1.06-1.79) if the affected relative had onset after the age of 45 years, and an RR of 1.71 (95% CI = 1.13-2.61) if the affected relative had onset at or before the age of 45. A family history of prostate cancer in the absence of a family history of breast cancer was associated with an RR of 1.19 (95% CI = .90-1.56). However, a family history of both breast and prostate cancers was associated with RRs of 2.06 (95% CI = 1.23-3.45) and 2.35 (95% CI = .97-5.67) for breast cancer onset in relatives of greater than 45 and less than or equal to 45 years, respectively. CONCLUSIONS: These observations are concordant with recent reports that suggest a shared familial risk (inherited or environmental) for these hormone-dependent malignancies.

Aged↗

PubMed1995

Radon and cancers other than lung cancer in underground miners: a collaborative analysis of 11 studies.

BACKGROUND: Exposure to the radioactive gas radon and its progeny (222Rn and its radioactive decay products) has recently been linked to a variety of cancers other than lung cancer in geographic correlation studies of domestic radon exposure and in individual cohorts of occupationally exposed miners. PURPOSE: This study was designed to characterize further the risks for cancers other than lung cancer (i.e., non-lung cancers) from atmospheric radon. METHODS: Mortality from non-lung cancer was examined in a collaborative analysis of data from 11 cohorts of underground miners in which radon-related excesses of lung cancer had been established. The study included 64,209 men who were employed in the mines for 6.4 years on average, received average cumulative exposures of 155 working-level months (WLM), and were followed for 16.9 years on average. RESULTS: For all non-lung cancers combined, mortality was close to that expected from mortality rates in the areas surrounding the mines (ratio of observed to expected deaths [O/E] = 1.01; 95% confidence interval [CI] = 0.95-1.07, based on 1179 deaths), and mortality did not increase with increasing cumulative exposure. Among 28 individual cancer categories, statistically significant increases in mortality for cancers of the stomach (O/E = 1.33; 95% CI = 1.16-1.52) and liver (O/E = 1.73; 95% CI = 1.29-2.28) and statistically significant decreases for cancers of the tongue and mouth (O/E = 0.52; 95% CI = 0.26-0.93), pharynx (O/E = 0.35; 95% CI = 0.16-0.66), and colon (O/E = 0.77; 95% CI = 0.63-0.95) were observed. For leukemia, mortality was increased in the period less than 10 years since starting work (O/E = 1.93; 95% CI = 1.19-2.95) but not subsequently. For none of these diseases was mortality significantly related to cumulative exposure. Among the remaining individual categories of non-lung cancer, mortality was related to cumulative exposure only for cancer of the pancreas (excess relative risk per WLM = 0.07%; 95% CI = 0.01-0.12) and, in the period less than 10 years since the start of employment, for other and unspecified cancers (excess relative risk per WLM = 0.22%; 95% CI = 0.08-0.37). CONCLUSIONS: The increases in mortality from stomach and liver cancers and leukemia are unlikely to have been caused by radon, since they are unrelated to cumulative exposure. The association between cumulative exposure and pancreatic cancer seems likely to be a chance finding, while the association between cumulative exposure and other and unspecified cancers was caused by deaths certified as due to carcinomatosis (widespread disseminated cancer throughout the body) that were likely to have been due to lung cancers. This study, therefore, provides considerable evidence that high concentrations of radon in air do not cause a material risk of mortality from cancers other than lung cancer. IMPLICATIONS: Protection standards for radon should continue to be based on consideration of the lung cancer risk alone.

Adult↗

PubMed2001

Second primary cancers following breast cancer in the Japanese female population.

To assess the risk of developing second primary cancers following breast cancer in Japanese females, we performed a retrospective cohort study of 2786 patients who were newly diagnosed with breast cancer at our hospital between 1970 - 1994, until the end of 1995 (average follow-up period, 8.6 years). The expected number of each second primary cancer was calculated by multiplying the number of appropriate person-years at risk by the corresponding age- and calendar period-specific cancer incidence rates for women obtained from the Osaka Cancer Registry. One hundred and seventeen patients developed a second primary cancer other than subsequent breast cancer, yielding an observed-to-expected ratio (O / E) of 1.3 [95% confidence interval (CI) = 1.1 - 1.6]. The risk for developing a second primary cancer was significantly elevated during the first year following the diagnosis of breast cancer, and decreased with the passage of time to unity. A significantly increased risk was noted for the development of ovarian cancer (O / E = 2.4, 95% CI = 1.0 - 4.6), thyroid cancer (O / E = 3.7, 95% CI = 1.5 - 7.6) and non-Hodgkin's lymphoma (NHL) (O / E = 3.5, 95% CI = 1.4 - 7.1) among the breast cancer patients compared with the general population. Patients who received hormonal therapy as the breast cancer treatment showed a significantly increased risk for ovarian cancer (O / E = 5.5, 95% CI = 1.8 - 12.9). Patients who received chemotherapy as the breast cancer treatment had an increased risk for NHL (O / E = 5.0, 95% CI = 1.6 - 11.6). These findings indicate that Japanese female patients with breast cancer had a 30% higher risk of developing a second primary cancer than the general population, the higher risk being manifested in the early period following the diagnosis of breast cancer. Medical surveillance of breast cancer patients for NHL, as well as for ovarian cancer and thyroid cancer, is required.

Adult↗

PubMed2006

Gastric cancer patients at high-risk of having synchronous cancer.

AIM: To identify patients with a high-risk of having a synchronous cancer among gastric cancer patients. METHODS: We retrospectively analyzed the prospective gastric cancer database at the National Cancer Center, Korea from December 2000 to December 2004. The clinicopathological characteristics of patients with synchronous cancers and those of patients without synchronous cancers were compared. Multivariate analysis was performed to identify the risk factors for the presence of a synchronous cancer in gastric cancer patients. RESULTS: 111 of 3291 gastric cancer patients (3.4%) registered in the database had a synchronous cancer. Among these 111 patients, 109 had a single synchronous cancer and 2 patients had two synchronous cancers. The most common form of synchronous cancer was colorectal cancer (42 patients, 37.2%) followed by lung cancer (21 patients, 18.6%). Multivariate analyses revealed that elderly patients with differentiated early gastric cancer have a higher probability of a synchronous cancer. CONCLUSION: Synchronous cancers in gastric cancer patients are not infrequent. The physicians should try to find synchronous cancers in gastric cancer patients, especially in the elderly with a differentiated early gastric cancer.

Adult↗

PubMed1990

Occupational cancer in Denmark. Cancer incidence in the 1970 census population.

Data sources and creation of data files. The cohort of persons who were 20-64 years of age at the time of the 1970 census has been followed for cancer incidence for a ten-year period. The study was made by linkage of individual records from the 1970 census, the Central Population Register, death certificates, and cancer registrations. Data were included on individual characteristics recorded in the census on prevalent cancer cases at the time of the census and on deaths, emigrations, and incident cancer cases during the ten-year follow-up period. The study includes a total of 2.8 million persons, of whom 2.0 million were economically active at the time of the 1970 census. A total of 115,000 incident cancer cases were registered during the follow-up period, and 77,000 of these occurred in persons who were economically active in 1970. The classifications used in the census included 218 codes for occupation and 245 codes for industry. The Cancer Registry data included 639 codes for diagnosis. Cancer incidence by social groups in Denmark. The cancer incidence was tabulated across 32 socioeconomic groups for 43 cancer sites among the men and 45 cancer sites among the women. The study showed an almost twofold difference in the overall cancer incidence between the socioeconomic groups of the men. Self-employed farmers were at low risk (RR 0.68), and unskilled workers in shipping/fishing were at high risk (RR 1.28) when the cancer incidence among all economically active men was used for the comparison. The social pattern in cancer incidence correlated well with the pattern for cancer mortality among men. As a rough estimate, the cumulative incidence for all cancer among persons under 75 years of age could be reduced by 32% if all Danish men had the cancer incidence of farmers. There was a fivefold or larger difference between the socioeconomic groups in the incidence for nine cancer sites. These nine cancer sites together represented 7% of the cumulative incidence for all cancer. Estimated in a similar way, the cumulative incidence could be reduced by 44% if all Danish men had the site-specific cancer incidence of the respective low-risk groups. The overall cancer incidence among the women varied from a relative risk of 0.71 for unskilled workers in agriculture to a relative risk of 1.18 for self-employed women in other industries I (dentists, lawyers, etc) when the cancer incidence among all economically active women was used for the comparison.(ABSTRACT TRUNCATED AT 400 WORDS)

Adult↗

PubMed1990

[Clinicopathological study of early cancer-like advanced gastric cancer].

We had clinicopathologically studied early cancer-like advanced gastric cancer in relation to peptic ulcer (UI). Early cancer-like advanced cancers with the difficulty to distinguish from early gastric cancer were selected for materials. Result were as followed: 1) Early cancer-like advanced cancers were consisted of 133 lesions, of which 128 lesions (96.2%) had peptic ulcer in cancerous lesion (73 lesions were active stage and 55 lesions were scarring stage). 2) Early cancer-like advanced cancers were 17.0% in all advanced gastric cancers. Proper muscle cancer (in which depth of cancerous invasion is up to proper muscle coat) was more common in early cancer-like advanced cancers than in Borrmann type advanced cancers. 3) Early cancer-like advanced cancers with peptic ulcer showed wide intramucosal cancerous infiltration. Thus, average of maximum diameter was 51.8 mm. 4) Those ulcer were commonly reaching to proper muscle coat or subserosa. Submucosal fibrosis was prominent and scattered proliferation of tumor cells were often seen within fibrosis. 5) Extent of cancerous infiltration in mucosa was more wide than that in submucosa. The above findings have led us to consider that early cancer-like advanced cancers have grown because of high degree submucosal fibrosis by the deep ulcerations due to "malignant cycle".

Fibrosis↗

PubMed1985

Second cancer following cancers of the buccal cavity and pharynx in Denmark, 1943-80.

Cancers of the buccal cavity and the pharynx are not only anatomically related but, except for the nasopharynx, also have risk factors in common. Multifocal occurrence of cancers in the buccal cavity and pharynx must be kept in mind when one is interpreting findings on multiple tumors. However, susceptibility to common risk factors, predominantly alcohol and tobacco, seem to be in operation among males, inasmuch as excess lung cancer followed cancers of the tongue [relative risk (RR) = 2.2], other parts of the mouth (RR = 2.2), and pharynx (RR = 2.0). Among females, lung cancer was in excess after cancers of the tongue (RR = 3.7) and mouth (RR = 3.6). Among males, esophageal cancer was elevated after cancers of the mouth (RR = 4.7) and tongue (RR = 5.7). Other combinations of tobacco-related cancers among males include those of the bladder (RR = 2.5) after cancer of the tongue and larynx (RR = 5.4) after pharyngeal cancer. Common etiologic factors or the multifocal nature of tumors of the buccal cavity might also account for the increases of cancer of the mouth (RR = 2.6) following lip cancer and cancer of the tongue (RR = 14) following mouth cancers among males. Among females, cancer of the mouth (RR = 17) was elevated after tongue, tongue (RR = 31) after mouth, and tongue (RR = 10) after salivary gland tumors. The excess of pharyngeal cancers in women (RR = 19) following cancer of the lip may be explained by common risk factors. Observed deficits of colon cancer following cancer of the lip in males and after tongue and salivary gland tumors in females could reflect low socioeconomic status, although a deficit of stomach cancer among males (RR = 0.1) also followed cancer of the salivary glands.

Denmark↗

PubMed1995

The volume of prostate cancer in the biopsy specimen cannot reliably predict the quantity of cancer in the radical prostatectomy specimen on an individual basis.

Previous studies suggest that prostate cancer with a volume of 0.5 ml. or less and a Gleason score of less than 7 may be clinically insignificant and may be managed with watchful waiting. A proposed method of determining the volume of cancer in the prostate gland has been the grade and volume of cancer present in the transrectal needle biopsy specimen. Volume of cancer in the biopsy specimen as a predictor of volume of cancer in the prostate gland was studied in 130 men who underwent radical retropubic prostatectomy for adenocarcinoma. Of the men 46 (35%) had clinical stage T1c (nonpalpable) disease, while 84 (65%) had clinical stage T2 (palpable) disease. Each radical prostatectomy specimen was whole-mounted and step-sectioned for accurate cancer volume determination. Three parameters for measuring volume of cancer in the biopsy specimen (percentage of biopsy cores involved, millimeters of cancer per biopsy core and percentage of cancer in the biopsy specimen) were determined and compared by Spearman rank correlation analysis. The percentage of cancer in the biopsy specimen was marginally better than the percentage of cores involved and the millimeters of cancer per biopsy core as a predictor of cancer volume in the radical prostatectomy specimen. While regression analysis revealed a direct correlation between the volume of cancer in the biopsy and radical prostatectomy specimens (r = 0.51), there was significant variability in prostate cancer volume for a given percentage of cancer in the biopsy specimen since the standard error of the estimate was 6.1 ml. Of the 13 patients with 5% or less cancer volume and a Gleason score of less than 7 in the biopsy specimen 1 (8%) had a cancer smaller than 0.5 ml. in volume in the radical prostatectomy specimen. Therefore, the risk of removing clinically insignificant prostate cancer, even when the biopsy parameter indicates low volume disease, is less than 10%. Overall, only 3 study patients (2.3%) had a prostate cancer volume of less than 0.5 ml. With 97.7% of the men having a clinically significant cancer by a volume criterion, it is apparent that the majority of clinically insignificant prostate cancers remained undetected and untreated. Currently, transrectal needle biopsy does not provide adequate information for differentiating between clinically insignificant and life threatening prostate cancer on an individual basis.

Adenocarcinoma↗

PubMed2001

Familial breast cancer: collaborative reanalysis of individual data from 52 epidemiological studies including 58,209 women with breast cancer and 101,986 women without the disease.

BACKGROUND: Women with a family history of breast cancer are at increased risk of the disease, but no study has been large enough to characterise reliably how, over women's lives, this risk is influenced by particular familial patterns of breast cancer. This report, on the relevance of breast cancer in first-degree relatives, is based on combined data from 52 epidemiological studies. METHODS: Individual data on breast cancer in first-degree relatives (mothers, sisters, and daughters) of 58209 women with breast cancer and of 101986 controls were collected, checked, and analysed centrally. Risk ratios for breast cancer were calculated by conditional logistic regression, stratified by study, age, menopausal status, number of sisters, parity, and age when the first child was born. Breast-cancer incidence and mortality rates for particular family histories were calculated by applying age-specific risk ratios to breast-cancer rates typical for more-developed countries. FINDINGS: Altogether 7496 (12.9%) women with breast cancer and 7438 (7.3%) controls reported that one or more first-degree relatives had a history of breast cancer: 12% of women with breast cancer had one affected relative and 1% had two or more. Risk ratios for breast cancer increased with increasing numbers of affected first-degree relatives: compared with women who had no affected relative, the ratios were 1.80 (99% CI 1.69-1.91), 2.93 (2.36-3.64), and 3.90 (2.03-7.49), respectively, for one, two, and three or more affected first-degree relatives (p<0.0001 each). The risk ratios were greatest at young ages, and for women of a given age, were greater the younger the relative was when diagnosed. The results did not differ substantially between women reporting an affected mother (9104) or sister (6386). Other factors, such as childbearing history, did not significantly alter the risk ratios associated with a family history of breast cancer. For women in more-developed countries with zero, one, or two affected first-degree relatives, the estimated cumulative incidence of breast cancer up to age 50 was 1.7%, 3.7%, and 8.0%, respectively; corresponding estimates for incidence up to age 80 were 7.8%, 13.3%, and 21.1%. Corresponding estimates for death from breast cancer up to age 80 were 2.3%, 4.2%, and 7.6%. The age when the relative was diagnosed had only a moderate effect on these estimates. INTERPRETATION: Eight out of nine women who develop breast cancer do not have an affected mother, sister, or daughter. Although women who have first-degree relatives with a history of breast cancer are at increased risk of the disease, most will never develop breast cancer, and most who do will be aged over 50 when their cancer is diagnosed. In countries where breast cancer is common, the lifetime excess incidence of breast cancer is 5.5% for women with one affected first-degree relative and 13.3% for women with two.

Adult↗

PubMed2006

Family history of breast cancer as a risk factor for ovarian cancer in a prospective study.

BACKGROUND: A family history of breast cancer has been associated with increased ovarian cancer risk. However, few studies have assessed risk according to characteristics that suggest an inherited cancer susceptibility disorder, such as earlier-than-usual age at cancer diagnosis, family members with double primary cancers of different types, multiple relatives with cancer, and cancer in both members of paired organs. METHODS: Ovarian cancer risk was assessed according to a detailed breast cancer family history among 49,975 participants in the Breast Cancer Detection Demonstration Project Breast Cancer Defection Demenstration Project (BCDDP) Follow-up Study (1979-1998). In all, 362 incident ovarian cancers were identified during follow-up and rate ratios (RRs) were calculated by Poisson regression. RESULTS.: Breast cancer in a first- or second-degree relative was associated with increased risk of ovarian cancer (RR = 1.4; 95% confidence interval [CI] = 1.1-1.7). Having 2 or more affected first-degree relatives was associated with increased risk (RR = 1.8; 95% CI = 1.1-2.8), especially for women diagnosed with ovarian cancer before age 60 (RR = 4.2; 95% CI = 1.9-9.2) or with a personal history of breast cancer (RR = 3.7; 95% CI 1.8-7.7). Risk was also particularly high for women with 2 or more first-degree relatives with breast cancer and at least 1 affected relative diagnosed before age 50 (RR = 2.6; 95% CI = 1.4-4.8) or with bilateral breast cancer (RR = 4.2; 95% CI = 1.7-10). CONCLUSIONS: A detailed breast cancer family history as well as an individual's age and personal history of breast cancer are useful for identifying women at elevated genetic risk of ovarian cancer.

Age Factors↗

PubMed1993

Familial effects of prostate and other cancers on lifetime breast cancer risk.

Lifetime probabilities of developing breast cancer were calculated for first-degree female relatives of three groups of breast cancer patients: 114 with bilateral cancer, 186 unselected, and 88 males. The patients were classified according to whether they had a family history of prostate, endometrial, or ovarian cancer, or no family history of these cancers. In families of unselected female and male patients with no family history of prostate, endometrial, or ovarian cancer, the lifetime probability of developing breast cancer was 11.4%. The risk increased slightly to 13.5% when these other cancers may or may not have present (i.e., they were ignored, which is the usual method in computing risks) and increased further to 25.5% when prostate, endometrial, or ovarian cancer was present in the family. In families of patients with bilateral cancer the respective risks were 10.9%, 17.3%, and 34.4%. A family history of prostate cancer increased lifetime risk consistently in each of the groups, to 29.0% in the unselected and male groups and to 38.2% in the bilateral group. Endometrial cancer increased risk only in the bilateral group (to 41.8%) as did ovarian cancer (to 54.6%). Increased risk of breast cancer with a family history of endometrial or ovarian cancer appeared to be influenced by families with hereditary breast-ovarian cancer or the cancer family syndrome. The results indicate that prostate cancer, and endometrial and ovarian cancers in some families, can significantly increase breast cancer risk and should be taken into account when counseling women about their breast cancer risk.

Adult↗

PubMed1991

Aetiological parallel between anal cancer and cervical cancer.

It has been postulated that an infectious agent and/or specific sexual behaviour is involved in the aetiology of anal cancer, in analogy with the aetiology established for cancer of the cervix. A case-control study of 29,648 women with cancers registered in the Danish Cancer Registry during 1968-87 tested the hypothesis that anal cancer patients were more likely than patients with colon, stomach, or vulva cancer to have had a previous diagnosis of cervical intraepithelial neoplasia (CIN) or invasive cervical cancer. The odds ratio of CIN, adjusted for age and year of diagnosis, for anal vs colon cancer was 5.2 (95% confidence interval [CI] 3.3-8.3), that for anal vs stomach cancer 3.6 (2.1-6.0), and that for anal vs vulva cancer 1.6 (0.9-2.9). The median time from diagnosis of CIN to diagnosis of the registered cancer was 151 months for anal, 112 months for vulva, 114 months for colon, and 126 months for stomach cancer. The association with previous invasive cervical cancer was also investigated; no patient with cervical cancer in this second analysis had been included in the CIN analysis. The odds ratios were similar. In addition, anal cancer patients were significantly more likely to have had cervical cancer than were patients with vulva cancer (odds ratio 1.8 [1.0-3.9]). The strong association between anal cancer and CIN/invasive cervical cancer suggests that these cancers share common risk factors. The association is at least as strong as that between cervical and vulva cancer.

Adolescent↗

PubMed2000

Second primary ovarian cancer among women with cancer.

PURPOSE: Some studies suggest women with certain types of cancers are at increased risk for ovarian cancer. This study assessed the risk of second primary ovarian cancer among U.S. women who have cancer by anatomic site, age, race, and time since diagnosis of the first primary cancer.METHODS: We analyzed data from SEER cancer registries for women diagnosed with invasive cancer between 1973 and 1996. Person-years were accumulated from 2 months after initial cancer diagnosis to date of ovarian cancer diagnosis, death, loss to follow-up, or end of follow-up, December 31, 1996. The expected number of cases was obtained by multiplying 5-year age and calendar year interval specific ovarian cancer rates by the accumulated person-years at risk. We calculated the risk (observed [O]/expected numbers [E]) of second primary ovarian cancer by cancer site and age (<50 years, >/=50 years), race (all, white, black), and time since first cancer (0-4, 5-9, 10-14, 15-24 years). Statistical tests and 95% confidence intervals (CI) were based on the assumption of a Poisson distribution.RESULTS: A significant increased risk of ovarian cancer was found for women aged <50 years at time of diagnosis with melanoma (O/E = 3.5, 95% CI = 2.1-5.5) and cancer of the breast (O/E = 6.0, 95% CI = 4.9-7.2), cervix (O/E = 4.2, 95% CI = 2.6-6.3), corpus uteri (O/E = 11.91, 95% CI = 7.3-18.4), colon (O/E = 17.9, 95% CI = 11.1-27.3), and ovary (O/E = 4.9, 95% CI = 2.7-8.2); no increased risk was found for women aged >/=50 years. Ovarian cancer risk remained elevated following all of these first primary cancers 5-9 years after diagnosis; for women with breast and colon cancer, risk remained elevated 15-24 years after diagnosis. A significant increased risk was found for all of these cancers among white women <50 years at diagnosis; risk was increased among black women <50 years with cancer of the breast, cervix, and colon.CONCLUSIONS: We found an ovarian cancer risk higher than expected for women with certain types of cancer; however, the risk was limited to women <50 years of age.

Journal Article↗

PubMed2004

Cancer incidence, mortality from cancer and survival in men of different occupational classes.

Low social class is associated with higher mortality from cancer at several sites and in patients with cancer low social class is known to be associated with a poorer chance of survival. Social differences in cancer incidence are less consistent. The present study was undertaken to assess the relation between occupational class and cancer incidence, mortality and survival from cancer in a large population of 7001 men aged 51-59, free of diagnosed cancer at baseline in 1970--1972. The main outcome measures were cancer incidence and cancer mortality until 1992 according to the Swedish national cancer and cause-specific death registries. Cancer survival was analysed in a subgroup of 904 men diagnosed with cancer before 1990. There were 1329 incident cases of cancer including 620 deaths from cancer. Overall cancer incidence during follow-up did not vary significantly by occupational class, but respiratory cancers were significantly more common among men with manual occupations; p = 0.0004. This was not be explained by differences in tobacco smoking, which were minor at the start of the study and did not increase much during follow-up. Overall mortality from cancer was significantly higher among men with manual occupations. Among professionals and higher officials 336 per 100,000 observation years died from cancer, compared to 391 among intermediate officials, 509 among lower officials, 474 among skilled and 548 among non-skilled workers; p for trend = 0.0003. This difference was mainly due to mortality from respiratory cancer, with a threefold difference between manual workers and professionals; this did not change after adjustment for smoking. Among the 904 men diagnosed before 1990 with cancer at any site (except non-melanoma skin cancer) the adjusted relative risk of dying from cancer was 1.75 (95% confidence interval 1.22-2.50) in unskilled workers compared to higher officials (p for trend 0.015).

Case-Control Studies↗

PubMedDate not supplied

Male patients with diagnoses of both breast cancer and prostate cancer.

Recently cancer susceptibility syndromes have been characterized that suggest possible genetic linkages between breast cancer and prostate cancer within families. Despite these connections, male breast cancer and prostate cancer in an individual man has rarely been reported. The clinical features of 10 patients with both of these cancers are described here. One hundred sixty-one patients with male breast cancer were seen at the Dana-Farber Cancer Institute and Massachusetts General Hospital between 1977 and 2000. Of these, 10 were identified who also had prostate cancer. A retrospective review of records from these 10 patients was performed. Breast cancer preceded prostate cancer in eight of these men. The mean age of diagnosis of breast cancer was 65.7 years (range 47-72 years). Twenty percent had nodal involvement at diagnosis and two patients ultimately developed evidence of metastatic disease. The mean age of diagnosis of prostate cancer was 68.0 years (range 51-76 years) with a median prostate-specific antigen (PSA) level at diagnosis of 6 ng/ml (range 1.8-47.5 ng/ml). Seven patients had a family history of female breast cancer in a first-degree relative, while one had a family history of prostate cancer. At a median follow-up of 6.5 years from initial cancer diagnosis, one patient had died of metastatic breast cancer and another had died of metastatic prostate cancer. The clinical features and course of the breast cancers diagnosed in this series do not appear significantly different from those described for the general population of male breast cancer patients. In addition, these men do not appear to develop prostate cancer at an earlier age or more aggressive stage than the general population.

Adenocarcinoma↗

PubMed1994

Family history of cancer and colon cancer risk: the Utah Population Database.

BACKGROUND: Family history of colon cancer has been shown to be related to the risk of developing colon cancer. The impact that a comprehensive family history of colon or other cancers has on the risk of colon cancer has not been thoroughly studied. PURPOSE: The purpose of this study was to assess the risk of developing colon cancer associated with having a family history of colon, rectal, breast, ovarian, endometrial, or prostate cancer. METHODS: A case-control study was conducted using data from the Utah Population Database. Case patients had first primary colon cancers (n = 2543). Three control subjects per case were individually matched to case patients on year of birth, place of birth, marital status, and sex. RESULTS: Those case patients with the highest familial standardized incidence ratio were at an increased risk of developing colon cancer (for men, odds ratio [OR] = 2.51 and 95% confidence interval [CI] = 1.88-3.29; for women, OR = 2.90 and 95% CI = 2.17-3.82). A second- or third-degree relative with colon cancer increased risk from 25% to 52%. Risk associated with family history was greater in those patients diagnosed before age 50 (for men, OR = 3.61 and for women, OR = 7.18) than in those diagnosed at 50 or more years of age (for men, OR = 2.44 and for women, OR = 2.73). The risk associated with a family history of colon cancer was greatest for the distal segment of the colon. Women were at an increased risk of colon cancer if they had a first-degree relative with breast (OR = 1.59; 95% CI = 1.25-2.03), uterine (OR = 1.50; 95% CI = 0.99-2.26), ovarian (OR = 1.63; 95% CI = 1.41-1.89), or prostate (OR = 1.49; 95% CI = 1.21-1.82) cancer; men were at increased risk of colon cancer if they had a first-degree relative with breast (OR = 1.30; 95% CI = 1.02-1.66), uterine (OR = 1.96; 95% CI = 1.34-2.87), or ovarian (OR = 1.59; 95% CI = 0.90-2.81) cancer. CONCLUSIONS: These findings support previous observations that people with a family history of colon cancer are at increased risk of colon cancer. Those with a second- or third-degree relative with colon cancer or a first-degree relative with breast, ovarian, uterine, or prostate cancer also have an increased risk of developing colon cancer. IMPLICATIONS: These data support the recommendations that individuals who have a first-degree, and possibly a second- or third-degree, relative with colon cancer should have regular screening for colon cancer.

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