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PubMed1999

Familial risks in second primary breast cancer based on a family cancer database.

The nationwide Swedish Family Cancer Database was used to analyse the risk of breast cancer in daughters of mothers presenting second, bilateral breast cancer. The database contained information on family relationships and cancers of mothers and daughters when the daughter was born after 1940, totalling 55,411 maternal and 9966 daughters' primary breast cancers. Some 95% of the second breast cancers were diagnosed in the contralateral breast. Familial risk of breast cancer in daughters was 1.70 when the mothers had first breast cancer and 3.28 when the mothers had bilateral breast cancer. Thus, the increased familial effect of the second breast cancer was 1.93. The risk was highest in daughters diagnosed at a young age when the mother was diagnosed before 50 years of age. If the mothers had breast cancer following any other type of cancer, the familial effect was as for the first breast cancer (1.03). The age of onset for breast cancer in daughters was 0.7 years younger for those whose mother had bilateral as compared with unilateral breast cancer, although the difference was not statistically significant. The mothers with bilateral breast cancer whose daughters also had breast cancer were diagnosed with the first breast cancer 3.8 years younger than mothers whose daughters did not have breast cancer. The present results apply to a relatively young population of daughters (< 54 years of age).

Adolescent↗

PubMed2003

Men with colorectal cancer are predisposed to prostate cancer.

BACKGROUND: The objective of the present study was to investigate the relationship between colorectal and prostate cancer. METHODS: All Victorian men who developed metachronous colorectal and prostate cancer with the first primary diagnosed between 1982 and 1993 were identified retrospectively from the Victorian Cancer Registry and were followed up to the end of 1995. Analyses were stratified by age group and years of follow up. The cause of death in those men who had prostate cancer following colorectal cancer was determined. The stage of colorectal cancer was compared between men with and without second primary prostate cancer and the grade of prostate cancer was compared with men who did not have a prior colorectal cancer. RESULTS: Men who develop colorectal cancer are at increased risk of prostate cancer, with the greatest risk in men under the age of 65 (Relative risk approximately 2). Men with first primary colorectal cancer are more likely to develop prostate cancer than colorectal second primaries, and men who develop second primary prostate cancer are more likely to die of prostate cancer than colorectal cancer. CONCLUSIONS: Younger men diagnosed with colorectal cancer are at increased risk of prostate cancer. However, there is no direct evidence that screening for prostate cancer leads to a reduction in mortality. This should be considered when discussing long-term follow up.

Age Factors↗

PubMedDate not supplied

[Relation of breast cancer tumour stage and the degree of registration in a population-based cancer registry].

UNLABELLED: Population-based cancer registries provide a large database of cancer cases which can be used for evaluation of cancer epidemiological and care-related questions. In particular, the latest projects in breast cancer screening and quality assured breast cancer diagnostics represent appropriate databases in the use of cancer registry data for further evaluation. For breast cancer the tumour stage distribution is a well suited, early available indicator for evaluating such interventions. The problem in using data from cancer registries occurs with the rather long time period until registration can be completed (up to 3 years). Thus, early usage of cancer registry data remains rather questionable. AIM OF THE STUDY: This analysis aims to show whether the distribution of breast cancer tumour stage depends on the completeness of registration and whether a valid estimate of the tumour stage distribution is possible at an early stage, on the basis of a not fully completed registration. METHODS: The cancer registry records all new cancer cases of the Federal State of Schleswig-Holstein. For the period from 1998 to the beginning of 2003 all breast cancer cases and their tumour stage distribution were extracted at three-month' intervals. Completeness of registration for each date was estimated on the basis of cancer data from the Federal State of Saarland. The expected number of breast cancer cases for Schleswig-Holstein was set to 100%. RESULTS: In total, 7,418 patients with new breast cancer were analysed. Already at a degree of 50% of registration a stable distribution of tumour stage could be observed. For example, the variability of the T1-category (tumour size < or = 2 cm) showed a maximum of three per cent in the range from 50% up to 100% completeness. Also for lymph nodes and distant metastases just a small degree of variability from one to three per cent points could be shown. A 75% completeness of breast cancer registration was established about six months after the end of the year of diagnosis. Complete registration could only be reached significantly later, approximately after two years. CONCLUSION: For the cancer registry of Schleswig-Holstein a significant relation of the tumour stage distribution in the degree of registration could not be detected. A stable distribution could be shown with a completeness of 50-75%. Hence, it appears to be methodically justified to analyse the tumour stage of breast cancer data with sufficient validity with a completeness of 75 %. The tumour stage distribution can be used as an early indicator (about six months after the end of the year of diagnosis) for evaluation of projects like mammography screening, quality management or research on medical care.

Breast↗

PubMed1993

Descriptive clinicopathologic study of 17 patients with endometrial cancer during or after adjuvant tamoxifen in early breast cancer.

BACKGROUND: Studies have shown that patients with early-stage endometrial cancer who have previously used endogenous estrogen (oral contraceptives or estrogen replacement therapy) have a favorable prognosis. This has not yet been demonstrated for patients with early-stage endometrial cancer who have received tamoxifen. In addition, studies have raised the question of whether women receiving tamoxifen are at increased risk of endometrial cancer. PURPOSE: Our aim was to determine whether the prognosis is favorable for patients with diagnosis of endometrial cancer after adjuvant treatment with tamoxifen for breast cancer. METHODS: We matched 931 patients from the Stockholm Adjuvant Tamoxifen Trial in early breast cancer against the Swedish Cancer Registry and identified 17 who subsequently had endometrial cancer. These patients had been randomly assigned to receive 40 mg/d tamoxifen orally for 2 years beginning 4 weeks after surgery for breast cancer. Histologic specimens, patient records, and death certificates were reviewed to verify treatment and causes of death. RESULTS: Thirteen of the 17 patients diagnosed with endometrial cancer were alive; for three of the four who had died, the cause of death was endometrial cancer. All 16 evaluable tumors except one were World Health Organization (WHO) histologic grades I-II. Only one patient had advanced disease (stage IV); the remaining tumor was a mixed mesodermal malignant tumor that could not be classified under the WHO grading system. Median time for adjuvant tamoxifen use was 24 months (range, 6-60 months) with a median cumulative tamoxifen dose of 29 g (range, 7-72 g). Median time from initiation of adjuvant tamoxifen to diagnosis of endometrial cancer was 32 months (range, 6-130 months). Ten-year actuarial survival after diagnosis of endometrial cancer for the 17 patients treated with tamoxifen was 73%. CONCLUSION: Because of the small number of patients, our results do not rule out the possibility of a favorable prognosis for patients with a diagnosis of endometrial cancer following tamoxifen treatment. IMPLICATIONS: The incidence of secondary endometrial cancer reported in this study following treatment of breast cancer patients with tamoxifen at doses of 40 mg/d in a large clinical trial is higher than that reported for previous large trials of tamoxifen at doses of 20 mg/d. Thus, tamoxifen dosage may be a critical factor in the subsequent occurrence of endometrial cancer. Our results also suggest two important considerations for improved follow-up in long-term tamoxifen trials: careful registration of second cancers and routine gynecologic examinations to ensure early detection of endometrial cancer.

Aged↗

PubMed1994

Lung cancer risk and radiation dose among women treated for breast cancer.

BACKGROUND: Evidence shows ionizing radiation can cause lung cancer, but few studies have quantified risk in relation to radiation dose. PURPOSE: This study evaluated the long-term risk of lung cancer among women treated with radiation for breast cancer. METHODS: In this case-referent study, the Connecticut Tumor Registry was used to identify women diagnosed with histologically confirmed invasive breast cancer between 1935 and 1971 who survived for at least 10 years (8976) and to ascertain lung cancers occurring in this group between 1945 and 1981. Seventy-six cases of lung cancer were identified; however, 15 cases did not meet the criteria for inclusion. For the 61 remaining lung cancer case patients and 120 reference subjects (selected from the same registry and matched according to race, age at breast cancer diagnosis, year of breast cancer diagnosis, and survival without a second primary tumor), hospital charts were reviewed to collect medical history and radiotherapy information. A medical physicist estimated radiation dose to different segments of the lungs on the basis of radiotherapy reports and experimental simulations of treatments. RESULTS: For these 10-year survivors of breast cancer, the overall relative risk (RR) of lung cancer associated with initial radiotherapy for breast cancer was 1.8 (95% confidence interval [CI] = 0.8-3.8), and the RR increased with time following treatment. The RR for periods of 15 years or more after radiotherapy was 2.8 (95% CI = 1.0-8.2). Mean dose was 15.2 Gy to the ipsilateral lung, 4.6 Gy to the contralateral lung, and 9.8 Gy for both lungs combined. The excess RR was 0.08 per Gy, based on average dose to both lungs, and 0.20 per Gy to the affected (cancerous) lung. CONCLUSIONS: Breast cancer radiotherapy regimens in use before the 1970s were associated with an elevated lung cancer risk many years following treatment. The estimated risk coefficients are lower than those reported for atomic bomb survivors. The lower than expected risk might be attributable to high-dose cell killing or the fractionated nature of the exposure. IMPLICATIONS: Approximately nine cases of radiotherapy-induced lung cancer per year would be expected to occur among 10,000 women who received an average lung dose of 10 Gy and survived for at least 10 years. Current radiotherapy for breast cancer results in less extensive exposure of the lungs in comparison to treatments of years past, and the risk of secondary lung cancer need not play a major role in clinical decisions regarding treatment for breast cancer. Nonetheless, efforts to reduce unnecessary exposure of the lungs and heart should continue to further reduce possible adverse radiation effects.

Adult↗

PubMed1994

Systematic population-based assessment of cancer risk in first-degree relatives of cancer probands.

BACKGROUND: Cancer has long been recognized to have a familial component. Elevated risks for cancers at the same site for relatives of cancer probands have been reported for both common cancers and a number of the rarer cancer sites. For a particular cancer site, however, the estimated risks to relatives have varied considerably depending on criteria for selection of probands, how cancers were determined in relatives, and overall study design. Not surprisingly, the estimated risks of other cancers in relatives of probands with cancer at a given site have been subject to even more variation. PURPOSE: The aim of this study was to use the Utah Population Database resource to systematically study familial clustering of 28 distinct cancer site definitions among first-degree relatives (parents, siblings, and off-spring) of cancer probands. METHODS: We estimated familial relative risks from the Utah Population Database by identifying all cases of cancer in these first-degree relatives. These observed values were compared with those expected based on cohort-specific internal rates calculated from 399,786 relatives of all individuals in the Utah Population Database known to have died in Utah. RESULTS: All sites showed an excess of cancers of the same site among relatives, with thyroid and colon cancers and lymphocytic leukemia showing the highest familial risks. When the analyses were restricted to cases with early ages at diagnosis, increased familial components for most cancer sites became evident. A significant difference in familial relative risk (FRR) between male (FRR = 4.04; 95% confidence interval [CI] = 3.13-5.07) and female (FRR = 2.24; 95% CI = 1.54-3.08) probands was found for colon cancer. Highly significant familial associations (one-sided; P < .001) were found among breast, colon, and prostate cancers and between breast and thyroid cancers. Statistically significant (one-sided, P < .01) associations were also found between tobacco-associated sites (lung, larynx, lip, and cervix). CONCLUSIONS: This study represents a unique comprehensive population-based study of familial cancer. The familial associations reported here will be useful in generating hypotheses about specific genetic and environmental factors that can be tested in genetic linkage and case-control studies.

Aged↗

PubMed2003

Annual report to the nation on the status of cancer, 1975-2000, featuring the uses of surveillance data for cancer prevention and control.

BACKGROUND: The American Cancer Society, the Centers for Disease Control and Prevention (CDC), the National Cancer Institute (NCI), and the North American Association of Central Cancer Registries (NAACCR) collaborate annually to update cancer rates and trends in the United States. This report updates statistics on lung, female breast, prostate, and colorectal cancers and highlights the uses of selected surveillance data to assist development of state-based cancer control plans. METHODS: Age-adjusted incidence rates from 1996 through 2000 are from state and metropolitan area cancer registries that met NAACCR criteria for highest quality. Death rates are based on underlying cause-of-death data. Long-term trends and rates for major racial and ethnic populations are based on NCI and CDC data. Incidence trends from 1975 through 2000 were adjusted for reporting delays. State-specific screening and risk factor survey data are from the CDC and other federal and private organizations. RESULTS: Cancer incidence rates for all cancer sites combined increased from the mid-1970s through 1992 and then decreased from 1992 through 1995. Observed incidence rates for all cancers combined were essentially stable from 1995 through 2000, whereas the delay-adjusted trend showed an increase that had borderline statistical significance (P =.05). Increases in the incidence rates of breast cancer in women and prostate cancer in men offset a long-term decrease in lung cancer in men. Death rates for all cancer sites combined decreased beginning in 1994 and stabilized from 1998 through 2000, resulting in part from recent revisions in cause-of-death codes. Death rates among men continued to decline throughout the 1990s, whereas trends in death rates among women were essentially unchanged from 1998 through 2000. Analysis of state data for the leading cancers revealed mixed progress in achieving national objectives for improving cancer screening, risk factor reduction, and decreases in mortality. CONCLUSIONS: Overall cancer incidence and death rates began to stabilize in the mid- to late 1990s. The recent increase in the delay-adjusted trend will require monitoring with additional years of data. Further reduction in the burden of cancer is possible but will require the continuation of strong federal, state, local, and private partnerships to increase dissemination of evidence-based cancer control programs to all segments of the population.

Age Distribution↗

PubMed2000

Second cancers after adjuvant tamoxifen therapy for breast cancer in Japan.

BACKGROUND: Women treated with tamoxifen for breast cancer are at increased risk of endometrial cancer. We conducted a retrospective cohort study to evaluate the risk of second primary cancers after adjuvant tamoxifen therapy for breast cancer in Japan. PATIENTS AND METHODS: The subjects of the study were 6148 women who had been diagnosed with stage I, II, or IIIA unilateral primary breast cancer and had received surgical treatment during the period from January 1982 through December 1990 at nine institutions in Japan. The information on each patient was obtained from medical records or a prospectively compiled computer database at each institution. RESULTS: Of the 6148 women, 3588 (58.4%) were administered tamoxifen as an adjuvant treatment and 2560 (41.6%) were not administered. Median follow-up periods were 7.64 years for tamoxifen-treated patients and 8.10 years for non-tamoxifen-treated patients, respectively. The duration of tamoxifen treatment was mostly two years or less (80.7%), and few patients received tamoxifen for more than five years. The cumulative incidence rates of all second cancers at 10 years were 4.61% and 4.09% among tamoxifen-treated and non-tamoxifen-treated patients (P = 0.62), respectively, and the incidence rate ratio (IRR) for all second cancers was 1.06 (95% confidence interval (CI): 0.77-1.47) after adjustment of several covariates. The numbers of endometrial cancers was 9 and 3 among tamoxifen-treated and non-tamoxifen-treated patients, respectively, and the IRR was 2.37 (95% CI: 0.64-8.77, P = 0.20). Of the 12 patients who developed endometrial cancer, 4 died of cancer (for 3 of them, the cause of death was breast cancer), and the other 8 patients were alive as of March 1996. Stomach cancer was the most frequent second cancer and the IRR was 1.34 (95% CI: 0.76-2.38, P = 0.31). There was no substantial increase in any other type of gastrointestinal cancer such as colorectal and liver cancers among tamoxifen-treated patients. CONCLUSIONS: The incidence and risk of second primary cancers associated with tamoxifen therapy is low. The potential benefit of adjuvant tamoxifen therapy in breast cancer patients outweighs the risk of second primary cancers for Japanese breast cancer patients.

Adult↗

PubMed2005

Increased risk of cancer among relatives of patients with lung cancer in China.

BACKGROUND: Genetic factors were considered as one of the risk factors for lung cancer or other cancers. The aim of this work was to determine whether a genetic predisposition accounts for such familial aggregation of cancer among relatives of lung cancer probands. METHODS: A case-control study was conducted in 800 case families identified by lung cancer patients (probands), and in 800 control families identified by the probands'spouses. The data were analysed with logistic regression analysis model. RESULTS: The data revealed a significantly greater overall risk of cancer (OR = 1.82, P < 0.01) in the proband group. The relatives of lung cancer probands maintained an increased risk of non-lung cancer (P < 0.05) after adjusting for confounder factors. The crude odds ratio of a proband family having one family member with cancer was 1.67 compared with control families. Proband families were 2.56 times more likely to have two other family members with cancer. For three cancers and four or more cancers, the risk increased to 3.50 and 5.91, respectively. The most striking differences in cancer prevalence between proband and control families were noted for cancer risk among female relatives. The strongest effects were for not only lung cancer in any female relatives (OR 2.17, 95%CI 1.60-3.64) and mothers (OR 2.78, 95%CI 1.23-5.12) and sisters (OR 2.03, 95%CI 1.26-3.97), but also non-lung cancer in females and mothers (OR 2.00, 95%CI 1.26-3.01, and OR 2.34, 95%CI 1.28-4.40, respectively). CONCLUSION: These data support the hypothesis of a genetic susceptibility to cancer in families with lung cancer, and the female genetic susceptibility to cancer might be greater than male.

Adult↗

PubMed2006

Menopausal hormone therapy and other breast cancer risk factors in relation to the risk of different histological subtypes of breast cancer: a case-control study.

INTRODUCTION: Breast cancers of different histology have different clinical and prognostic features. There are also indications of differences in aetiology. We therefore evaluated the risk of the three most common histological subtypes in relation to menopausal hormone therapy and other breast cancer risk factors. METHODS: We used a population-based case-control study of breast cancer to evaluate menopausal hormone therapy and other breast cancer risk factors for risk by histological subtype. Women aged 50 to 74 years, diagnosed with invasive ductal (n = 1,888), lobular (n = 308) or tubular (n = 93) breast cancer in Sweden in 1993 to 1995 were compared with 3,065 age-frequency matched controls randomly selected from the population. Unconditional logistic regression was used to calculate odds ratios (ORs) and 95% confidence intervals (CIs) for ductal, lobular, and tubular cancer. RESULTS: Women who had used medium potency estrogen alone were at increased risks of both ductal and lobular cancer. Medium potency estrogen-progestin was associated with increased risks for all subtypes, but the estimates for lobular and tubular cancer were higher compared with ductal cancer. We found OR 5.6 (95% CI 3.2-9.7) for lobular cancer, OR 6.5 (95% CI 2.8-14.9) for tubular cancer and OR 2.3 (95% CI 1.6-3.3) for ductal cancer with > or =5 years use of medium potency estrogen-progestin therapy. Low potency oral estrogen (mainly estriol) appeared to be associated with an increased risk for lobular cancer, but the association was strongest for short-term use. Reproductive and anthropometric factors, smoking, and past use of oral contraceptives were mostly similarly related to the risks of the three breast cancer subtypes. Recent alcohol consumption of > 10 g alcohol/day was associated with increased risk only for tubular cancer (OR 3.1, 95% CI 1.4-6.8). CONCLUSION: Menopausal hormone therapy was associated with increased risks for breast cancer of both ductal and lobular subtype, and medium potency estrogen-progestin therapy was more strongly associated with lobular compared with ductal cancer. We also found medium potency estrogen-progestin therapy and alcohol to be strongly associated with tubular cancer. With some exceptions, most other risk factors seemed to be similarly associated with the three subtypes of breast cancer.

Adenocarcinoma↗

PubMed2006

Predicting perceived vulnerability for breast cancer among women with an average breast cancer risk.

OBJECTIVES: The purpose of the present study was to investigate predictors of perceived vulnerability for breast cancer in women with an average risk for breast cancer. On the basis of empirical findings that suggested which variables might be associated with perceived vulnerability for breast cancer, we investigated whether knowledge of breast cancer risk factors, cancer worry, intrusions about breast cancer, optimism about not getting cancer and perceived health status have a predictive value for perceived breast cancer vulnerability. DESIGN: In a 3-step approach, we recruited 292 women from the general public in Germany who had neither a family history of breast cancer nor breast cancer themselves. After receiving an initial informational letter about study objectives, the women were interviewed by telephone and then asked to fill in a self-administered questionnaire. METHODS: We used structural equation modelling and hypothesized that each of the included variables has a direct influence on perceived vulnerability for breast cancer. RESULTS: We found a valid model with acceptable fit indices. Optimism about not getting cancer, intrusions about breast cancer and women's perceived health status explained 32% of the variance of perceived vulnerability for breast cancer. Cancer worry and knowledge about breast cancer did not influence perceived vulnerability for breast cancer. CONCLUSION: Perceived vulnerability for breast cancer is associated with health-related variables more than with knowledge about breast cancer risk factors.

Adult↗

PubMed1999

Is history of squamous-cell skin cancer a marker of poor prognosis in patients with cancer?

BACKGROUND: Nonmelanoma skin cancer is associated with increased occurrence of subsequent cancer and death from cancer, but it is not known whether a history of skin cancer is associated with poor prognosis after a second diagnosis of cancer. OBJECTIVE: To determine whether history of squamous-cell skin cancer is a marker of poor prognosis in patients with cancer. DESIGN: Population-based cohort study. SETTING: Sweden, 1958 to 1996. PATIENTS: All patients in the Swedish Cancer Registry with or without a first diagnosis of squamous-cell skin cancer and a subsequent or first diagnosis of non-Hodgkin lymphoma (including chronic lymphocytic leukemia) or cancer of the colon, breast, prostate, or lung. MEASUREMENTS: Relative risk (RR) for death determined by using Cox proportional hazards regression analysis. RESULTS: Patients with a history of squamous-cell skin cancer had a significantly greater risk for death than those with no such history after receiving a diagnosis of non-Hodgkin lymphoma (RR, 1.33), colon cancer (RR, 1.24), breast cancer (RR, 1.19), or prostate cancer (RR, 1.17). Patients with lung cancer and a history of squamous-cell skin cancer who survived for 1 year after diagnosis of lung cancer also had an increased risk for death (RR, 1.29). CONCLUSION: Patients with a registered history of squamous-cell skin cancer have a poor prognosis after diagnosis of subsequent cancer and warrant careful medical attention.

Adult↗

PubMed1999

Increased serum angiogenin concentration in colorectal cancer is correlated with cancer progression.

We have previously demonstrated that the increased expression of angiogenin (ANG) in pancreatic cancer is related to cancer aggressiveness; however, the relationship between ANG expression and its clinical relevance in colorectal cancer has not been demonstrated. We therefore investigated the correlation between serum ANG (sANG) concentration and colorectal cancer progression or the changes in sANG concentrations before and after cancer resection. To determination sANG concentration by ELISA, sera were obtained from colorectal cancer patients (the cancer group) preoperatively (n = 34) and postoperatively (n = 25), from hernia patients (the nonneoplastic group) preoperatively (n = 9) and postoperatively (n = 4), and from 23 healthy volunteers. The amount of ANG in the colorectal cancer tissues (n = 19) was determined by the same method. Before surgery, the mean sANG concentration in the cancer group (411.8 +/- 106.3 ng/ml) was significantly higher than that in both the nonneoplastic group (344.0 +/- 60.7 ng/ml; P = 0.04) and in the healthy volunteers (321.7 +/- 59.7 ng/ml; P = 0.0001). The degree of elevation of sANG concentration in the cancer group was more significant in the more progressed subgroups as compared with that in the normal group (versus T(is) + T1 + T2 cancer, P = 0.01; versus T3 + T4 cancer, P = 0.002; versus stage 0 + I cancer, P = 0.02; versus >stage III cancer, P = 0.001; versus Dukes' A cancer, P = 0.02; versus Dukes' C cancer, P = 0.006). After cancer resection, the mean sANG concentrations in each subgroup decreased to the same levels as those of the normal group; the degrees of reduction were more significant in the more progressed subgroups. The tissue ANG amount correlated significantly with sANG concentration (P = 0.007). These results suggest that the increased concentration of sANG that is derived from colorectal cancer correlates with cancer progression.

Adenocarcinoma↗

PubMed1999

Prospectively detected cancer in familial breast/ovarian cancer screening.

BACKGROUND: Early diagnosis and treatment are shown to improve survival of breast and ovarian cancer. Identification and medical follow-up of high-risk groups may be important for early diagnosis. METHODS: A prospective study of 845 women from breast/ovarian- and ovarian cancer kindreds who were classified according to pre-set inclusion criteria (Table I), were offered genetic counseling and annual medical examinations of breasts and ovaries. The material consisted of three series: 1) 754 unaffected women, 2) 49 women with breast cancer, and 3) 42 women with ovarian cancer. RESULTS: In series 1) nine ovarian cancers and 20 breast cancers, in series 2) seven ovarian cancers, and in series 3) three breast cancers were found. All but one of the ovarian cancers were 40 years or older, and 4/16 (25%) were Borderline cancer. All breast cancers were 30 years or older, and 89% were detected before spread. CONCLUSIONS: This is to our knowledge the first prospective report of the combined breast/ovarian cancer findings in breast/ovarian cancer kindreds. A woman with both breast and ovarian cancer is the hallmark of inherited breast/ovarian cancer, and 50% of the ovarian cancers were detected in these families. Borderline ovarian cancer may represent a manifestation of this syndrome. If prophylactic oophorectomy prevents ovarian cancer, oophorectomy at age 45 would have prevented 75% of such cancers. Based on these results we revised our protocol for annual follow-up in these kindreds: 1) clinical breast examination and mammography (ultrasound/cytology if indicated) from 30 years of age, 2) gynecologic examination (including vaginal ultrasound, serum-CA125) from 35 years of age, and 3) discuss oophorectomy at 45 years of age.

Adolescent↗

PubMed2003

The epidemiology of colorectal cancer: what can we learn from the New Zealand Cancer Registry?

AIM: Colorectal cancer (CRC) is a major cause of cancer death in New Zealand. Incidence and mortality rates are regularly reported but more detailed information concerning the epidemiology of the disease is not readily available. The aim of this study is to describe the epidemiology of colorectal cancer, with particular reference to gender; subsite distribution; stage at diagnosis; tumour grade; the contribution of recognisable aetiological factors; and the resection rate and type of surgery performed for rectal cancer. METHODS: All 2272 pathology reports of colorectal cancer submitted to the National Cancer Registry for the year 2000 were reviewed and restaged according to the classical Dukes system. Age, gender, stage, subsite distribution, differentiation, tumour type, associated pathology and type of rectal cancer specimen were recorded. RESULTS: The gender ratio for all cases was equal. One third of resected cancers were in the rectum, one third in the left colon and one third were proximal to the splenic flexure. Men had more rectal cancer (M:F 1.6:1) and women more colon cancer (0.9:1). Right-sided cancers were of significantly higher grade than left-sided cancers. The proportion of right-sided cancers increased with advancing age in both men and women. Three per cent of patients had synchronous tumours and 0.2% of patients had phenotypic features of familial adenomatous polyposis (FAP). Fourteen per cent of patients were Dukes stage A at diagnosis, 43% stage B and 43% stage C. Rectal cancers were more likely to be stage A than colon cancers (odds ratio 1.6). Stage and grade of CRC were significantly associated. Ninety one per cent of cancers were resected; 29% of patients with rectal cancer had an abdominoperineal resection and 6% a local excision. CONCLUSIONS: The current stage distribution of CRC is in keeping with a predominantly unscreened population. The subsite distribution of cancer and its relationship to age and gender are similar to other high-risk countries; however, its relationship to grade of tumour has not previously been reported. An abdominoperineal resection rate of 29% reflects the mix of specialised colorectal and general surgical units treating rectal cancer in New Zealand and is in line with or better than recent overseas data that reflect national or regional practice.

Adenocarcinoma↗

PubMed1985

Second cancer following cancer of the male genital system in Connecticut, 1935-82.

The risk of a second primary cancer developing was evaluated in nearly 20,000 men with cancers of the prostate or testis in Connecticut, 1935-82. Among 18,135 men with prostate cancer, a significant 15% deficit of all second cancers was observed [1,053 vs. 1,241; relative risk (RR) = 0.85; 95% CI = 0.80-0.90], most notably for respiratory (RR = 0.7) and digestive cancers (RR = 0.8). The absence of a colon cancer risk lends little support to the idea of common risk factors such as dietary fat consumption. Only the risk for salivary gland cancer was significantly increased, possibly due to chance. Leukemia was significantly elevated among men observed for 10 and more years (RR = 2.2). In contrast to most other index tumors, the prostate stands out as being associated with an overall low risk of second cancer development. The reasons for these deficiencies have not been explained. Among 1,446 men with testis cancer, a significant twofold risk of second cancers was seen (104 vs. 50.1). A fivefold risk of leukemia (8 vs. 1.5) was not related to treatment or age. Contralateral testis cancer (6 vs. 0.5) was elevated in men treated with and without radiation. Risks for kidney cancer (5 vs. 1.5), bladder cancer (9 vs. 3.4), pancreatic cancer (6 vs. 1.5), non-Hodgkin's lymphoma (6 vs. 1.5), and prostate cancer (12 vs. 5.9) were significantly increased. No trends over time were noted for any cancer. Overall risk of second cancer development tended to be higher in younger men with testis cancer. The relationship of leukemia to testis and prostate cancers should be investigated in future research.

Connecticut↗

PubMed1994

Are women with breast, endometrial, or ovarian cancer at increased risk for colorectal cancer?

OBJECTIVES: Evidence is accumulating supporting the use of screening for colorectal cancer. Patients at higher risk for colorectal cancer are more likely to benefit from screening. Women with breast, endometrial, or ovarian cancer are often classified as at high risk for subsequent colorectal cancer, and are urged to undergo screening, but the basis for this is uncertain. METHODS: We performed a meta-analysis of published data to assess the risk of colorectal cancer after these cancers. RESULTS: Based on 154,270 women and 779,251 person-yr of observation (PYO) after breast cancer, 37,266 women and 229,498 PYO after endometrial cancer, and 41,366 women and 126,688 PYO after ovarian cancer, the age-adjusted relative risk (95% CI) for colorectal cancer after breast cancer was 1.1 (1.07, 1.19), after endometrial cancer 1.4 (1.32, 1.55), and after ovarian cancer 1.6 (1.40, 1.80). CONCLUSIONS: 1) Women with a history of breast, endometrial, or ovarian cancer are at a statistically significant increased risk for subsequent colorectal cancer. 2) Women with a history of endometrial or ovarian cancer are at higher risk than are women with breast cancer, but ascertainment bias from heightened medical surveillance after the diagnosis of a gynecologic malignancy may contribute to this observed increase in risk. 3) The association between these cancers and colorectal cancer suggests common etiologic factors, either environmental or genetic, but the degree of increased risk is small.

Aged↗

PubMed1996

[Risk of second primary cancer in two-year survivors of small cell lung cancer].

A total of 498 patients with small cell lung cancer received chemotherapy with or without chest irradiation at Osaka Prefectural Habikino Hospital from October 1977 through December 1991. Sixty-one who survived for more than two years were evaluated to determine the incidence and anatomic patterns of redevelopment of small cell lung cancer and development of second primary cancers. The numbers of expected cancers were estimated by cumulating person years of observation from 2 years after the start of treatment for small cell lung cancer to the date of death. Second primary cancers were observed in seven patients (four cases of non-small cell lung cancer, two of gastric cancer, and one of prostate cancer). The risk of a second primary cancer was 3.2 times greater than in the general population (95% Cl: 1.3-6.6). the relations between occurrence of a second primary cancer and family history of cancer, smoking history, smoking cessation after treatment of small cell lung cancer, and thoracic irradiation were studied. Occurrence of a second primary cancer correlated with family history (relative risk 7.5, 95% Cl: 1.5-22) and smoking cessation (relative risk 3.2, 95% Cl: 1.2-6.9). Long-term survivors were more likely to have a second primary cancer than a relapse of small cell lung cancer. Therefore, long-term survivors should be closely monitored for second primary cancers. Meta-analyses of studies done at several institutions may provide more detailed information on the occurrence of second primary cancers after small cell lung cancer.

Adenocarcinoma↗