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PubMed2006

Breast cancer as a second primary in patients with prostate cancer--estrogen treatment or association with family history of cancer?

PURPOSE: In a large population based study we reported an increased risk of male breast cancer after prostate cancer. In the current study we performed a comprehensive investigation of whether treatment for prostate cancer and/or family history is responsible for the excess risk. MATERIALS AND METHODS: This study had 2 parts. 1) We performed a nested case-control study in 41 men who had previously been identified with first prostate cancer, followed by male breast cancer and in 81 matched controls with prostate cancer only. The medical records of these men were retrieved and clinical data such as stage, grade and treatment were extracted. 2) We also performed a family study including relatives of men with a diagnosis of prostate as well as breast cancer, irrespective of which was first. The 878 relatives were identified through parish offices and linked to the Swedish Cancer Registry to evaluate the occurrence of breast, prostate and other cancers and calculate if there were any excess risks for different cancers. RESULTS: Cases with prostate plus breast cancer received estrogen treatment more often than controls with prostate cancer only (p = 0.03). The period of estrogen treatment was longer in the cases, although it was not statistically significant. Mean time from prostate cancer diagnosis to breast cancer diagnosis was 47.6 months. Cases and controls did not differ in grade or stage. In the family study an increased risk of prostate cancer was found in relatives (SIR 2.14, 95% CI 1.09 to 3.18). For other cancers no significantly increased risks were found. In 2 families pedigree analysis using the BRCAPRO program (http://www3.utsouthwestern.edu/cancergene/) revealed an estimated 100% and 49% probability in families 1 and 2, respectively, that the proband was a BRCA2 carrier. CONCLUSIONS: Our data suggest that most of the increased risk of breast cancer following prostate cancer can be explained by estrogen treatment. However, in a small number of men with prostate as well as breast cancer pedigree analysis suggests that BRCA2 mutation might be the underlying cause.

Aged↗

PubMed2003

Second primary cancers in men with prostate cancer: an increased risk of male breast cancer.

PURPOSE: Evaluation of second primary cancers provides valuable insight about etiology and shared risk factors. Studies of second primary cancers following prostate cancer conclude that overall risk of second primary cancers decreases. However, risk of bladder cancer and kidney cancer increases. We examine the risk of common and rare second primary cancers following prostate cancer in a large population based cohort to identify possible common etiological factors. MATERIALS AND METHODS: All prostate cancer cases in the Swedish Cancer Registry (135, 713) from 1958 to the end of 1996 constituted the study base. Risk (standardized incidence ratio) of second primary cancers was calculated as the ratio between observed and expected number of cancers. We used 2-tailed 95% confidence intervals (CI) to test significance. RESULTS: An overall increased risk (standardized incidence ratio 1.17, 95% CI 1.15-1.19) of second primary cancers was found but was only seen in the first 6 months of followup (ratio 3.45, 3.32-3.57). The most interesting finding was an increased risk (ratio 2.01, 95% CI 1.44-2.74) of male breast cancer. Other tumor sites with increased risk were the small intestine (standardized incidence ratio 1.39, 95% CI 1.09-1.51), skin melanoma (ratio 1.33, 95% CI 1.16-1.51) and endocrine tumors (ratio 1.41, 95% CI 1.13-1.74). CONCLUSIONS: A small but increased risk of second primary cancers following prostate cancer was found, most likely due to increased surveillance during the first 6 months after diagnosis. However, following prostate cancer there is an increased risk of endocrine related second primary cancers such as male breast cancer and carcinoids in the small intestine. To our knowledge these associations have not been reported previously, and they warrant more study.

Adenocarcinoma↗

PubMed1997

Prevalence and contribution of BRCA1 mutations in breast cancer and ovarian cancer: results from three U.S. population-based case-control studies of ovarian cancer.

We investigate the familial risks of cancers of the breast and ovary, using data pooled from three population-based case-control studies of ovarian cancer that were conducted in the United States. We base estimates of the frequency of mutations of BRCA1 (and possibly other genes) on the reported occurrence of breast cancer and ovarian cancer in the mothers and sisters of 922 women with incident ovarian cancer (cases) and in 922 women with no history of ovarian cancer (controls). Segregation analysis and goodness-of-fit testing of genetic models suggest that rare mutations (frequency .0014; 95% confidence interval .0002-.011) account for all the observed aggregation of breast cancer and ovarian cancer in these families. The estimated risk of breast cancer by age 80 years is 73.5% in mutation carriers and 6.8% in noncarriers. The corresponding estimates for ovarian cancer are 27.8% in carriers and 1.8% in noncarriers. For cancer risk in carriers, these estimates are lower than those obtained from families selected for high cancer prevalence. The estimated proportion of all U.S. cancer diagnoses, by age 80 years, that are due to germ-line BRCA1 mutations is 3.0% for breast cancer and 4.4% for ovarian cancer. Aggregation of breast cancer and ovarian cancer was less evident in the families of 169 cases with borderline ovarian cancers than in the families of cases with invasive cancers. Familial aggregation did not differ by the ethnicity of the probands, although the number of non-White and Hispanic cases (N = 99) was sparse.

Adult↗

PubMed2002

Risk of ovarian cancer in breast-cancer patients with a family history of breast or ovarian cancer: a population-based cohort study.

BACKGROUND: Patients with breast cancer who have mutations in the high penetrance genes BRCA1 and BRCA2, have an increased risk of ovarian cancer. Because these mutations are rare, easily obtained information such as age and family history of breast or ovarian cancer might be preferable for assessment of ovarian cancer risk in clinical practice. METHODS: We linked data from the Swedish Cancer Register to the Swedish Generation Register and generated a cohort of 30552 breast-cancer patients born after 1931, with information on breast and ovarian cancer diagnosis from 146117 first-degree relatives. Standardised incidence ratios (SIRs) with 95% CIs were calculated with nationwide rates of ovarian cancer, adjusted for age and calendar year. FINDINGS: During a mean follow-up of 6 years, 122 incident ovarian cancers were identified in the cohort, yielding an overall SIR of 2.0 (95% CI 1.6-2.4). The risk was higher in breast-cancer patients diagnosed before the age of 40 years, with a family history of breast cancer (5.6; 1.8-13.1) or ovarian cancer (17.0; 3.5-50.0). A consistently increased risk was noted in patients with a relative who was diagnosed before the age of 50 years, with either breast or ovarian cancer. Women with a family history of ovarian cancer have an almost 10% risk of developing ovarian cancer before the age of 70. INTERPRETATION: In young women with breast cancer, the risk of ovarian cancer is greatly raised when a family history of breast or ovarian cancer is present. Close medical surveillance, and perhaps even prophylactic oophorectomy, might be justified in high-risk groups.

Adult↗

PubMed2005

Management of cancer-related anemia in patients with breast or gynecologic cancer: new insights based on results from the European Cancer Anemia Survey.

The incidence, prevalence, and treatment of anemia (hemoglobin [Hb] <12 g/dl) in women with breast cancer and gynecologic cancer were evaluated using data from the European Cancer Anemia Survey (ECAS). Adult patients with newly diagnosed treated or untreated disease, persistent/recurrent disease, and disease in remission were enrolled and followed for up to six chemotherapy cycles or six evaluation points within a 6-month period. At enrollment, 30.4% of breast cancer patients and 49.1% of gynecologic cancer patients were anemic. A significant correlation was shown between low Hb level and poor performance status (World Health Organization criteria) at enrollment for both breast cancer and gynecologic cancer patients. In all, 62.4% of breast cancer patients and 81.4% of gynecologic cancer patients were anemic at some time during the survey. The incidence of anemia, determined in a carefully defined population, was 59.8% for breast cancer patients and 74.8% for gynecologic cancer patients. Despite the high prevalence and incidence of anemia, only 26.3% and 42.7% of patients in the respective groups received anemia treatment. In breast cancer patients, the mean Hb trigger was 10 g/dl for epoetin treatment and 8.6 g/dl for transfusion; corresponding values for gynecologic cancer patients were 10.1 g/dl and 9.1 g/dl. Logistic regression analyses in the overall ECAS population identified five factors as significant and suitable predictors of anemia: lower initial Hb, having lung or gynecologic cancer versus gastrointestinal/colorectal cancer, any other cancer versus gastrointestinal/colorectal cancer, treatment with platinum chemotherapy, and being female. The ECAS data highlight the need for greater awareness of the adverse impact of anemia on cancer patients and for optimal anemia management to ensure maximal patient quality of life.

Adult↗

PubMed2004

Breast cancer after childhood cancer: a report from the Childhood Cancer Survivor Study.

BACKGROUND: Survivors of childhood cancer are at risk for secondary breast cancer. Other than previous chest radiation therapy, risk factors for secondary breast cancer have not been established. OBJECTIVE: To identify risk factors for breast cancer among female survivors of childhood cancer. DESIGN: Retrospective cohort study. SETTING: The Childhood Cancer Survivor Study (CCSS), a multicenter study of persons who survived more than 5 years after childhood cancer diagnosed from 1970 to 1986. PARTICIPANTS: Among 6068 women in the CCSS, 95 women had 111 confirmed cases of breast cancer. MEASUREMENTS: Standardized incidence ratios for breast cancer were calculated by using age-specific incidence rates in the general population. Breast cancer incidence was evaluated with respect to primary cancer diagnosis and therapy, age at and time since primary diagnosis, menstrual and reproductive history, and family history of cancer. RESULTS: Breast cancer risk was increased in survivors who were treated with chest radiation therapy (standardized incidence ratio, 24.7 [95% CI, 19.3 to 31.0]) and survivors of bone and soft-tissue sarcoma who were not treated with chest radiation therapy (standardized incidence ratios, 6.7 and 7.6, respectively). Family history of breast cancer (relative rate, 2.7 [CI, 1.3 to 5.0]) and history of thyroid disease (relative rate, 1.7 [CI, 1.1 to 2.6]) were independently associated with increased risk, and exposure to pelvic radiation was protective (relative rate, 0.6 [CI, 0.4 to 0.9]). Age at primary cancer diagnosis and menstrual and reproductive histories did not statistically significantly modify risk. LIMITATIONS: This cohort has not yet attained an age at which breast cancer risk is greatest. CONCLUSION: Survivors of childhood sarcomas and those who received chest radiation therapy are at risk for secondary breast cancer. When assessing a survivor's risk, clinicians should consider primary diagnosis, previous radiation therapy, family cancer history, and history of thyroid disease.

Adult↗

PubMed2005

Risk factors and prognostic factors in patients with double primary cancer: epithelial ovarian cancer and breast cancer.

BACKGROUND AND OBJECTIVE: The most important known risk factor for ovarian cancer is the BRCA1-2 mutation, which is clinically often manifested through a positive family history of cancer of the breast and/or ovary. Whether other risk factors and prognostic factors in women with a positive family history of cancer of the breast and/or ovary and/or with BRCA1-2 mutation are important remains to be elucidated. Recent studies have shown that in the double primary breast and ovarian cancer (DPBOC), BRCA1-2 mutation is present in at least 86% of cases. Therefore, the group of patients with DPBOC, especially with epithelial ovarian cancer and breast cancer, is the most suitable for such an analysis. The aim of this study was to verify the hypothesis that, in this group, some other risk factors, in addition to a specific family history of cancer, as well as unfavourable pathomorphological prognostic factors, are more expressed than in a control group of patients with sporadic epithelial ovarian cancer only. METHODS: We compared the study group of 31 patients with DPBOC (epithelial ovarian cancer) to a control group of 62 patients with a single, sporadic epithelial ovarian cancer and negative specific family history. The data were obtained from the Cancer Registry of Slovenia and from clinical records. For every patient, we filled-in a protocol and analysed the data, comparing other risk factors in addition to specific family history and prognostic, clinical, and pathomorphological factors. Statistical analysis was performed using descriptive statistics, chi-square test and t-test. Multivariate analysis was also planned, but the necessary conditions were not met. RESULTS: In the study group, we found a higher percentage of positive non-specific family histories than in the control group, but the difference was not statistically significant. No difference in procreative risk factors was observed between the groups. There was a higher percentage of borderline significance of women from the study group that developed ovarian cancer between 45 and 59 years of age. In the study group, ovarian cancer was significantly more often found at Stage I, although the groups did not differ in detection procedures. Also, we did not find any differences in the distribution of tumour grades or histologic tumour types. CONCLUSION: The results did not confirm our hypothesis, yet they indicated some differences between the groups regarding the risk factors for ovarian cancer. Regarding the prognostic factors, we even found a significantly higher percentage of Stage I epithelial ovarian cancer in the study group, with no difference in the mode of detection. Considering the results that are not typical of BRCA-related cancer (what double primary cancer of the ovary and breast is supposed to be) and previous reports, we find it more likely that the patients with BRCA1-2 mutations represent only a subgroup within the group of patients with double primary breast and ovarian cancer.

Adult↗

PubMed1996

[Incidence of synchronous or metachronous multiple primary cancers and aggregation of cancers in families of patients with endometrial cancer].

We evaluated the incidence of synchronous or metachronous multiple primary cancer, hereditary or familial cancer, and the familial aggregation of cancer in 142 patients who were treated for endometrial cancer at Tsukuba University Hospital in the period 1977 to 1995. Synchronous multiple primary cancers were identified in 6 of the 142 patients (4.2%). Eleven patients (7.7%) had a history of extraendometrial cancer. Patients with endometrial cancer had a significantly high incidence of a history of breast cancer. Endometrial cancer was diagnosed in two patients who were screened before menopause. Four patients with endometrial cancer (2.8%) subsequently developed extraendometrial forms of cancer. One patient (0.7%) was considered to have a hereditary form of cancer, and 5 patients (3.5%) had familial forms of cancer. A total of 86 cases of cancer were found among 53 kindred (37.3%). More detailed studies are needed to elucidate the aggregation of cancers in the families of patients with endometrial cancer in Japan. Patients with a history of breast cancer should be screened for the presence of endometrial cancer.

Adenocarcinoma↗

PubMed1995

Genetic services for familial cancer patients: a survey of National Cancer Institute cancer centers.

In the past decade, significant progress has been made in understanding the genetic component of familial cancers. Genes associated with familial colon and breast cancers have recently been isolated and molecular diagnostic tests are expected to become available in the near future. Clinicians now have the opportunity to recognize and counsel individuals with elevated risk of cancer by identifying risk factors and genes associated with cancer predisposition. The rapid advances in molecular technology are a direct challenge to the medical community and cancer centers to supply specialized clinical services for familial cancers. We sought to ascertain the activities of cancer centers in the development of programs and the provision of genetic services for familial cancer. We surveyed 41 centers with National Cancer Institute (NCI) cancer center support grants. One half of the centers responding (17 of 34) reported that they provide some genetic services for familial cancer. About one half of these 17 centers (eight [57%] of 14; the three remaining clinics that responded had incomplete information on this indicator) see a variety of patient types on a small scale (fewer than 100 patients per year), and most provide four basic clinical evaluations: medical evaluation, cancer risk assessment, genetic counseling, and pedigree analysis. Staffing of each center varied widely, as did the types of screening services offered (including molecular diagnostic testing). Several centers (six [35%] of 17) indicated that they were in the developmental stages for serving familial cancer patients, and many seem to be increasing their activities in this area. The remaining 17 NCI-supported centers that responded, however, currently provide no genetic services for familial cancers. The results of this survey suggest that there is interest in developing clinical programs for familial cancers by NCI-supported cancer centers, but most of these programs are in developmental stages. A base line has been established to monitor future progress for the provision of cancer genetic services.

Cancer Care Facilities↗

PubMed1995

Second primary cancer after treatment for cervical cancer. An international cancer registries study.

BACKGROUND: The pattern of second cancers after treatment for cervical cancer provides important information on the risk of radiation-induced malignancies. Large numbers of women survive many years and can be studied for late effects. METHODS: Incident second cancers in 86,193 patients with cervical cancer reported to 13 population-based cancer registries in 5 countries were evaluated to estimate the risk of second cancer among very long term survivors. RESULTS: Overall, 7543 second cancers were observed versus 6015 cancers expected based on population rates (observed/expected = 1.2). Lung cancer accounted for nearly half of the excess cancers. Among the 49,828 women treated with radiation, 3750 survived 30 or more years and a two-fold risk of cancers of heavily irradiated organs was seen. Most of the excess cancers were of the rectum, vagina, vulva, ovary, and bladder. Patterns of risk over time since treatment were consistent with a radiation etiology. Significant increases of nonchronic lymphocytic leukemia and cancers of the bone and kidney were also linked to radiotherapy. Women treated surgically were also at significant risk of second cancers, in all likelihood related to cigarette smoking and risk factors similar to those of cervical cancer. CONCLUSIONS: Curative therapy for cervical cancer results in large numbers of long term survivors who develop second cancers very late in life. Radiation is an important cause of this increase and there is no evidence that risk returns to normal levels.

Europe↗

PubMed2005

Long-term mortality from heart disease and lung cancer after radiotherapy for early breast cancer: prospective cohort study of about 300,000 women in US SEER cancer registries.

BACKGROUND: Radiotherapy for early breast cancer can decrease breast cancer mortality but increase other mortality, mainly from heart disease and lung cancer. The mean cardiac dose from irradiation of a left-sided breast cancer can be two or three times that for a right-sided breast cancer. The mean ipsilateral (ie, on the same side as the breast cancer) lung dose can also be two or three times the mean contralateral lung dose. Particularly during the 1970s, when typical heart and lung exposures were greater than now, the laterality of an irradiated breast cancer could measurably affect cardiac mortality and mortality from cancer of the right or the left lung decades later. This study aimed to assess the hazards in the general US population from routine cancer-registry and death-certificate data. METHODS: We analysed data for 308 861 US women with early breast cancer of known laterality (left-sided or right-sided) who were registered in the US Surveillance Epidemiology and End Results (SEER) cancer registries during 1973-2001 and followed prospectively for cause-specific mortality until Jan 1, 2002. FINDINGS: 115 165 (37%) received radiotherapy. Among those who did not, tumour laterality was of little relevance to subsequent mortality. For women diagnosed during 1973-82 and irradiated, the cardiac mortality ratio (left versus right tumour laterality) was 1.20 (95% CI 1.04-1.38) less than 10 years afterwards, 1.42 (1.11-1.82) 10-14 years afterwards, and 1.58 (1.29-1.95) after 15 years or more (trend: 2p=0.03). For women diagnosed during 1983-92 and irradiated, the cardiac mortality ratio was 1.04 (0.91-1.18) less than 10 years afterwards and 1.27 (0.99-1.63) 10 or more years afterwards. For women diagnosed during 1993-2001 and irradiated the cardiac mortality ratio was 0.96 (0.82-1.12), with none yet followed for 10 years. Among women irradiated for breast cancer who subsequently developed an ipsilateral or contralateral lung cancer, the lung cancer mortality ratio (ipsilateral versus contralateral) for women diagnosed during 1973-82 and irradiated was 1.17 (0.62-2.19), 2.00 (1.00-4.00), and 2.71 (1.65-4.48), respectively, less than 10 years, 10-14 years, and 15 or more years afterwards (trend: 2p=0.04). For women irradiated after 1982 there is, as yet, little information on lung cancer risks more than 10 years afterwards. INTERPRETATION: US breast cancer radiotherapy regimens of the 1970s and early 1980s appreciably increased mortality from heart disease and lung cancer 10-20 years afterwards with, as yet, little direct evidence on the hazards after more than 20 years. Since the early 1980s, improvements in radiotherapy planning should have reduced such risks, but the long-term hazards in the general populations of various countries still need to be monitored directly.

Adult↗

PubMed1998

Cancer predisposition, radiosensitivity and the risk of radiation-induced cancers. IV. Prediction of risks in relatives of cancer-predisposed individuals.

Individuals carrying cancer-predisposing germline mutations are known to be at a higher risk for cancers than those who do not carry them. This is also true of their biological relatives because they have a higher probability of being carriers of such mutant genes than unrelated individuals in the population. Further, there are now sufficient grounds for assuming that cancer-predisposed individuals may also be at a higher risk for cancers induced by ionizing radiation. In our earlier work, we examined the impact of this heterogeneity (with respect to cancer predisposition and radiosensitivity differentials) on risks of radiation-induced cancer at the population level. This paper is focused on the question of risks of radiation-induced cancer in relatives of cancer-predisposed individuals. Using an autosomal dominant model of cancer predisposition and radiosensitivity developed earlier and applying it to breast cancer risks associated with mutations in the BRCA1 gene, we show that: (1) The risk ratio (i.e. the ratio of risk of radiation-induced cancer in relatives to that in unrelated individuals) in the population increases with the degree of biological relatedness of the relative, being higher for close than for distant relatives; incomplete penetrance of the mutant gene "dilutes" this risk ratio. (2) The proportion of excess radiation-induced cancers in relatives (i.e. the attributable fraction) is higher than in unrelated individuals. (3) In relatives, the proportion of excess cancers due to radiosensitivity differentials alone depends on the strength of predisposition, the radiosensitivity differentials assumed, the radiation dose, the proportion of cancers due to predisposition, the mutant gene frequency and the penetrance of the mutant gene. This is in contrast to the situation for unrelated individuals, for whom the above-mentioned proportion is dependent on the first three but not on the last three of these factors. Further, even when the proportion of excess cancers is small, most of it is due to radiosensitivity differential alone both in unrelated individuals and in relatives. (4) For values of predisposition strength and radiosensitivity differential <10, even when the estimated frequency of a mutant BRCA1 gene is 0.0047 and the proportion of breast cancers due to these mutations is 38% (as is the case for Ashkenazi Jewish women under age 30), the increase in breast cancer risks is only marginal even for first-degree relatives. (5) These findings support the conclusion that increases in radiation risks to relatives (compared to those in unrelated individuals), to be detectable epidemiologically, will occur only when the mutant alleles are common and the strength of predisposition and radiosensitivity differentials are conjointly dramatic.

Breast Neoplasms↗

PubMed1997

Use of multiple primary cancers to indicate associations between smoking and cancer incidence: an analysis of 500,000 cancer cases diagnosed in Norway during 1953-93.

The occurrence of multiple primary cancers is relatively rare, but may provide indications of common or opposite risk factors for different types of cancer. In the present study, the occurrence of multiple primary cancers was used to indicate possible associations between smoking and the incidence of cancers other than those generally accepted as smoking-associated. All cancer cases in persons above the age of 30, registered at the population-based Cancer Registry of Norway (1953-1993), were used in the analysis. For each type of cancer, the observed occurrence of smoking-associated cancers in the patients was compared with the expected occurrence if the patients had the same risk as the general population. Similar comparisons were made for the occurrence of other cancers in patients with a smoking-associated cancer. The results were presented as standardized incidence ratio (SIR), the ratio of the observed and the expected numbers of cases. The results indicated that uterine cervical cancer may share some important risk factor(s) with the cancers generally accepted as smoking-associated. This is in accordance with the literature, where an association between smoking and uterine cervical cancer has been found consistently. In addition, the results for liver cancer and leukemia indicated that these types of cancer also share some risk factor(s) with the smoking-associated cancers.

Adult↗

PubMed2006

Cancer screening and risk-reducing behaviors of women seeking genetic cancer risk assessment for breast and ovarian cancers.

PURPOSE/OBJECTIVES: To examine breast and ovarian cancer screening and risk-reducing behaviors of women seeking genetic cancer risk assessment (GCRA). DESIGN: Descriptive, cross-sectional. SETTING: An insurance-based clinic that serves high-risk patients in a southern California cancer center. SAMPLE: 134 women with breast or ovarian cancer (affected group) and 80 women with a family history of breast or ovarian cancer (unaffected group). The mean age of the sample was 48 years (range = 21-86), 79% were Caucasian, 66% were married, 60% were college educated, and 78% had children. Most affected women had early-stage disease. Unaffected women had a family history of breast (86%) or ovarian (14%) cancer. METHODS: Mailed surveys assessed pre-GCRA health behaviors and health and family histories. MAIN RESEARCH VARIABLES: Breast cancer screening (mammograms, clinical breast examination [CBE], breast self-examination), ovarian cancer screening (CA-125, pelvic ultrasound), and breast and ovarian cancer risk-reducing strategies (tamoxifen, bilateral mastectomy, oral contraceptive pills, bilateral salpingo-oophorectomy). FINDINGS: Twenty-one percent of the women who should have been having a mammogram had not had an annual examination as recommended, and 30% of affected women had not had annual CBEs. Few women took tamoxifen or oral contraceptive pills or had a bilateral salpingo-oophorectomy or bilateral mastectomy for cancer risk reduction. Twelve percent likely had unnecessary ovarian cancer screening. About 35% used other means, including herbs and homeopathy, for cancer prevention. CONCLUSIONS: Nearly a third of the affected women had not had appropriate breast cancer screening. About 12% used unsubstantiated, potentially harmful cancer "prevention" measures (e.g., herbs). IMPLICATIONS FOR NURSING: Nurses should assess clients' personal and family breast and ovarian cancer histories and promote cancer screening and risk-reducing behaviors that are appropriate for age and risk level.

Adult↗

PubMed2002

Radiosurgery for residual or recurrent nonfunctioning pituitary adenoma.

OBJECT: Nonfunctioning pituitary adenomas comprise approximately 30% of all pituitary tumors. The purpose of this retrospective study is to evaluate the efficacy and role of gamma knife radiosurgery (GKS) in the management of residual or recurrent nonfunctioning pituitary adenomas. METHODS: A review was conducted of the data obtained in 42 patients who underwent adjuvant GKS at the University of Pittsburgh between 1987 and 2001. Prior treatments included transsphenoidal resection, craniotomy and resection, or conventional radiotherapy. Endocrinological, ophthalmological, and radiological responses were evaluated. The duration of follow-up review varied from 6 to 102 months (mean 31.2 months). Fifteen patients were observed for more than 40 months. The mean radiation dose to the tumor margin was 16 Gy. Conformal radiosurgery planning was used to restrict the dose to the optic nerve and chiasm. Tumor control after GKS was achieved in 100% of patients with microadenomas and 97% of patients with macroadenomas. Gamma knife radiosurgery was equally effective in controlling adenomas with cavernous sinus invasion and suprasellar extension. No patient developed a new endocrinological deficiency following GKS. One patient's tumor enlarged with an associated decline in visual function. Another patient experienced a deterioration of visual fields despite a decrease in tumor size. CONCLUSIONS: Gamma knife radiosurgery can achieve tumor control in virtually all residual or recurrent nonfunctioning pituitary adenomas. Dose sparing facilitates tumor management even when the adenoma is close to the optic apparatus or invades the cavernous sinus.

Adenoma↗

PubMed2006

Guidelines for colonoscopy surveillance after cancer resection: a consensus update by the American Cancer Society and the US Multi-Society Task Force on Colorectal Cancer.

Patients with resected colorectal cancer are at risk for recurrent cancer and metachronous neoplasms in the colon. This joint update of guidelines by the American Cancer Society and the US Multi-Society Task Force on Colorectal Cancer addresses only the use of endoscopy in the surveillance of these patients. Patients with endoscopically resected Stage I colorectal cancer, surgically resected Stages II and III cancers, and Stage IV cancer resected for cure (isolated hepatic or pulmonary metastasis) are candidates for endoscopic surveillance. The colorectum should be carefully cleared of synchronous neoplasia in the perioperative period. In nonobstructed colons, colonoscopy should be performed preoperatively. In obstructed colons, double-contrast barium enema or computed tomography colonography should be performed preoperatively, and colonoscopy should be performed 3 to 6 months after surgery. These steps complete the process of clearing synchronous disease. After clearing for synchronous disease, another colonoscopy should be performed in 1 year to look for metachronous lesions. This recommendation is based on reports of a high incidence of apparently metachronous second cancers in the first 2 years after resection. If the examination at 1 year is normal, then the interval before the next subsequent examination should be 3 years. If that examination is normal, then the interval before the next subsequent examination should be 5 years. Shorter intervals may be indicated by associated adenoma findings (see "Guidelines for Colonoscopy Surveillance After Polypectomy: A Consensus Update by the US Multi-Society Task Force on Colorectal Cancer and the American Cancer Society"). Shorter intervals also are indicated if the patient's age, family history, or tumor testing indicate definite or probable hereditary nonpolyposis colorectal cancer. Patients undergoing low anterior resection of rectal cancer generally have higher rates of local cancer recurrence compared with those with colon cancer. Although effectiveness is not proven, performance of endoscopic ultrasound or flexible sigmoidoscopy at 3- to 6-month intervals for the first 2 years after resection can be considered for the purpose of detecting a surgically curable recurrence of the original rectal cancer.

Colectomy↗

PubMed1993

Characteristics of prostate cancers detected in a multimodality early detection program. The Investigators of the American Cancer Society-National Prostate Cancer Detection Project.

BACKGROUND: Few data are available to describe the clinical and pathologic characteristics of prostate cancers detected through early detection programs. The American Cancer Society National Prostate Cancer Detection Project (ACS-NPCDP) is a multimodality, multicenter study of the feasibility of early prostate cancer detection using digital rectal examination (DRE), transrectal ultrasound (TRUS), and prostate specific antigen (PSA). One hundred fifty-six prostate cancers are available from this project for analysis. METHODS: The ACS-NPCDP is a prospective, comparative study of a cohort of 2,999 men between 55 and 70 years of age not suspected of having prostate cancer. DRE, TRUS, and PSA are performed for each subject on an annual basis for as long as 5 years. Biopsies are performed on the basis of recommendations from DRE or TRUS results. Although elevated PSA alone was not typically a basis for biopsy, in some instances biopsies were recommended because of the degree of elevation in PSA. Diagnoses are confirmed by participating pathologists and by pathologic analysis. RESULTS: A small proportion of cancers detected were advanced in terms of the clinical stage at time of diagnosis. A total of only six cancers were stage C1 to D1, and five of these were preexisting cancers detected at the first examination. Cancers detected by DRE tended to be more advanced than those found on the basis of only TRUS or PSA. A large proportion of patients received curative therapy, involving radical prostatectomy for 67.9% and radiation therapy for 17.9%. Of 100 men presumed to have organ confined disease and treated by prostatectomy, 64 actually proved to have localized cancer, a rate of upstaging of 36.0%. PSA level and PSA density were associated with the detection of organ confined cancer, but several advanced cancers had PSA levels in the normal range, limiting the usefulness of these measures for staging. CONCLUSIONS: The cancers resulting from this multimodality detection effort represented a spectrum of pathologic findings. These data, however, suggest that early detection interventions in men not suspected to have prostate cancer will yield tumors with a favorable stage distribution that are likely to benefit from treatment. Further follow-up evaluation is needed to determine whether these benefits are reflected in long-term mortality and survival experience.

Aged↗

PubMed2002

Germline mutations in E-cadherin do not explain association of hereditary prostate cancer, gastric cancer and breast cancer.

Somatic mutations in the E-cadherin (CDH1) gene have frequently been reported in cases with diffuse gastric and lobular breast cancers. Recently, germline mutations have been identified in families with diffuse gastric cancers. In families with hereditary prostate cancer (HPC), a significant association of prostate cancer, gastric and/or breast cancer has been observed in epidemiological studies. The aim of this study was to investigate if germline mutations in CDH1 could explain the risk for cancer in HPC families with an excess of gastric and breast cancer. In total, 17 members from 13 HPC families and 3 members from 3 families with hereditary gastric cancer (HGC) were screened for germline CDH1 sequence alterations using PCR/Denaturing HPLC for initial screening of nucleotide variants followed by confirmatory direct sequencing analysis. The frequency of identified novel germline mutations were tested for in 136 cases with hereditary prostate cancer and 215 cases of sporadic prostate cancer with 422 age matched controls in an allelic discrimination assay. In total, 8 sequence variants were detected in 20 samples tested. In the HPC families, we found 2 missense mutations, A592T in exon 12 and a novel D777N in exon 15 and a mutation in intron 5, 687+92T>A. A previously known polymorphism in exon 13 and 3 sequence variations in introns and untranslated regions were also found, of which the significance is unknown. In HGC-023 with early onset diffuse gastric cancer a truncating mutation, R335X, was identified in exon 7. None of the missense mutations or 687+92T>A were found in the extended HPC material or in the sporadic prostate cancer cases with age-matched controls in the allelic discrimination assay. We found several germline mutations of unknown clinical significance in the CDH1 gene that probably do not explain the association of prostate, gastric and/or breast cancers in the HPC-families. Two missense mutations and a mutation in intron 5 were identified that do not influence the risk of hereditary or sporadic prostate cancer in general and are considered to be pedigree specific. In a family with hereditary gastric cancer of the diffuse type, we identified the first truncating germline mutation in a Scandinavian family.

Adult↗