Family history of breast cancer in first-degree relatives and triple-negative breast cancer risk

Triple-negative breast cancer accounts for less than 20% of breast cancers overall, but is the predominant subtype among carriers of mutations in BRCA1. However, few studies have assessed the association between breast cancer family history and risk of triple-negative breast cancer. We examined the relationship between having a family history of breast cancer in first-degree relatives and risk of triple-negative breast cancer, and risk of two other breast cancer subtypes defined by tumor marker expression. We evaluated data collected by the Breast Cancer Surveillance Consortium from 2,599,946 mammograms on 1,054,466 women, among whom 15% reported a first-degree family history of breast cancer. Using Cox regression in this cohort, we evaluated subtype-specific associations between family history and risk of triple-negative (N = 705), estrogen receptor-positive (ER+, N = 10,026), and hormone receptor-negative/HER2-expressing (ER−/PR−/HER2+, N = 308) breast cancer among women aged 40–84 years. First-degree family history was similarly and significantly associated with an increased risk of all the subtypes [hazard ratio (HR) = 1.73, 95% confidence interval (CI): 1.43–2.09, HR = 1.62, 95% CI: 1.54–1.70, and HR = 1.56, 95% CI: 1.15–2.13, for triple-negative, ER+, and ER−/PR−/HER2+, respectively]. Risk of all the subtypes was most pronounced among women with at least two affected first-degree relatives (versus women with no affected first-degree relatives, HR_{triple-negative} = 2.66, 95% CI: 1.66–4.27, HR_ER+ = 2.05, 95% CI: 1.79–2.36, HR_ER−_/PR−_/HER2+ = 2.25, 95% CI: 0.99–5.08). Having a first-degree family history of breast cancer was associated with an increased risk of triple-negative breast cancer with a magnitude of association similar to that for the predominant ER+ subtype and ER−/PR−/HER2+ breast cancer.     

Cancer mortality in relatives of women with breast cancer: The OPCS study

Mortality from cancer and other causes in male and female first-degree relatives of women with breast cancer diagnosed before age 60 has been examined in a large population-based cohort study, providing estimates of familial risks free from ascertainment or recall bias. Relatives of 3,295 patients with breast cancer diagnosed in the UK between 1954 and 1981 were identified through a register of households established in 1939. The 11,678 first-degree relatives thus identified were followed up through national records until the end of 1992. Over this period 5,421 deaths (including 1,527 cancer deaths) occurred in these relatives. Mortality from breast cancer was significantly raised in first-degree relatives (SMR 187, 248 deaths), and there was also significant excess mortality from cancers of the larynx (SMR 177, 17 deaths), endometrium (SMR 166, 29 deaths) and unspecified neoplasms (SMR 153, 70 deaths). The SMR for ovarian cancer was 130, based on 58 deaths (p = 0.06). There was no marked excess for other sites or for non-neoplastic causes of death, but there was a significant deficit in mortality from cervical cancer (SMR 63, 18 deaths). The SMR for breast cancer increased significantly with decreasing age of the relative. After allowing for age, sisters of cases had a slightly (though non-significantly) higher risk than mothers (ratio of SMRs 1.22). These results, together with penetrance estimates from linked families, suggest that approximately one woman in 800 carries BRCAI, the susceptibility gene on chromosome 17q, and that this gene causes about 1% of all breast cancers. © 1996 Wiley-Liss, Inc.     

DNA repair proficiency in breast cancer patients and their first-degree relatives

Defective DNA repair capacity as measured by enumerating chromatid aberrations induced in G₂ phase by X-irradiation may explain increased risk of breast cancer among relatives of patients. In the present study, chromatid damage was determined in peripheral blood lymphocytes (PBL) following in vitro exposure to 50R X-irradiation in G₂ phase from 14 breast cancer (BrCa) patients, 19 first-degree relatives (FDR) of BrCa patients and 17 control women who had no family history of cancer for the last 3 generations. Controls, BrCa patients and their FDR had comparable frequency of gaps and breaks when cells were arrested with Colcemid (30 min) after X-irradiation. A steep decline in chromatid damage was observed in cells of controls when arrested after 30, 90 and 120 min of X-irradiation. BrCa patients and their FDR showed higher frequencies of lymphocytic chromatid damage as compared to controls. Chromatid damage (95 gaps + breaks per 100 cells) observed among controls at 90 min post X-irradiation was considered as the optimal level of efficient DNA repair. Thirty-five percent of controls, 93% of BrCa patients and 79% of FDR showed sub-optimal DNA repair. Amongst the FDR, the likelihood of having suboptimal DNA repair was 7 times higher and the risk of developing breast cancer was 2.7 times higher as compared to controls. Moreover, in the BrCa patients, there was frequent involvement of chromosomes 1 and 2, and chromosomes of B, D and E groups, while in FDR, involvement of chromosome 2 and chromosomes of B, D and E groups was more frequent. Int. J. Cancer 73:20–24, 1997. © 1997 Wiley-Liss, Inc.     

Risk of breast cancer to relatives of young breast cancer patients

Breast cancer risk among sisters and mothers of a population-based series of 1,137 breast cancer patients diagnosed in Metropolitan Detroit before the age of 55 years was compared with risk to the same relatives of 1,001 age-matched, population-based controls. After adjusting for age of the relative, for age of the case or control, and for race, the odds ratio for breast cancer for women with affected sisters was 2.2; for women with affected daughters, 3.2; and for women with affected mothers and sisters, 9.9. Breast cancer in aunts had no independent influence on risk. Among white women, cumulative risk of breast cancer before the age of 50 years was approximately 1% for relatives of controls, 3% for sisters of older cases, but about 17% for women either with sisters diagnosed before the age of 40 years or with affected sisters and mothers. Sisters of the older patients had a 13% risk of breast cancer by 70 years of age, compared to 5% for sisters of controls. White women with affected mothers and sisters were at 50% risk by 65 years of age. This study identifies the criteria for women who could receive particular benefit from screening for breast cancer.     

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

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

Risk of malignancy in first-degree relatives of patients with pancreatic carcinoma

BACKGROUND: Approximately 5-10% of pancreatic carcinoma (PC) patients report a family history of the disease. In some families, mutations of tumor suppressor genes have been elucidated, but for most the causative gene remains unidentified. Counseling the families of PC patients regarding their risk of cancer remains problematic because little information is available. METHODS: The authors analyzed family history questionnaires completed by 426 unselected, sequential Mayo Clinic patients with PC. The prevalence of malignancy reported among 3355 of their first-degree relatives was compared with the Surveillance, Epidemiology, and End Results Project (SEER) 9 (2000) registry. Age-adjusted and gender-adjusted standardized incidence ratios (SIRs) were generated. RESULTS: Greater than 130,000 person-years at risk for cancer among the first-degree relatives were analyzed. The risk of PC was found to be increased among the first-degree relatives of patients with PC (SIR of 1.88; 95% confidence interval [95% CI], 1.27-2.68), as was the risk of liver carcinoma (SIR of 2.70; 95% CI, 1.51-4.46). Lymphoma (SIR of 0.28; 95% CI, 0.12-0.55), bladder carcinoma (SIR of 0.55; 95% CI, 0.31-0.89), breast carcinoma (SIR of 0.73; 95% CI, 0.57-0.92), lung carcinoma (SIR of 0.62; 95% CI, 0.47-0.80), and prostate carcinoma (SIR of 0.71; 95% CI, 0.54-0.92) were found to be underrepresented. When the proband was age < 60 years, the risk of PC to first-degree relatives was found to be increased further (SIR of 2.86; 95% CI, 1.15-5.89). In this subgroup, no other malignancies were found to be significantly increased, although the risks of melanoma (SIR of 1.73; 95% CI, 0.70-3.57), ovarian carcinoma (SIR of 2.20; 95% CI, 0.72-5.12), and colon carcinoma (SIR of 1.37; 95% CI, 0.80-2.19) were suggestive. CONCLUSIONS: There was a nearly twofold increased risk of PC in the first-degree relatives of PC probands. This risk was found to increase nearly threefold when patients were diagnosed before age 60 years. At the current time, in the absence of a pedigree suggestive of known familial cancer syndromes, the current study results do not support targeted screening for other malignancies in the first-degree relatives of patients with sporadic PC.     

Risk factors for breast cancer in Turkish women: a hospital-based case-control study

The aim of this study was to investigate the association between risk factors and breast cancer in Turkish women. In a hospital-based case-control study in Istanbul, 405 patients with histologically confirmed breast cancer were compared with 1050 controls, who were admitted to different departments of the same hospital. Unadjusted odds ratios (ORs) and 95% confidence intervals (CIs) for each risk factor were obtained from logistic regression analyses. Risk factors for breast cancer were found to be early menarche age (OR 3.87, 95% CI 2.46-6.08), use of alcohol (OR 3.87, 95% CI 1.79-8.37), history of diabetes (OR 3.31, 95% CI 2.36-4.64) or hypertension (OR 3.44, 95% CI 2.07-5.71), oral contraceptive use (OR 1.98, 95% CI 1.38-2.85) and hormone replacement therapy (HRT) use (OR 1.94, 95% CI 1.15-3.29). The findings of the present study indicated that history of diabetes or hypertension, use of alcohol, oral contraceptive and HRT, never having breastfed and delayed age at first birth associated with changing of lifestyle led to an increased risk of breast cancer in Turkish women.     

Risk of second cancer among women with breast cancer

A large number of women survive a diagnosis of breast cancer. Knowledge of their risk of developing a new primary cancer is important not only in relation to potential side effects of their cancer treatment, but also in relation to the possibility of shared etiology with other types of cancer. A cohort of 525,527 women with primary breast cancer was identified from 13 population-based cancer registries in Europe, Canada, Australia and Singapore, and followed for second primary cancers within the period 1943-2000. We used cancer incidence rates of first primary cancer for the calculation of standardized incidence ratios (SIRs) of second primary cancer. Risk of second primary breast cancer after various types of nonbreast cancer was also computed. For all second cancer sites combined, except contralateral breast cancer, we found a SIR of 1.25 (95% CI = 1.24-1.26) on the basis of 31,399 observed cases after first primary breast cancer. The overall risk increased with increasing time since breast cancer diagnosis and decreased by increasing age at breast cancer diagnosis. There were significant excesses of many different cancer sites; among these the excess was larger than 150 cases for stomach (SIR = 1.35), colorectal (SIR = 1.22), lung (SIR = 1.24), soft tissue sarcoma (SIR = 2.25), melanoma (SIR = 1.29), non-melanoma skin (SIR = 1.58), endometrium (SIR = 1.52), ovary (SIR = 1.48), kidney (SIR = 1.27), thyroid gland (SIR = 1.62) and leukaemia (SIR = 1.52). The excess of cancer after a breast cancer diagnosis is likely to be explained by treatment for breast cancer and by shared genetic or environmental risk factors, although the general excess of cancer suggests that there may be additional explanations such as increased surveillance and general cancer susceptibility.     

Intra-arterial chemotherapy in patients with breast cancer: a feasibility study.

The aim of this study was to assess the practicality of treating patients with various stages of breast cancer by means of regional (intra-arterial) chemotherapy. Three groups of patients received a median of four (range 2-4) cycles of combination chemotherapy: group I operable primary (n = 10); group II, locally advanced disease (n = 20); group III, recurrent locoregional disease (n = 22). The response rates (complete response, partial response and mixed response) in these groups of patients were 100% in groups I and II and 86% in group III. Morbidity included drug streaming and dysaesthesia in the hand. Patients in groups I and II had their tumours downstaged, allowing surgery to be performed. Local control was also achieved in group III when other treatment modalities had failed.     

Risk factors associated with the development of intestinal metaplasia in first-degree relatives of gastric cancer patients.

Family relatives of gastric cancer patients have a higher risk of gastric cancer and premalignant gastric lesions. We sought to determine the risk factors associated with the presence of intestinal metaplasia in a large cohort of gastric cancer relatives. First-degree relatives of gastric cancer patients were invited for screening gastroscopy. Endoscopic gastric biopsies were obtained from the antrum and corpus. Gastric biopsies were analyzed for Helicobacter pylori infection, severity of inflammation, and presence of intestinal metaplasia. Stepwise logistic regressions were used to identify for risk factors associated with presence of intestinal metaplasia in cancer relatives. Two hundred seventy cancer relatives underwent screening endoscopy (median age, 42; 47% male and 48% siblings). Among them, 161 (59.6%) were H. pylori positive and 81 (30%) had confirmed intestinal metaplasia. The following factors were found to be associated with the presence of intestinal metaplasia: age, male sex, H. pylori infection, birth order, alcohol use, siblings with stomach cancer, childhood living conditions, and water supply. Individuals with intestinal metaplasia had more severe acute and chronic inflammation in the antrum and corpus (P < 0.003). With multiple logistic regression, H. pylori infection [odds ratio (OR), 3.23], male gender (OR, 2.09), age (OR, 1.07), and a history of gastric cancer in siblings (OR, 1.91) were independent factors associated with the development of intestinal metaplasia in cancer relatives. In conclusion, we have identified risk factors associated with gastric intestinal metaplasia in stomach cancer relatives, which may be useful in the understanding of gastric carcinogenesis in these high-risk individuals.     

Breast cancer in first-degree relatives and risk of lung cancer: assessment of the existence of gene sex interactions

BACKGROUND: Previous studies have shown the sex differences in lung cancer and the associations between estrogen-related genes and non-small cell lung cancer. In the present study, we assumed the existence of shared candidate genes that are common in lung and breast cancers, and examined whether women with a family history of breast cancer are at increased risk of lung cancer compared with men, especially adenocarcinoma, in a case-only study. METHODS: This case-only study was conducted based on the Lung Cancer Database Project at the National Cancer Center Hospital East. A total of 1566 patients with newly diagnosed primary lung cancer were consecutively recruited between 1999 and 2003. Information on their family history of cancer and smoking habit was obtained from a self-administered questionnaire. To assess an interactions between two factors, odds ratios for interaction (ORis) and 95% confidence intervals (CIs) were calculated by case-only contingency table. RESULTS: A statistically significant ORi was observed between a family history of breast cancer in first-degree relatives (parent and siblings, not including children) and the sex of a patient (ORi: 2.22, 95% CI: 1.02-4.81). A stratified analysis by histologic subtypes showed a statistically significant ORi only for adenocarcinoma (ORi: 3.27, 95% CI: 1.19-8.98). No other family history of cancer, such as stomach, colon and lung cancer, showed a statistically significant ORi. CONCLUSION: This study suggests the possibility of gene-sex interaction in lung cancer.     

Cancer-related beliefs and health behavior change among breast cancer survivors and their first-degree relatives

It is unclear why some cancer survivors and their relatives are motivated by the (personal or vicarious) cancer experience to make positive health behavior changes while others are not. Consistent with Leventhal's Commonsense Model, we hypothesized that breast cancer survivors and their first-degree relatives (FDRs) would change behaviors they believed: (1) had caused the survivor's cancer or (2) could prevent a future cancer incidence. Sixty-five breast cancer survivors (stages 0-III) and 33 FDRs were recruited. Assessments occurred within three months of the survivor completing treatment (i.e. all surgery, chemotherapy, and radiation) and again three months later. Findings indicate that survivors who believed that unhealthy diet, insufficient exercise, or alcohol consumption contributed to their cancer were more likely to modify the relevant behavior. Likewise, survivors were more likely to implement healthy changes they believed would ward off a recurrence. Findings were similar when data from FDRs was added to the sample. Thus, healthy lifestyle changes after a personal (and possibly a vicarious) cancer diagnosis are tied to whether individuals believe changes can affect cancer outcomes. Given the role of health behavior change in reducing medical risks, these findings have important implications for maintaining the health of cancer survivors.     

Aggregation of cancer in first-degree relatives of patients with glioma.

BACKGROUND: Previous studies have been inconclusive in estimating the risk of different cancer sites among close relatives of glioma patients; however, malignant melanoma has consistently been described. METHODS: We obtained family history information from 1,476 glioma patients under age 75 years who registered at M. D. Anderson Cancer Center between June 1992 and June 2006. The number of observed cancers (N=1,001) among 8,746 first-degree relatives (FDR) was compared with the number expected from age-, sex-, and calendar year-specific rates from the Surveillance, Epidemiology, and End Results Program using standardized incidence ratios (SIR). RESULTS: The overall SIR for any cancer was 1.21 (95% confidence interval, 1.14-1.29). Among FDRs under 45 years the overall SIR was 5.08, and for relatives >45 years the overall SIR was 0.95. The SIRs were significantly elevated for brain tumors (2.14), melanoma (2.02), and sarcoma (3.83). We observed an excess of pancreatic cancer, which was significantly higher only among mothers. CONCLUSION: We observed an overall 21% increase in cancer among the FDRs of glioma patients including excess cases of brain tumors and melanoma, which could point to similar genetic contributions to these two malignancies. A large international linkage study is under way to examine potential genomic regions important for familial glioma.     

Risk of second primary cancer in the contralateral breast in women treated for early-stage breast cancer: a population-based study

PURPOSE: To study the potential risk factors, including radiotherapy (RT) for contralateral breast cancer (CBC), in patients treated for early-stage breast cancer. METHODS AND MATERIALS: The Surveillance, Epidemiology, and End Results database (1973-1996) was used to study the incidence of CBC after breast cancer. The Cox proportional hazards regression model was used to estimate the relative risk (RR) of CBC, with adjustment for confounders, including age, race, histologic subtype, and use of RT. Information on the use of hormonal therapy and chemotherapy was not available in the Surveillance, Epidemiology, and End Results database. RESULTS: A CBC was documented in 5679 (4.2%) of the 134501 localized invasive or intraductal breast cancer patients surviving at least 3 months. The 10- and 20-year actuarial rate of CBC was 6.1% and 12%, respectively. In multivariate analysis, medullary carcinoma (RR = 1.18, 95% confidence interval [CI] 1.02-1.37), black race (RR = 1.20, 95% CI 1.08-1.33), and age >55 years at initial diagnosis (RR = 1.15, 95% CI 1.08-1.22) were associated with increased CBC risk. A total of 1234 (3.3%) of 37,379 patients who received RT developed CBC, and 4445 (4.6%) of 97122 patients who did not receive RT developed CBC. Overall, RT was not associated with an increased risk of CBC (RR = 1.04, 95% CI 0.97-1.10) in multivariate analysis. The CBC risk associated with RT varied substantially with the length of follow-up. During the first 5 years of follow-up, RT was not associated with an increased CBC risk (age-adjusted RR = 0.96, 95% CI 0.88-1.04). For patients surviving for >5 years, RT was associated with a 14% increase in CBC risk (RR = 1.14, 95% CI 1.03-1.26). The increased CBC risk with RT was evident in patients aged <45 years (RR = 1.32, p = 0.01) and >55 years (RR = 1.15, p = 0.04) at initial diagnosis. The 5-, 10-, 15-, and 20-year actuarial rate of CBC was 2.9%, 6.5%, 10.2%, and 13.4%, respectively, for patients with RT; the corresponding rates were 3.0%, 6.0%, 8.9%, and 11.8% for patients without RT. The absolute increase in CBC risk associated with RT was 0.5%, 1.3%, and 1.6% in the 10-, 15-, and 20-year actuarial rate, respectively. CONCLUSION: CBC is not uncommon after breast cancer, especially for certain subsets of patients. RT was associated with a very small increased long-term CBC risk. This minimal increase in CBC risk should not affect clinical decision-making in treatment selection for patients with localized invasive breast cancer or ductal carcinoma in situ. Unnecessary radiation exposure to the contralateral breast should be avoided for all patients with early-stage breast cancer.     

Risk for breast cancer among women with endometriosis

Although several risk factors are common to endometriosis and breast cancer, the results of observational studies of an association have so far been inconsistent. We evaluated the relationship between endometriosis and breast cancer on the basis of data on selected cancers and medical histories from the Danish nationwide cancer and hospital registries used in a large case-cohort study. A total of 114,327 women were included in the study of whom 1,978 women had received a diagnosis of endometriosis and 16,983 had had a diagnosis of breast cancer between 1978 and 1998. Of the women with endometriosis, 236 subsequently received a diagnosis of breast cancer. The crude overall rate ratio for breast cancer after endometriosis was 1.00 and after adjustment for reproductive factors, calendar-period, bilateral oophorectomy and benign breast disease, the rate ratio was 0.97 (95% confidence interval, 0.85-1.11). The risk for breast cancer increased with age at diagnosis of endometriosis, so that women in whom endometriosis was diagnosed at a young age (approximately <40 years) had a reduced risk for breast cancer and women in whom endometriosis was diagnosed at older ages (approximately > or =40 years) tended to have an increased risk for breast cancer. The reduced risks observed among young women may reflect their exposure to drugs with antiestrogenic effects. The increased risk associated with endometriosis among postmenopausal women may be due to common risk factors between postmenopausal endometriosis and breast cancer or an altered endogenous estrogen.     

Tumour morphology of early-onset breast cancers predicts breast cancer risk for first-degree relatives: the Australian Breast Cancer Family Registry

ABSTRACT: INTRODUCTION: We hypothesised that breast cancer risk for relatives of women with early-onset breast cancer could be predicted by tumour morphological features. METHODS: We studied female first-degree relatives of a population-based sample of 452 index cases with a first primary invasive breast cancer diagnosed before the age of 40 years. For the index cases, a standardised tumour morphology review had been conducted for all, estrogen (ER) and progesterone receptor (PR) status was available for 401 (89%), and 77 (17%) had a high-risk mutation in a breast cancer susceptibility gene or methylation of the BRCA1 promoter region in peripheral blood. We calculated standardised incidence ratios (SIR) by comparing the number of mothers and sisters with breast cancer to the number expected based on Australian incidence rates specific for age and year of birth. RESULTS: Using Cox proportional hazards modelling, absence of extensive sclerosis, extensive intraductal carcinoma, absence of acinar and glandular growth patterns, and presence of trabecular and lobular growth patterns were independent predictors with between a 1.8 and 3.1-fold increased risk for relatives (all p < 0.02). Excluding index cases with known genetic causes or BRCA1 promoter methylation, absence of extensive sclerosis, circumscribed growth, extensive intraductal carcinoma and lobular growth pattern were independent predictors with between a 2.0 and 3.3-fold increased risk for relatives (all p < 0.02). Relatives of the 128 (34%) index cases with none of these four features were at population risk (SIR = 1.03, 95% CI = 0.57-1.85) while relatives of the 37 (10%) index cases with two or more features were at high risk (SIR = 5.18, 95% CI = 3.22-8.33). CONCLUSIONS: This wide variation in risks for relatives based on tumour characteristics could be of clinical value, help discover new breast cancer susceptibility genes, and be an advance on the current clinical practice of using ER and PR as pathology-based predictors of familial and possibly genetic risks.     

Addressing fear of cancer recurrence among women with cancer: a feasibility and preliminary outcome study

Background

Evidence suggests that fear of cancer recurrence (FCR) is one of the most frequently cited unmet needs among cancer survivors and is associated with psychological distress, stress-response symptoms, and lower quality of life, as well as increased use of health care resources. Despite these factors, few manualized interventions exist to address FCR among cancer survivors.

Purpose

To develop, manualize, and pilot test the feasibility and preliminary efficacy of a 6-week cognitive-existential (CE) group intervention designed to address FCR in women with breast or ovarian cancer.

Methods

This study was a single-arm multi-site study with pre-, post-, and 3-month follow-up measurement occasions.

Results

A total of 56 breast or ovarian cancer survivors enrolled in the study; 44 completed the CE group intervention. Following the intervention, women experienced a reduction in the primary study outcome measure of FCR and secondary study outcome measures of cancer-specific distress and uncertainty. They also reported improvements in secondary study outcome measures of quality of life and coping. The effect sizes of the observed changes were for the most part in the medium to large effect range; furthermore, almost all changes were sustained at 3-month follow-up.

Conclusion

This brief intervention appears feasible and has shown promising results in addressing FCR and related secondary outcomes of cancer-specific distress, uncertainty, quality of life, and coping; however, it should be further tested using a randomized controlled study design to more definitively assess its efficacy.

Implications for Cancer Survivors

FCR is a near-universal worry for cancer survivors that, when left unaddressed, tends to remain stable over time. This study has important implications for all cancer survivors as it is the first published intervention that provides preliminary evidence of its efficacy in decreasing fear of cancer recurrence.     

Risk assessment in first degree female relatives of breast cancer patients using the alkaline Comet assay

First degree female relatives (FDFRs) of breast cancer patients have been reported to have a 2- to 3-fold increase in breast cancer risk as compared with the general population. Assessment of genetic instability (DNA damage and repair efficiency) is an important parameter concerning mutagenesis and carcinogenesis. In an attempt to identify individuals at high risk of breast cancer in the FDFRs of breast cancer patients, two tests were used: the alkaline Comet assay on leucocytes and the micronucleus test (MNT) on buccal epithelial cells. In addition to FDFRs, two other categories of subjects were included: breast cancer patients and controls. The Comet assay was used to study basal DNA damage, DNA susceptibility to a mutagen (N-methyl N-nitro N-nitrosoguanidine) and DNA repair efficiency. In addition, the MNT served as an indicator of chromosome breakage/aneuploidy. A significant increase in DNA damage (basal and after treatment with a mutagen, as well as after allowing repair to take place) and micronucleus frequency was observed from controls to FDFRs and from FDFRs to breast cancer patients. There was considerable variability in the subjects with respect to both of these parameters. Outliers identified among the FDFRs based on 3 SD limits of DNA damage and micronucleus frequency were considered as high risk individuals.     

Familial occurrence of nonmedullary thyroid cancer: a population-based study of 5673 first-degree relatives of thyroid cancer patients from Norway.

The purpose of this study was to estimate the occurrence of familial nonmedullary thyroid cancer (FNMTC) in a large population-based study. Of the 5274 cases of thyroid cancer on record in the Norwegian Cancer Registry between 1960 and 1995, a total of 1025 patients could be identified with verified thyroid cancer, a unique personal identification number, and a link to at least one parent. For patients with nonmedullary carcinoma, 5457 first-degree relatives in 970 families were found, compared with 216 first-degree relatives in 37 families for the medullary cancers. A standardized incidence ratio (SIR) was calculated among the relatives based on rates from the Cancer Registry of Norway. A significantly increased risk of thyroid cancer was found among the 5457 relatives of nonmedullary index cases, both for males [SIR, 5.2; confidence interval (CI), 2.1-10.7; 7 cases] and females (SIR, 4.9; CI, 3.0-7.7; 19 cases). All of these 26 thyroid cancer cases were of the nonmedullary type. Furthermore, an increased risk was found among 4282 relatives of papillary index cases, for both males (SIR, 5.8; CI, 2.1-12.6; 6 cases) and females (SIR, 4.0; CI, 2.1-7.1; 12 cases). The 36 familial papillary thyroid cancer patients had an average age at diagnosis of 43 years. Genetic influence is probably only modest for the familial nonmedullary cases and clearly weaker than for the classic familial type of medullary thyroid cancer.