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PubMed2000

Leads to cancer control based on cancer patterns in a rural population in South India.

OBJECTIVE: Cancer patterns and incidence rates for a rural population (359,674) resident in 384 villages spread over 2058 km2 in Palani and Oddanchathram taluks of Dindigul District, Tamil Nadu, in South India, are described in this paper. METHODS: A population-based cancer registry was established in 1995 to register incident invasive and in-situ cancers. Cases were found and details abstracted by cancer registry staff visiting 26 data sources, comprising cancer hospitals, tertiary and secondary care hospitals, pathology laboratories and death registration offices. A customized version of CANREG-3 software was used for data entry and analysis. RESULTS: During the period 1996-1998, 783 invasive cancers (310 male and 473 females) were registered, yielding an all-cancer crude incidence rate of 56.8/100,000 males and 88.5/100,000 females; the corresponding age standardized incidence rates (ASR) were 83.3 and 122.3 respectively. In males, mouth cancer (ASR 11.5) was the most frequently recorded malignancy followed by tongue (ASR 8.6), hypopharynx (ASR 7.8), esophagus (ASR 7.8) and larynx (ASR 7.8). Thus head and neck cancers accounted for half of the male cases. In females, cervical cancer (ASR 65.4) accounted for more than half of the cancers followed by breast (ASR 14.2) and mouth (ASR 10.2). Ambillikai Cancer Registry (ACR) reports the second highest incidence of cervical cancer in the world. More than four-fifths of cervical cancer cases were diagnosed in stages II B and III B; a third of these cancer patients either did not have, or did not complete, treatment. CONCLUSIONS: The observed cancer patterns in this population establish that measures directed at prevention and early detection (linked with treatment) of cervix and head and neck cancers are of paramount importance for cancer control in this and other rural populations of India where three-fourths of the total population live.

Adolescent↗

PubMed1993

Multiple primary cancers in the Vaud Cancer Registry, Switzerland, 1974-89.

Data collected by the Cancer Registry of the Swiss Canton of Vaud (whose population in 1980 was about 530,000 inhabitants) were used to estimate the incidence of second metachronous primary cancers following any specific neoplasm. Among 34,615 cases of incident neoplasms registered between 1974 and 1989 and followed through integrated active follow-up to the end of 1989, for a total of 118,241 person-years at risk, there were 2,185 second primaries (1,280 males, 905 females). For both sexes, the standardised incidence ratios (SIR) were significantly elevated by about 20%. Overall significantly elevated ratios were registered for cancers of the oral cavity and pharynx (SIR = 1.6 for males, 2.0 for females), oesophagus in males (SIR = 1.5), lung in males (SIR = 1.4), skin melanoma (SIR = 1.7 for males, 1.5 for females), non-melanomatous skin cancers (SIR = 1.6 for males, 1.5 for females), female breast (SIR = 1.3), kidney (SIR = 1.5 for males, 1.9 for females), and thyroid in males (SIR = 2.4). When specific first cancer sites were considered, the SIR following a cancer of the oral cavity and pharynx was around 3 in both sexes, mainly on account of a substantial excess of second primaries of the oral cavity, oesophagus, larynx and lung. The overall SIR following laryngeal cancer was 3.0, and significant excesses were observed for oral cavity and pharynx, oesophagus and lung. After lung cancer, the overall SIR was 1.7 for males and 2.6 for females, and significantly elevated SIRs were observed for oral cavity, lung and oesophagus. Following non-melanomatous skin cancers, elevated SIRs were observed in both sexes for skin melanoma and non-melanomas. The incidence of any cancer after breast cancer was significantly elevated (SIR = 1.2), mainly on account of an elevated risk of subsequent breast cancer (SIR = 1.7). With reference to cervical cancer, there was a significant excess for any subsequent primary (SIR = 1.6), and for lung cancer (SIR = 7.8). Significantly elevated SIRs were observed for kidney following bladder cancer, and for bladder after kidney cancer. In both sexes, the incidence of cancers of any site was elevated following leukaemias (SIR = 1.7 for males, 2.5 for females), and a significant excess was registered for lung in males and non-melanomatous skin cancers in both sexes.(ABSTRACT TRUNCATED AT 400 WORDS)

Female↗

PubMed2004

Role of cancer-associated stromal fibroblasts in metastatic colon cancer to the liver and their expression profiles.

The cancer microenvironment and interaction between cancer and stromal cells play critical roles in tumor development and progression. The molecular features of cancer stroma are less well understood than those of cancer cells. Cancer-associated stromal fibroblasts are the predominant component of stroma associated with colon cancer and its functions remain unclear. Fibroblast cell cultures were established from metastatic colon cancer in liver, liver away from the metastatic lesions, and skin from three patients with metastatic colorectal cancer. We generated expression profiles of cancer-associated fibroblasts using oligochip arrays and compared them to those of uninvolved fibroblasts. The conditioned media from the cancer-associated fibroblast cultures enhanced proliferation of colon cancer cell line HCT116 to a greater extent than cultures from uninvolved fibroblasts. In microarray expression analysis, cancer-associated fibroblasts clustered tightly into one group and skin fibroblasts into another. Approximately 170 of 22,000 genes were up-regulated in cancer-associated fibroblasts (fold change > 2, P < 0.05) as compared to skin fibroblasts, including many genes encoding cell adhesion molecules, growth factors, and COX2. By immunohistochemistry in-vivo, we confirmed COX2 and TGFB2 expression in cancer-associated fibroblasts in metastatic colon cancer. The distinct molecular expression profiles of cancer-associated fibroblasts in colon cancer metastasis support the notion that these fibroblasts form a favorable microenvironment for cancer cells.

Cell Line, Tumor↗

PubMed1993

Detection of preinvasive cancer of the cervix and the subsequent reduction in invasive cancer.

BACKGROUND: Cytologic screening and follow-up can reduce the incidence of cervical cancer by detection and removal of precursor lesions. It is unknown, however, whether differences in histopathologic criteria for these precursor lesions affect the benefit of screening. These criteria may be difficult to study, but they are likely to be reflected in reported incidence of in situ cancer in small areas of Sweden. PURPOSE: Our purpose was to test the hypothesis that the benefit of screening can be predicted by histopathologic criteria as reflected in the reported incidence of cancer in situ. METHODS: Incidence data were from the Swedish National Cancer Registry. Regression models showing the relationship between in situ and invasive cancer were formulated and estimated. Each county (total, 24) was a unit of measurement, and adjustment was made for the incidence of invasive cancer before screening. RESULTS: During population-based screening in Sweden, the incidence of cancer in situ varied about fourfold among the 24 counties, which indicates that the criteria used to diagnose cancer in situ differed markedly. No statistically significant (P < .05) associations were found between the incidence of cancer in situ in 1965, 1970, or 1975 and the reduction in invasive cancer 5, 10, or 15 years later. According to the best-fitting model, detection of 100 extra cases of cancer in situ per 100,000 women per year in 1975 resulted in a reduction of 1.0 (95% confidence interval [CI] = -1.6-3.7) cases of invasive cancer 10 years later. The corresponding best model estimate implied a reduction of 4.6 cases (95% CI = 1.5-7.7) in a model restricted to cancer in situ in patients aged 20-50 years (when organized screening took place), invasive cancer in patients aged 30-60 years, and cancer in situ measured in 1970. CONCLUSIONS: The absent, or at most weak, association between detection of cancer in situ and subsequent reduction in invasive cancer indicates that relaxed histopathologic criteria for cancer in situ may result in extensive, unnecessary treatment of lesions that would regress spontaneously. IMPLICATION: Further studies are urgently needed to enable identification of neoplasms likely to progress to invasive, fatal disease.

Adult↗

PubMed1994

Endometrial cancer in tamoxifen-treated breast cancer patients: findings from the National Surgical Adjuvant Breast and Bowel Project (NSABP) B-14.

BACKGROUND: Tamoxifen is advantageous in treating all stages of breast cancer. However, studies have suggested that incidence and severity of endometrial cancer increase in women treated with tamoxifen. PURPOSE: We compared rates of endometrial and other cancers in tamoxifen- and non-tamoxifen-treated patients and described the pathologic characteristics of the endometrial cancers. METHODS: Data were analyzed on 2843 patients with node-negative, estrogen receptor-positive, invasive breast cancer randomly assigned to placebo or tamoxifen (20 mg/d) and on 1220 tamoxifen-treated patients registered in NSABP B-14 subsequent to randomization. Average time on study is 8 years for randomly assigned patients and 5 years for registered patients. RESULTS: The incidence rates of liver, gastrointestinal, urinary tract, and nonuterine genital tumors were not increased by tamoxifen treatment. Twenty-five endometrial cancers were originally reported, one of which was reclassified after subsequent review. Two cases occurred in the placebo group in patients whose medical status subsequent to random assignment had required tamoxifen treatment. Twenty-three occurred in the tamoxifen groups. Twenty-one of the 24 originally reported endometrial cancers were FIGO stage 1; 18 of 23 gradable cases were of good to moderate histologic grade. Four tamoxifen-treated women died of uterine cancer. The average annual hazard rate of endometrial cancer as a first event within the first 5 years of follow-up in the randomized, tamoxifen-treated group was 1.2/1000 patient-years; the cumulative hazard rate was 6.3/1000. Findings for the registered, tamoxifen-treated group were similar. Including all originally reported endometrial cancers, the annual hazard rate through all follow-up was 0.2/1000 in the placebo group and 1.6/1000 in the randomized, tamoxifen-treated group; the relative risk of endometrial cancer for the latter versus the former group was 7.5. Again for the latter group, using population-based rates of endometrial cancer from SEER data and information from another NSABP (B-06) trial, relative risks were 2.2 and 2.3, respectively. The 5-year cumulative hazard rate for disease-free survival in the randomized tamoxifen group was 38% less than that in the placebo group. Some data in this paper were provided by an investigator who submitted fraudulent data to the NSABP [see the "News" section]; therefore, the reader must read the entire text including Table 10 and the Editor's notes. In brief, data on 182 of the 2843 randomly assigned patients and 37 of the 1220 registered patients were provided by the investigator in question. After review, 24 of the 182 records showed falsification, all involving characteristics of patients prior to random assignment. Of the 37 registered-patient records, 8 showed falsification. CONCLUSIONS: Risk of endometrial cancer increases following tamoxifen therapy for invasive breast cancer; however, net benefit greatly outweighs risk. Endometrial cancers occurring after tamoxifen therapy do not appear to be of a different type with a worse prognosis than are such tumors in non-tamoxifen-treated patients. IMPLICATIONS: Tamoxifen treatment for breast cancer should continue. In addition, the relative risk of endometrial cancer observed in B-14 tamoxifen-treated patients is consistent with the twofold relative risk used in the initial risk-benefit computation for the NSABP breast cancer prevention trial.

Adult↗

PubMed2000

Causes of death in elderly prostate cancer patients and in a comparison nonprostate cancer cohort.

BACKGROUND: Prostate cancer tends to affect older men and to progress relatively slowly. Since the prevalence of comorbidity increases with advancing age, competing causes of death are important contributors to death rates among prostate cancer patients. Accurate determination of the underlying causes of death in older men dying with prostate cancer may thus also be more difficult. METHODS: We compared the distribution of underlying causes of death in decedents from a population-based cohort of elderly prostate cancer patients to that from a population-based comparison cohort of elderly men without prostate cancer. Among decedents from the prostate cancer patient cohort, we examined associations of patient demographics, disease stage, and initial treatment, with assignment of a prostate cancer underlying cause of death (versus any other cause) by use of multivariable logistic regression. In the subgroup of prostate cancer patient decedents having underlying causes of death other than prostate cancer, the underlying cause distribution was compared with that in nonprostate cancer cohort decedents. RESULTS: Prostate cancer was the underlying cause for 39% (95% confidence interval [CI] = 36.3-41.9) of the decedents in the prostate cancer cohort. Causes of death among prostate cancer patients not dying of prostate cancer were similar to those among the nonprostate cancer cohort decedents. However, in those who were aggressively treated, the adjusted odds of other cancer causes of death were 51% higher (odds ratio [OR] = 1.51; 95% CI = 1.08-2.10) than that in nonprostate cancer patient decedents, while in those treated with watchful waiting the adjusted odds were 34% lower (OR = 0.66; 95% CI = 0.47-0.93). CONCLUSIONS: Initial treatment may influence the underlying cause of death reported in vital statistics for prostate cancer patients.

Aged↗

PubMed2002

Changing area socioeconomic patterns in U.S. cancer mortality, 1950-1998: Part II--Lung and colorectal cancers.

BACKGROUND: Lung cancer and colorectal cancer are leading causes of U.S. cancer mortality. Because mortality rates for many cancers vary by socioeconomic characteristics, we used area socioeconomic indices to examine patterns in U.S. lung and colorectal cancer mortality between 1950 and 1998. METHODS: A factor-based area socioeconomic index was linked to 1950-1998 county mortality data to generate annual lung and colorectal cancer mortality rates for each area socioeconomic group. Joinpoint regression analysis was used to model and identify statistically significant changes in the mortality trends. RESULTS: Area socioeconomic patterns in U.S. lung cancer mortality changed dramatically between 1950 and 1998. Men aged 25-64 years and those aged 65 years or older in higher socioeconomic areas generally had higher lung cancer mortality than did those in lower socioeconomic areas during 1950-1964 and 1950-1980, respectively. Area socioeconomic differences in lung cancer mortality began to reverse and widen by the early 1970s for younger men and by the mid-1980s for older men. In 1998, lung cancer mortality was 56% (95% confidence interval [CI] = 49% to 64%) higher for younger men and 38% higher (95% CI = 34% to 43%) for older men in the lowest area socioeconomic group than for the same age groups in the highest area socioeconomic group. Lung cancer mortality among older women in all socioeconomic groups increased sevenfold to eightfold between 1950 and 1998, with higher mortality in higher area socioeconomic groups. The positive socioeconomic gradient in colorectal cancer mortality diminished substantially over time. Although colorectal cancer mortality among women in all area socioeconomic groups showed a consistent downward trend, colorectal cancer mortality among men in low area socioeconomic groups, but not in high area socioeconomic groups, showed an upward trend. CONCLUSIONS: Socioeconomic gradients in male lung cancer mortality reversed between 1950 and 1998, and those in colorectal cancer mortality narrowed over that time. Area measures may be useful for monitoring socioeconomic disparities in cancer mortality and for identifying areas for potential cancer control interventions.

Adult↗

PubMed1998

Validity of self-reported cancers in a prospective cohort study in comparison with data from state cancer registries.

The accuracy of self-reported cancer diagnoses in a prospective study was compared with population-based cancer registry data in four states. The study cohort included 65,582 men and women aged 39-96 years who were participants in the Cancer Prevention Study II Nutrition Survey, begun by the American Cancer Society in 1992. Estimates of sensitivity (the proportion of study participants with a registry-documented cancer who self-reported the cancer) ranged from 0.79 for an exact match of cancer site and year of diagnosis (+/- 1 year) to 0.93 for a match of any reported cancer. The sensitivity of exact matches varied considerably by cancer site and was highest for breast, prostate, and lung cancers (0.91, 0.90, and 0.90, respectively) and lowest for rectal cancer and melanoma (0.16 and 0.53, respectively). Sensitivity also varied slightly by the age, education, and smoking status of study participants. Estimates of sensitivity were virtually identical for each of the four states. The positive predictive value (the proportion of self-reported cancers that were confirmed by the registries) was 0.75 overall and also varied by cancer site. Unlike sensitivity, however, this proportion varied considerably by state. All self-reports of cancer that were not confirmed by the registries were further investigated by repeat questionnaires and acquisition of medical records. Low positive predictive values were due to underascertainment of true cancer cases by the registries, inaccurate reporting on the part of study participants, and problems with the algorithm used by the state to link the study population to the registry data. In conclusion, the ability of members of this cohort to report a past diagnosis of cancer accurately is quite high, especially for cancers of the breast, prostate, lung, and colon, or for the occurrence of any cancer.

Aged↗

PubMed1999

The association between biliary tract cancers and cancers of other sites.

OBJECTIVE: Cancers of the biliary tract, including cancers of the gallbladder and bile duct, generally carry a very poor prognosis. Little is known about their etiology. The pattern of co-occurrence of two cancers may give clues to shared etiological risk factors. We therefore investigated the association of biliary tract cancer with other cancers, especially with estrogen- and tobacco-related cancers. METHODS: We used data from the Surveillance, Epidemiology, and End Results Program of the National Cancer Institute. Associations between biliary tract cancer and other cancers were evaluated using the standardized incidence ratio as an estimate of the relative risk of a second primary malignancy. RESULTS: Estrogen-related cancers of the breast and uterine corpus and smoking-related upper aerodigestive tract cancers were not associated with biliary tract cancer. The risk of gallbladder cancer was inversely related to the risk of prostate cancer in men, but positively related to the risk of cervical cancer in women. CONCLUSIONS: This study suggests that smoking and estrogen exposure have minimal roles in the pathogenesis of biliary tract cancer. Our finding of an inverse relationship between prostate cancer and gallbladder cancer requires confirmation by further studies.

Adult↗

PubMed2002

All-cause mortality among breast cancer patients in a screening trial: support for breast cancer mortality as an end point.

BACKGROUND: It has recently been suggested that all-cause mortality is a more appropriate end point than disease specific mortality in cancer screening trials, and that disease specific mortality is biased in favour of screening. This suggestion is based partly on supposed inconsistencies between all-cause mortality results and disease specific results in cancer screening trials, and alleged increases in deaths from causes other than breast cancer among breast cancer cases diagnosed among women invited to screening. METHODS: We used data from the Swedish Two-County Trial of mammographic screening for breast cancer, in which 77 080 women were randomised to an invitation to screening and 55 985 to no invitation. We estimated relative risks (RRs) (invited v control) of death from breast cancer, death from other causes within the breast cancer cases, and death from all causes within the breast cancer cases. RRs were adjusted for age and took account of the longer follow up of breast cancer cases in the invited group due to lead time. RESULTS: There was a significant 31% reduction in breast cancer mortality in the invited group (RR 0.69, 95% confidence interval (CI) 0.58-0.80; p<0.001). There was no significant increase in deaths from other causes among breast cancer cases in the invited group (RR 1.12, 95% CI 0.96-1.31; p=0.14). A significant 19% reduction in deaths from all causes was observed among breast cancer cases in the group invited to screening (RR 0.81, 95% CI 0.72-0.90; p<0.001). A more conservative estimation gave a significant 13% reduction (RR 0.87, 95% CI 0.78-0.97; p=0.01). These findings are consistent with the magnitude of the reduction in breast cancer mortality. CONCLUSIONS: Invitation to screening was associated with a reduction in deaths from all causes among breast cancer cases, consistent with high participation rates in screening. There is no significant evidence of bias in cause of death classification in the Two-County Trial, and as breast cancer mortality is the targeted clinical outcome in breast cancer screening, it is the appropriate end point in a breast cancer screening trial. All-cause mortality is a poor and inefficient surrogate for breast cancer mortality.

Adult↗

PubMed2005

Influence of review design on percentages of missed interval breast cancers: retrospective study of interval cancers in a population-based screening program.

PURPOSE: To retrospectively investigate whether different review designs have an influence on the estimate of missed interval cancer in a population-based breast cancer screening program. MATERIALS AND METHODS: The Norwegian Breast Cancer Screening Program invites women aged 50-69 years to undergo biennial screening mammography. The current study was part of the evaluation and scientific aspects of the screening program and thus was covered by the general ethical approval of the screening program as a part of the Cancer Registry of Norway. All participants signed an informed consent that specified that data related to their screening visit could be used for evaluation and scientific purposes. Six radiologists (9-34 years of experience in mammography) reviewed previously obtained bilateral two-view screening and diagnostic mammograms of 231 interval cancers, 117 screening-detected cancers, and 373 normal cases. Four review designs were used: individual and paired blinded review and individual and consensus informed review. A five-point interpretation scale was used to reclassify the cancers into missed cancers, minimal signs, and true cancers. The number and proportion of subgroups were estimated with 95% confidence intervals. RESULTS: Of 231 interval cancers, 46 (19.9%) were reclassified as missed cancers with the mixed blinded individual review and 54 (23.4%) were classified as missed cancers with the mixed blinded paired review. Eighty-three cancers (35.9%) were classified as missed cancers with individual informed review, and 78 (33.8%) were classified as missed cancers with consensus informed review. Thirty-nine cancers (16.8%) were reclassified as missed when four or more radiologists assigned a score of 2 or more (probably benign or more suspicious); three cancers (1.3%) were reclassified as missed when a score of 4 or more (probably malignant or more suspicious) was assigned. CONCLUSION: The percentage of interval cancers classified as missed ranged from 1.3% to 35.9% according to review design. To encourage learning, a review protocol should include both blinded and informed designs.

Aged↗

PubMed2006

Distal colorectal cancers with microsatellite instability (MSI) display distinct gene expression profiles that are different from proximal MSI cancers.

Promoter methylation of the mismatch repair gene plays a key role in sporadic microsatellite instability (MSI) colorectal cancers. However, promoter methylation often occurs in proximal colon cancers, and molecular phenotypes underlying MSI cancers in distal colon have not been fully clarified. Our goal was to clarify the difference between MSI and microsatellite stability (MSS) cancers and, furthermore, to determine distinct characteristics of proximal and distal MSI cancers. By DNA microarray analysis of 84 cancers (33 MSI and 51 MSS), we identified discriminating genes (177 probe sets), which predicted MSI status with a high accuracy rate (97.6%). These genes were related to phenotypic characteristics of MSI cancers. Next, we identified 24 probe sets that were differentially expressed in proximal and distal MSI cancers. These genes included promoter methylation-mediated genes, whose expression was significantly down-regulated in proximal MSI cancers. Among discriminating genes between MSI and MSS, nine methylation-mediated genes showed down-regulation in MSI cancers. Of these, 7 (77.8%) showed down-regulation in proximal MSI cancers. Furthermore, methylation-specific PCR confirmed that frequency of hMLH1 promoter methylation was significantly higher in proximal MSI cancers (P = 0.0317). These results suggested that there is a difference between proximal and distal MSI cancers in methylation-mediated influence on gene silencing. In conclusion, using DNA microarray, we could distinguish MSI and MSS cancers. We also showed distinct characteristics of proximal and distal MSI cancers. The inactivation form of hMLH, per se, differed between proximal and distal MSI cancers. These results suggested that distal MSI cancers constitute a distinct subgroup of sporadic MSI cancers.

Adaptor Proteins, Signal Transducing↗

PubMed2006

A novel cancer testis antigen that is frequently expressed in pancreatic, lung, and endometrial cancers.

PURPOSE: To isolate cancer testis antigens that are expressed in pancreatic cancers and may be useful in clinical applications. EXPERIMENTAL DESIGN: To efficiently isolate cancer testis antigens, a testis cDNA library was immunoscreened (SEREX) with serum from a patient with pancreatic ductal adenocarcinoma. The expression of isolated antigens in various cancer cell lines and tissues was evaluated by reverse transcription-PCR and Northern blot analyses. The immunogenicity of the antigen in cancer patients was evaluated by detection of the IgG antibody in sera from patients with various cancers. RESULTS: Of the three clones isolated through screening of a total of 2 x 10(6) cDNA library clones, one clone (KU-CT-1) was found to be expressed in various cancers but only in testis among normal tissues, indicating that it was a novel cancer testis antigen. The KU-CT-1 gene is located on chromosome 10p12 and produces two splice variants, which encode proteins of 397 and 872 amino acids, respectively. KU-CT-1 was expressed in pancreatic cancer tissues (3 of 9, 33%), lung cancer tissues (9 of 24, 38%), and endometrial cancer tissues (7 of 11, 64%). Specific serum IgG antibodies were detected in 3 of 20 pancreatic cancer patients, 2 of 12 endometrial cancer patients, 1 of 18 colon cancer patients, and 1 of 10 prostate cancer patients but not detected in 30 healthy individuals. CONCLUSIONS: KU-CT-1 is a new cancer testis antigen that is expressed in pancreatic, lung, and endometrial cancers and may be useful for diagnosis and immunotherapy for patients with various cancers.

Amino Acid Sequence↗

PubMed2003

Features of second primary cancer in patients with gastric cancer.

BACKGROUND: In order to improve the prognosis of gastric cancer patients, the timely identification of second primary cancers is considered to be a crucial clinical problem. METHODS: We analyzed the clinicopathological data of 2250 patients with gastric cancer with regard to both synchronous and metachronous second primary cancers. RESULTS: Of 2250 patients, 95 (4.2%) had a second primary cancer. Both colorectal and lung cancer were frequently detected, followed by cancer in the liver, esophagus and breast. Regarding the time of detection for such second cancers, 65% of colorectal cancers were detected synchronously, while more than 80% of lung cancers were detected metachronously. The prognosis of gastric cancer patients with a second primary cancer was more negatively influenced by a second primary cancer than by a primary gastric cancer. CONCLUSION: Since gastric cancer patients may develop synchronous and metachronous second cancers in other organs, effective preoperative and postoperative diagnostic modalities both for second primary cancers, as well as for the recurrence of gastric cancer, need to be developed.

Aged↗

PubMed2006

Identifying related cancer types based on their incidence among people with multiple cancers.

BACKGROUND: There are several reasons that someone might be diagnosed with more than one primary cancer. The aim of this analysis was to determine combinations of cancer types that occur more often than expected. The expected values in previous analyses are based on age-and-gender-adjusted risks in the population. However, if cancer in people with multiple primaries is somehow different than cancer in people with a single primary, then the expected numbers should not be based on all diagnoses in the population. METHODS: In people with two or more cancer types, the probability that a specific type is diagnosed was determined as the number of diagnoses for that cancer type divided by the total number of cancer diagnoses. If two types of cancer occur independently of one another, then the probability that someone will develop both cancers by chance is the product of the individual probabilities for each type. The expected number of people with both cancers is the number of people at risk multiplied by the separate probabilities for each cancer. We performed the analysis on records of cancer diagnoses in British Columbia, Canada between 1970 and 2004. RESULTS: There were 28,159 people with records of multiple primary cancers between 1970 and 2004, including 1,492 people with between three and seven diagnoses. Among both men and women, the combinations of esophageal cancer with melanoma, and kidney cancer with oral cancer, are observed more than twice as often as expected. CONCLUSION: Our analysis suggests there are several pairs of primary cancers that might be related by a shared etiological factor. We think that our method is more appropriate than others when multiple diagnoses of primary cancer are unlikely to be the result of therapeutic or diagnostic procedures.

Journal Article↗

PubMed2005

Breast cancer and ovarian cancer genetics.

Breast and ovarian cancers are the second and fifth leading causes of cancer death, respectively, among women in the United States. Individuals with breast cancer have a 20--30% chance of having at least one relative with the disease. However, only 5--10% of the cases are a direct result of germline mutations in highly penetrable genes, such as BRCA1 and BRCA2 (BRCA1/2) as well as genes TP53 and PTEN. Since 1996, genetic testing for these mutations has been clinically available. A strategy for the management of women at increased familial risk of breast and ovarian cancers is described, which includes genetic assessment, chemoprevention, radiologic screening, and clinical and self-examination. Genetic testing should occur within a cancer genetic clinic after genetic counseling. A blood sample allows determination of the presence of the BRCA1 and BRCA2 genes, the TP53 gene, the PTEN gene, and the ATM gene. Tumor examination has identified a growth factor receptor gene, human epidermal growth factor receptor (HER-2). With regard to diet and lifestyle, women at increased risk of breast cancer could be advised to reduce dietary fat, avoid obesity, decrease alcohol consumption, and take regular exercise. Although chemoprotection is a valuable consideration, it is important to emphasize that the use of Tamoxifen in BRCA1 and BRCA2 mutation carriers is not established, nor is the optimum duration of benefit. An overview of the main outcomes of the current published studies confirms a 38% decrease in breast cancer incidence with Tamoxifen but recommends its use be restricted to women at high risk of breast cancer and low risk for potential side effects. The role of bilateral risk-reducing mastectomy or prophylactic mastectomy has been controversial for several reasons, including the psychosocial significance of the breast in Western cultures, the wide acceptance of breast conservation in surgery for early breast cancer, and the previous lack of data on its efficacy. The surgical procedure should aim to remove substantially all at-risk breast tissue. However, there is a balance between reduction of cancer risk and cosmetic outcome. Bilateral prophylactic oophorectomy can significantly decrease ovarian cancer risk in women who carry BCRA1 mutations. Oophorectomy lowers the risk of breast cancer, even in women who have previously used hormone replacement therapy. There are no published randomized controlled trials examining the effectiveness of mammographic screening in women under 50 years of age with a family history of breast cancer. However, the published studies do suggest that mammographic screening of a high-risk group of women under 50 years of age may detect cancer at a rate equivalent to that seen in women 10 years older with normal risk. Other initial studies also support MRI as having a greater sensitivity than mammography in high-risk women. Breast clinical and self-examination is often advocated, but its effectiveness is unproved, and only one randomized study has been undertaken in women at risk. On the basis of this study as well as one nonrandomized study, it can be concluded that clinical examination as well as mammography are essential in detecting breast cancer. under 50 years of age with a family history of breast cancer. However, the published studies do suggest that mammographic screening of a high-risk group of women under 50 years of age may detect cancer at a rate equivalent to that seen in women 10 years older with normal risk. Other initial studies also support MRI as having a greater sensitivity than mammography in high-risk women. Breast clinical and self-examination is often advocated, but its effectiveness is unproved, and only one randomized study has been undertaken in women at risk. On the basis of this study as well as one nonrandomized study, it can be concluded that clinical examination as well as mammography are essential in detecting breast cancer.

Breast Neoplasms↗

PubMed2001

Impact of cancer predisposition and radiosensitivity on the population risk of radiation-induced cancers.

This paper provides a brief overview of the current evidence for cancer predisposition and for an increased sensitivity of individuals carrying such predisposing mutations to cancers induced by ionizing radiations. We also discuss the use of a Mendelian one-locus, two-allele autosomal dominant model for predicting the impact of cancer predisposition and increased radiosensitivity on the risk of radiation-induced cancers in the population and in relatives of affected individuals using breast cancer due to BRCA1 mutations as an example. The main conclusions are the following: (1) The relative risk ratio of the risks of radiation-induced cancer in a heterogeneous population which has subgroups of normal and cancer-predisposed individuals to the risks in a homogeneous population (i.e., one which does not have these subgroups) increases with increasing dose; however, the dose dependence of the RR decreases at higher doses because of the fact that at high doses, the radiation risk to a homogeneous population will already be high. (2) The attributable risk (the proportion of cancers attributable to increased cancer susceptibility and increased radiosensitivity) follows a similar pattern. (3) When the proportion of cancers due to the susceptible genotypes is small (< 10%), as is likely to be the case for breast cancers in non-Ashkenazi Jewish women, the increases in risk ratios and attributable risks are small, and become marked only when there are very large increases in cancer susceptibility (> 1000-fold) and radiosensitivity (> 100-fold) in the susceptible group. (4) When the proportion of cancers due to the susceptible genotypes is appreciable (> or = 10%), as may be the case for breast cancers in Ashkenazi Jewish women, there may be significant increases in the risk ratios and attributable risk for comparatively moderate increases in cancer susceptibility (> 10-fold) and radiosensitivity (> 100-fold) in the susceptible subpopulation. (5) The ratio of the risk of radiation-induced cancer in relatives to that in unrelated individuals in the population increases with the biological relatedness of the relative, being higher for close than for distant relatives; however, even when the mutant BRCA1 gene frequency and the proportion of breast cancers due to these mutations are high, as in Ashkenazi Jewish women, for values of predisposition strength and radiosensitivity differential < 10, the increase in breast cancer risks is only marginal, even for first-degree relatives.

Alleles↗

PubMedDate not supplied

Twenty-year follow-up of the breast cancers diagnosed during the Breast Cancer Detection Demonstration Project.

This study reports on the 20-year follow-up of the women diagnosed with breast cancer in the Breast Cancer Detection Demonstration Project (BCDDP) between 1973 and 1980. This project provided 5 years of screening with physical examination and two-view mammography for 280,000 volunteer women across the United States. Based on a 96% follow-up from 1993 to 1995 of the 4,051 women with breast cancer available for analysis, 2,658 (66%) were alive and 1,393 (34%) were dead. A high proportion of the cancers were detected by mammography alone, and 28.6% of all the cancers were smaller than 1.0 cm. Survival rates were calculated by life table method with deaths from breast cancer as the outcome. The adjusted survival rate for the entire group was 80.5%, and the observed survival rate was 61.7%. Adjusted and observed survival rates were 97.2% and 78.5%, respectively, for women with non-invasive cancers and 78.2% and 59.3%, respectively, for those with invasive cancers. Lymph node status and the size of the cancer at diagnosis were prognostic indicators of survival in the BCDDP Women with invasive cancers and negative lymph nodes had an 85.5% breast cancer survival rate and a 65.6% observed survival rate. Adjusted survival rates for women with invasive breast cancers were 90.2% for cancers smaller than 1 cm, 80.5%, for cancers 1.0 to 1.9 cm, 70.5% for cancers 2.0 to 4.9 cm, and 60.6% for cancers larger than 5 cm. Women 40 to 49 years of age demonstrated a greater survival with noninvasive or invasive cancers smaller than 5.0 cm compared with women 50 to 59 and 60 to 69 years of age at diagnosis. These results from the BCDDP are discussed in the context of the recent decline in breast cancer incidence and mortality in the United States.

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