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PubMed2006

Breast cancer risk factors and second primary malignancies among women with breast cancer.

PURPOSE: To examine the association between breast cancer risk factors and second primary cancers (independent diagnoses occurring at least 12 months after the initial breast cancer diagnosis) among breast cancer survivors. METHODS: In this population-based study, cancer outcomes among breast cancer survivors first diagnosed during 1987-2000 were investigated. Invasive breast cancer cases were identified from the statewide tumor registry and interviewed regarding their pre-diagnosis risk factors, including reproductive and lifestyle characteristics, approximately 1 year after diagnosis. Data on second primary cancers (not recurrences) and deaths were obtained by linkage with tumor registry reports and death certificates through December 31, 2002. Hazard ratios (HR) were estimated using proportional hazards regression stratified by age and adjusted for stage and other factors. RESULTS: Among the 10,953 breast cancer cases, 10.8% experienced a second cancer diagnosis within an average of 7 years (including 488 breast, 132 colorectal, 113 endometrial, and 36 ovarian cancers). Risk of a second primary breast cancer increased according to low parity (P = 0.002), older age at menopause (P = 0.08), greater body mass index (P = 0.003) and adult weight gain (P = 0.02), and a family history of breast cancer-particularly among women with 2 or more first-degree affected relatives (HR = 1.8, 95% CI: 1.1-2.9). Reduced risk of colorectal cancer after breast cancer was observed in relation to older ages at menarche (P = 0.05), younger age at menopause (P = 0.04), postmenopausal hormone use (HR = 0.4, 95% CI: 0.3-0.7), normal body mass index (P = 0.07), and infrequent alcohol consumption (P = 0.01). Second endometrial cancer risk was associated with increasing body mass index (P < 0.01) and adult weight gain (P = 0.03). Risk of second ovarian cancer appeared related to recent alcohol intake and family history of breast cancer. Women who reported consuming any alcohol appeared to have a 55% reduction in ovarian cancer risk (95% CI: 0.2-1.0) compared to non-drinkers, while having 2 or more first-degree relatives with breast cancer was associated with an increased risk of ovarian cancer (HR = 4.3, 95% CI: 1.3-14.6). CONCLUSION: This study suggests that family history of breast cancer as well as potentially modifiable characteristics including body weight, alcohol intake, and postmenopausal hormone use may be associated with risk of a second cancer diagnosis among breast cancer cases.

Adolescent↗

PubMed2002

Are deaths within 1 month of cancer-directed surgery attributed to cancer?

BACKGROUND: Cancer mortality should include not only deaths from cancer but also deaths from cancer treatment. By convention, deaths within 30 days of a surgical procedure are considered treatment-related deaths in the calculation of operative mortality-that is, the chance of dying from surgery. How cause of death is attributed in patients who die within 1 month of cancer-directed surgery is unknown. METHODS: The National Cancer Institute's Surveillance, Epidemiology, and End Results (SEER) program data from 1994 through 1998 were used to examine the cause of death in patients diagnosed with one of 19 common solid tumors who had died within 1 month of diagnosis and had also received cancer-directed surgery. We determined the proportion of deaths not attributed to the cancer and the magnitude of the undercount in cancer-specific mortality. RESULTS: Among 4135 patients with only one cancer who died within 1 month of diagnosis and cancer-directed surgery, the proportion of deaths not attributed to the coded cancer was 41% (1714/4135), ranging from 13% (1/8) for cervical cancer to 81% (13/16) for laryngeal cancer. Selected intermediate values include 25% (14/56) for esophageal cancer, 34% (177/525) for lung cancer, 42% (719/1695) for colorectal cancer, 59% (110/186) for breast cancer, and 75% (80/106) for prostate cancer. Restricting the analysis to deaths following specific major procedures (e.g., esophagectomy, pneumonectomy, colectomy) had little effect on the findings. If all deaths within 1 month of cancer-directed surgery were attributed to cancer, cancer mortality would rise about 1%. CONCLUSION: Some deaths that are conventionally attributed to surgery are not being attributed to the cancer for which the surgery was performed. Although the estimated effect of this misclassification on overall cancer mortality is modest, it may be indicative of more widespread confusion about how to code treatment-related deaths of patients with cancer.

Databases as Topic↗

PubMed1999

Risk for colorectal cancer after gynecologic cancer.

BACKGROUND: Studies have suggested that women with previous diagnoses of gynecologic cancer (cervical, endometrial, or ovarian) have an increased risk for colorectal cancer. OBJECTIVE: To quantify risk for colorectal cancer after gynecologic cancer, both overall and for subgroups defined by age at diagnosis, cancer stage at diagnosis, ethnicity, and duration of follow-up. DESIGN: Retrospective cohort analysis of the Surveillance, Epidemiology, and End Results (SEER) program database from 1974 through 1995. SETTING: U.S. cancer registry. PATIENTS: 21,222 patients with cervical cancer, 51,680 patients with endometrial cancer, and 28,832 patients with ovarian cancer. MEASUREMENTS: Standardized incidence ratios (SIRs) were calculated for each gynecologic cancer site and for subgroups to represent the relative risk for colorectal cancer in women with previously diagnosed gynecologic cancer compared with women without gynecologic cancer. Poisson regression methods adjusting simultaneously for all study variables were used to estimate relative risks for colorectal cancer across subgroups with each gynecologic cancer. RESULTS: Overall, risk for colorectal cancer was elevated among women with previous ovarian cancer (SIR, 1.36 [95% CI, 1.21 to 1.53]). Risk was greatest in women who received a diagnosis before 50 years of age (SIR, 3.67 [CI, 2.74 to 4.80]) but was also elevated in women who received a diagnosis between 50 and 64 years of age (SIR, 1.52 [CI, 1.25 to 1.83]). The risk for colorectal cancer after endometrial cancer was also elevated substantially if endometrial cancer was diagnosed before the age of 50 (SIR, 3.39 [CI, 2.73 to 4.17]). No apparent risk elevation was associated with previous cervical cancer. CONCLUSIONS: Previous endometrial or ovarian cancer, particularly when diagnosed at an early age, increases subsequent risk for colorectal cancer. Greater emphasis on colorectal cancer screening in these populations may be necessary.

Adult↗

PubMed2003

Risk for smoking-related cancer among relatives of lung cancer patients.

Studies of familial aggregation of cancer provide indirect evidence for the role of genetic predisposition to cancer. In an ongoing case-control study, we evaluated whether first-degree relatives of lung cancer cases are at increased risk of lung and other cancers. Smoking-related cancers were defined as cancers of the lung, bladder, head and neck, kidney, and pancreas. The 806 probands included in this analysis were patients referred to The University of Texas M. D. Anderson Cancer Center (Houston, TX). We identified 663 controls, matched to the cases on age (+/-5 years), sex, ethnicity, and smoking history, who were recruited from a local multispecialty physician practice in the Houston metropolitan area. Self-reported cancer family history data were available for 6430 first-degree relatives of the cases and 4936 first-degree relatives of the controls. An excess of cancer in relatives was evaluated by comparing the observed cancer cases among relatives of the cases with relatives of the controls. We conducted further analysis after stratifying on age of lung cancer onset (age at study registration for controls) and smoking status (never, former, or current) of the probands. We also conducted Cox regression analysis and compared time to cancer diagnosis among the relatives of the cases and controls adjusted for age and smoking status of proband and family members. Siblings [relative risk (RR) = 1.85; P = 0.003] of cases had a significant excess of lung cancer and an excess of smoking-related cancers (RR = 1.29; P = 0.01). We observed evidence of familial aggregation (RR = 1.71; P < 0.001) of lung cancer among relatives of late-onset lung cancer cases. From the Cox regression, we observed a moderate risk for development of lung (RR = 1.25; P = 0.09) and other smoking-related cancers (RR = 1.23; P = 0.05). After adjustment for smoking behavior of probands and their relatives, the risks of lung cancer (RR = 1.33; P = 0.03) and smoking-related cancers (RR = 1.28; P = 0.02) were statistically significant. We further stratified on age at onset and observed no evidence (P = 0.81) of familial aggregation of lung cancer among young onset (<or=55 years of age) lung cancer cases. We also did not observe evidence of familial aggregation (P = 0.88) of smoking-related cancers in the same group. There was no evidence of increased risk (P = 0.77) of lung cancer among relatives of never-smokers. These findings support the need for additional study in the characterization and identification of genetic factors that influence and modulate cancer susceptibility in humans.

Adult↗

PubMed2006

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.

Adult↗

PubMed1995

Impact of family history of colon cancer on development of multiple primaries after diagnosis of colon cancer.

PURPOSE: The purpose of this study was to assess risk of developing multiple primaries after a diagnosis of colon cancer and to determine the impact that having a family history of cancer has on cancer risk. METHODS: Data from the Utah Cancer Registry and the Utah Population Database were used. A cohort of 2,236 first primary colon cancers were observed for the subsequent development of additional primary cancers. RESULTS: We observed a greater than expected incidence of colon, rectal, and pancreatic cancers among the cohort. The standardized incidence ratios were 2.77 (95 percent confidence interval (CI), 2.07-3.70), 2.26 (95 percent CI, 1.34-3.81), and 2.38 (95 percent CI, 1.32-4.30), respectively. Having a family history of colon or rectal cancer did not greatly influence risk of having a multiple primary. However, there was a trend toward increased risk of pancreatic cancer (hazard rate ratios, 1.99; 95 percent CI, 0.67-5.90) and bladder cancer (hazard rate ratios, 2.35; 95 percent CI, 0.77-7.18) among patients with a family history of rectal cancer. We also observed that risk of uterine cancer in the cohort was positively associated with family history of uterine cancer, risk of breast cancer was positively associated with family history of breast cancer, and risk of prostate cancer was positively associated with family history of prostate cancer. CONCLUSIONS: People with colon cancer are at a greater risk of developing colon, rectal, and possibly pancreatic cancer. Although a family history of colon or rectal cancer did not have a large impact on developing other cancers, a family history of other primary cancers did influence risk of other cancers.

Aged↗

PubMed2000

Multiple primary breast and thyroid cancers: role of age at diagnosis and cancer treatments (United States).

BACKGROUND: Breast and thyroid cancer have been observed to occur more frequently than expected as multiple primary tumors in women. The study presented herein focuses on the effects of age at diagnosis and treatment for the first cancer on the development of the second cancer. METHODS: This retrospective cohort study used a study population consisting of 38,632 women diagnosed with primary invasive breast cancer and 2189 women diagnosed with primary invasive thyroid cancer between 1974 and 1994. Cases were identified from records of the Cancer Surveillance System of western Washington and followed for subsequent cancer development through 1995. RESULTS: Seventy-one women were diagnosed during their lives with both breast and thyroid cancers. Including cancers diagnosed during the same month as or after the initial cancer, the relative risk (RR) of breast cancer among women with thyroid cancer was 1.5 (95% confidence interval [CI] 1.1-2.0), and the RR of thyroid cancer among women with breast cancer was 1.5 (95% CI 1.1-2.2). Among women with thyroid cancer, risk of breast cancer was greatest when the latter cancer was diagnosed under 45 years of age (RR = 2.3, 95% CI 1.1-4.4). First course of treatment, including radiation or hormonal therapy to treat thyroid cancer, and radiation, chemotherapy, or hormonal therapy to treat breast cancer, did not alter a woman's risk of developing the second cancer. CONCLUSIONS: The data suggest that the incidence of breast and thyroid cancer may be related, and that in particular women with thyroid cancer may be at a moderately increased risk of developing breast cancer before age 45.

Adult↗

PubMed1999

Cancer risk in close relatives of women with early-onset breast cancer--a population-based incidence study.

Inherited susceptibility to breast cancer is associated with an early onset and bilateral disease. The extent of familial risks has not, however, been fully assessed in population-based incidence studies. The purpose of the study was to quantify the risks for cancers of the breast, ovary and other sites of close relatives of women in whom breast cancer was diagnosed at an early age. Records collected between 1943 and 1990 at the Danish Cancer Registry were searched, and 2860 women were found in whom breast cancer was diagnosed before age 40. Population registers and parish records were used to identify 14 973 parents, siblings and offspring of these women. Cancer occurrence through to 31 December 1993 was determined within the Cancer Registry's files and compared with national incidence rates. Women with early-onset breast cancer were at a nearly fourfold increased risk of developing a new cancer later in life (268 observed vs. 68.9 expected). The excess risk was most evident for second cancer of the breast (181 vs. 24.5) and for ovarian cancer (20 vs. 3.3). For mothers and sisters, risks for cancers of the breast and ovary were significantly increased by two- to threefold. Bilateral breast cancer and breast-ovarian cancer were very strong predictors of familial risks, with one in four female relatives predicted to develop breast and/or ovarian cancer by age 75. Mothers had a slightly increased risk of colon cancer, but not endometrial cancer. The risk for breast cancer was also increased among fathers (standardized incidence ratio 2.5; 95% CI 0.5-7.4) and especially brothers (29; 7.7-74), although based on small numbers. The risk for prostatic cancer was unremarkable. In this large population-based survey, the first-degree relatives of women who developed breast cancer before age 40 were prone to ovarian cancer as well as male and female breast cancer, but not other tumours that may share susceptibility genes with breast cancer.

Adult↗

PubMed1996

Radiotherapy, alkylating agents, and risk of bone cancer after childhood cancer.

BACKGROUND: Individuals who had cancer in childhood are at higher risk of developing bone cancer than any other type of second primary cancer. PURPOSE: Using the population-based National Registry of Childhood Tumours in Britain, we investigated the incidence and etiology of second primary bone cancer after childhood cancer in a cohort study and in a case-control study. METHODS: A cohort study of 13,175 3-year survivors of childhood cancer diagnosed in Britain between 1940 and 1983 revealed 55 subsequent bone cancers. A largely nested case-control study comprised 59 case subjects developing second primary bone cancer, and 220 control subjects were selected and matched for sex, type of first cancer, age at first cancer, and interval between diagnosis of first cancer and subsequent bone cancer. Outcome measures were the incidence of bone cancer after childhood cancer, the cumulative dose of radiation received at the site of the second cancer in the case subject and at the corresponding anatomic site in the matched control subjects, and the cumulative dose of alkylating agents and vinca alkaloids received by case and control subjects. RESULTS: The percentage of 3-year survivors developing bone cancer within 20 years did not exceed 0.9%, except following heritable retinoblastoma (7.2%), Ewing's sarcoma (5.4%), and other malignant bone tumors (2.4%). The risk of bone cancer increased substantially with increased cumulative dose of radiation to the bone (P< .001, linear trend). At the highest levels of exposure, however, the risk appeared to decline somewhat (P=.065, nonlinearity). Exposure to less than 10 Gy was at worst, associated with only a small increased relative risk (RR) of bone cancer (RR= 0.7; 95% confidence interval = 0.2-2.2). The risk of bone cancer increased linearly (P= .04, one-tailed test) with increased cumulative dose of alkylating agents. IMPLICATIONS: This population-based study provides grounds for reassurance of the majority of survivors in that their risk of developing bone cancer within 20 years of 3-year survival did not exceed 0.9%. The higher risks found for bone cancer following the other specific rare types of childhood cancer provide a rational basis for surveillance. The RRs reported for bone cancer after specified levels of exposure to radiation should help in making decisions concerning future treatment protocols.

Adolescent↗

PubMed2002

The risk of subsequent primary cancers after colorectal cancer in southeast England.

BACKGROUND: Multiple cancers may occur in an individual because of a genetic predisposition, environmental exposure, cancer therapy, or immunological deficiency. Colorectal cancer is one of the most commonly diagnosed cancers, and inherited factors play an important role in its aetiology. AIMS: To characterise the occurrence of multiple primary cancers in patients diagnosed with colorectal cancer and explore the possibility of a common aetiology for different cancer sites. PATIENTS: The Thames Cancer Registry database was used to identify patients with a first colorectal cancer, resident in the North or South Thames region, diagnosed between 1 January 1961 and 31 December 1995. A total of 127 281 patients were included, 61 433 men and 65 848 women. METHODS: Observed numbers of cancers occurring after the diagnosis of colorectal cancer were compared with expected numbers, calculated using appropriate age, sex, and period specific rates, to obtain standardised incidence ratios. The occurrence of colorectal cancers subsequent to cancers at other sites was also examined. RESULTS: Small intestinal cancer was significantly increased in men diagnosed with colorectal cancer before the age of 60 years and in women diagnosed with colorectal cancer after the age of 65 years. Colorectal cancer was also significantly increased after a first diagnosis of cancer of the small intestine. Other cancer sites with a significant increase after colorectal cancer included the cervix uteri, corpus uteri, and ovary. CONCLUSIONS: Patients with colorectal cancer are at increased risk of developing cancer at a number of other sites. Some of these associations are consistent with the effects of known inherited cancer susceptibility genes.

Adult↗

PubMed2002

Familial cancer aggregation and the risk of lung cancer.

CONTEXT: Around 90% of lung cancer worldwide is attributable to cigarette smoking, although less than 20% of cigarette smokers develop lung cancer. Other factors such as diet, chronic lung diseases, occupation and possibly environmental agents also contribute to this cancer. Genetic factors seem to play a role in lung cancer, but the precise characteristics influencing lung cancer susceptibility are not known, since genetic factors are easily obscured by the strong environmental determinants of lung cancer, particularly smoking. OBJECTIVE: To estimate the effect that cancer occurrence among first-degree relatives has on the risk of lung cancer. DESIGN: Hospital-based case-control study. SETTING: The metropolitan region of São Paulo, Brazil. PARTICIPANTS: 334 incident lung cancer cases and 578 controls matched by hospitals. MAIN MEASUREMENTS: By means of a structured questionnaire, cases and controls were interviewed about cancer occurrence in first-degree relatives, tobacco smoking, exposure to passive smoking, occupation, migration and socioeconomic status. Non-conditional logistic regression was used to calculate the risk of familial cancer aggregation, the effect of cancer in first-degree relatives and smoking in conjunction, and for controlling confounders. RESULTS: The adjusted odds ratio (OR) revealed a slight, but not statistically significant, excess risk of lung cancer for subjects with a history of lung cancer in relatives (OR 1.21; 95% confidence interval [CI] 0.50 - 2.92). The same was found among those with a history of other tobacco-related cancers in relatives (OR 1.36; 95% CI 0.87 - 2.14). A step gradient effect was observed regarding lung cancer risk, in accordance with increases in the number of pack-years of cigarette consumption. An interaction between familial cancer aggregation and tobacco smoking was detected. CONCLUSIONS: A mildly elevated risk of lung cancer among persons with a positive history of lung and other tobacco-related cancers was observed. The finding of an interaction between the variables of familial cancer aggregation and smoking suggests that familial cancer aggregation could be considered as a marker of susceptibility, increasing the risk of lung cancer among smokers. These results improve our knowledge of lung carcinogenesis and can guide future cancer genetic studies.

Adult↗

PubMed1996

Mammographic appearance of cancer in the opposite breast: comparison with the first cancer.

OBJECTIVE: Patients who have had cancer in one breast are at high risk for cancer in the contralateral breast. These bilateral cancers may be synchronous or metachronous. If the manifestations on mammography were similar in both breasts, an aggressive search for the mammographic findings of the first breast cancer might lead to early detection of the contralateral cancer. The purpose of this study was to evaluate mammograms for patients with bilateral cancers to determine whether the mammographic appearance of the contralateral cancer is likely to be the same as that of the first cancer. MATERIALS AND METHODS: We retrospectively reviewed the pathologic and mammographic records of 69 patients with surgically proven bilateral primary breast cancer. Thirty four of 69 (49%) had synchronous cancer, and 35 (51%) had metachronous cancer. Mammographic appearances were classified as microcalcifications, spiculated mass, nonspiculated mass (whether circumscribed or poorly defined), asymmetric or developing density, architectural distortion, and normal. Multiple findings were subclassified as major and minor findings. All findings were compared between both breast cancers, and statistical significance was determined by the two-sample Z test. RESULTS: Forty six (67%) of 69 patients had different major mammographic findings in the contralateral cancer. Of 30 patients whose first cancers had microcalcifications, 20 (67%) had microcalcifications in the contralateral cancer. Of 39 patients whose first cancers lacked microcalcifications, 17 (44%) had microcalcifications in the contralateral cancer. This difference was statistically significant (p = .02). Of 26 patients whose first cancers had spiculated masses, 9 (35%) had a contralateral spiculated mass. Of 43 patients whose first cancers lacked spiculated masses, 12 (28%) had a contralateral spiculated mass. This difference was not statistically significant (p = .22). CONCLUSION: Our results show that contralateral tumors usually have major mammographic findings different from those of the first cancer, and the mammographic signs of the first cancer do not indicate the most likely appearance of cancer in the contralateral breast. Evaluation of a contralateral mammogram should be performed without regard for the mammographic findings for the first cancer.

Adult↗

PubMed1999

The American Cancer Society challenge goals. How far can cancer rates decline in the U.S. by the year 2015?

BACKGROUND: Cancer incidence and mortality rates both began to decline in the U. S. in the early 1990s. Recognizing the unprecedented potential benefits of accelerating this decline, the American Cancer Society (ACS) has set ambitious challenge goals for the American public for a 25% reduction in cancer incidence rates and a 50% reduction in cancer mortality rates by the year 2015. This analysis examined the feasibility of reaching those goals by estimating future changes in cancer rates that can result from past and future reductions in cancer risk factors. METHODS: Estimates for future declines in cancer risk factors in the U. S. under alternative scenarios were applied to conservative population-attributable risk estimates for cancer incidence and mortality rates in 1990 to estimate cancer rate trends in the year 2015. RESULTS: If the current trends toward a decline in the prevalence of cancer risk factors continue over the next decade, by the year 2015 one can expect a 13% decline in cancer incidence rates and a 21% decline in cancer mortality rates below their 1990 levels. With redoubled efforts to reduce the prevalence of known cancer risk factors further, by the year 2015 cancer incidence rates could be reduced by 19% and cancer mortality rates reduced by 29%. Such redoubled efforts would equate to approximately 100,000 cancer cases and 60,000 cancer deaths prevented each year by the year 2015. CONCLUSIONS: Past reductions in cancer risk factors in the U.S. population have led to recent declines in the rates of cancer incidence and mortality in the U.S. Redoubled efforts to act on current knowledge regarding how to prevent, detect, and treat cancer can result in attaining approximately 80% of the ACS challenge goal for cancer incidence rates and 60% of the ACS challenge goal for cancer mortality rates by the year 2015. New findings from cancer research are needed and will have to be applied quickly if the ACS challenge goals are to be met fully.

Forecasting↗

PubMedDate not supplied

Gastric remnant cancer compared with primary proximal gastric cancer.

BACKGROUND/AIMS: Recently, detections of early-stage gastric remnant cancer and small proximal gastric cancer are increasing. The aim of this study was to compare pathologic and prognostic data of gastric remnant cancer with those of primary proximal gastric cancer including upper gastric cancer based on a recent 15-year experience at a single institute in Japan. METHODOLOGY: Among 698 patients who underwent gastrectomy for cancer between 1984 and 1998, 15 (2.1%) were patients with gastric remnant cancer. During the same period, 139 patients underwent primary gastrectomy for proximal gastric cancer which included 71 with upper gastric cancer confined to the upper one-third of the stomach. Clinicopathologic findings of gastric remnant cancer were compared with those of proximal gastric cancer. RESULTS: Of 15 gastric remnant cancers, 8 (53%) were stage I tumors. Although gastric remnant cancer and proximal gastric cancer was not different in several clinicopathologic factors, gastric remnant cancer and upper gastric cancer confined to the upper one-third of the stomach was different with regard to the frequency of tumor size > or = 4 cm (60% vs. 32%, p < 0.05), poorly differentiated type (67% vs. 38%, p < 0.05), serosal invasion (40% vs. 11%, p < 0.01), lymph node metastasis (47% vs. 20%, p < 0.05), stage III or IV disease (47% vs. 10%, p < 0.01), and noncurative gastrectomy (20% vs. 1%, p < 0.01). The 5-year survival rate of gastric remnant cancer (69%) was higher than that of proximal gastric cancer (57%) and lower than that of upper gastric cancer (81%), although the differences were not statistically significant. CONCLUSIONS: In our recent series, a half of gastric remnant cancers are stage I tumors. Although gastric remnant cancers are similar to proximal gastric cancers, they are more advanced and their surgical results are less satisfactory when compared with upper gastric cancers confined to the upper one-third of the stomach.

Adenocarcinoma↗

PubMed1985

Second cancer following cancer of the respiratory system in Denmark, 1943-80.

A 10% increased risk of developing a second cancer was observed among approximately 36,000 persons reported to the Danish Cancer Registry with a cancer of the respiratory system during 1943-80. This estimate is markedly influenced by a striking tendency by physicians not to report or the Cancer Registry not to accept a report of a second lung cancer following a primary lung cancer (14 observed vs. 99 expected). A significant 30% excess of all second cancer was seen after laryngeal cancer (368 vs. 282), whereas the 22% excess following cancer of the nasal cavities and paranasal sinuses did not quite reach the level of statistical significance (95% CI = 0.9-1.6). For cancers of the lung and larynx, second cancers arose mainly in the buccal cavity, bladder, kidney (after lung cancer only) and lung (after laryngeal cancer only). These second cancers may be due to common carcinogenic factors, most likely tobacco. Elevated risks of second cancers of the breast, cervix uteri, and other female genital organs were found consistently. Radiotherapy may have contributed to the increased risk of breast cancer, but the excess risk of cancer of the female genital organs other than the cervix was unexpected. Although not significant, the risk of esophageal cancer following cancer of the larynx was below expectation (1 vs. 4.1), which was surprising because alcohol consumption and smoking are thought to be common risk factors for these 2 sites. Significant excesses of pancreatic cancer were observed following cancers of the lung, larynx, and nasal cavities, which might be due to more careful medical surveillance of these patients or to common risk factors such as cigarette smoking. Finally, the risk of a patient developing liver cancer after lung cancer was significantly elevated (22 vs. 11.6). This increase is unlikely to be due to misdiagnosed metastases from the lung, inasmuch as the risk was generally elevated throughout the observation period.

Denmark↗

PubMed1985

Second cancer following cancer of the respiratory system in Connecticut, 1935-1982.

The risk of a person developing a second primary cancer was evaluated in approximately 30,000 persons who developed cancer of the respiratory system in Connecticut between 1935 and 1982. A significant 44% excess of all second cancers was observed following cancer of the lung (614 observed vs. 426 expected). The excess of second tumors was 72% following cancer of the larynx (541 vs. 314) and 34% following cancer of the nasal cavities and sinuses (43 vs. 32). For cancers of the lung and larynx, second cancers arose mainly along the respiratory tract or other sites associated with cigarette smoking (oral cavity, bladder, kidney). A threefold excess of esophageal cancer followed cancer of the larynx, which was indicative of risk factors in common (alcohol and tobacco) and possibly an effect of radiotherapy. Radiotherapy may have contributed also to the increased risk of second lung and breast cancers. A slight excess risk of leukemia after lung cancer points to a possible effect of chemotherapy given for certain histologic types. An unexpected finding was a significant 50% increased risk of colon cancer following cancer of the larynx. Significant excesses of prostate cancer are probably artifacts associated with increased medical surveillance and higher autopsy rates among cancer patients than in the general population. No deficits of any second cancers were observed. The risk of a second cancer developing did not appear to vary by sex or time since initial diagnosis, except that the risks following cancer of the nasal cavities and sinuses returned to normal levels among long-term survivors. Among persons observed for 10 or more years after their initial diagnosis of cancers of the lung or larynx, the risk of developing a second cancer remained high, i.e., on the order of 50% above expectation. Further analytic studies should clarify the role of smoking, alcohol, other life-style and host factors, and various forms of therapy on the risk of second cancers following cancer of the respiratory system.

Connecticut↗

PubMed2000

Life expectancy gains from cancer prevention strategies for women with breast cancer and BRCA1 or BRCA2 mutations.

CONTEXT: Women with BRCA1- or BRCA2-associated breast cancer are at increased risk for contralateral breast cancer and ovarian cancer and therefore may consider secondary cancer prevention strategies, such as prophylactic surgery and tamoxifen therapy. It is not proven to what extent these strategies reduce risk of second cancers in such patients. OBJECTIVE: To examine the effect of tamoxifen therapy, bilateral prophylactic oophorectomy (PO), prophylactic contralateral mastectomy (PCM), and combinations of these strategies on life expectancy for women with unilateral breast cancer and a BRCA1 or BRCA2 gene mutation. DESIGN AND SETTING: Decision analysis using a Markov model. Probabilities for developing contralateral breast cancer and ovarian cancer, dying from these cancers, dying from primary breast cancer, and the reduction in cancer incidence and mortality due to prophylactic surgeries and/or tamoxifen were estimated from published studies. PARTICIPANTS: Hypothetical breast cancer patients with BRCA1 or BRCA2 mutations facing decisions about secondary cancer prevention strategies. INTERVENTIONS: Seven strategies, including 5 years of tamoxifen use, PO, PCM, and combinations of these strategies, compared with careful surveillance. MAIN OUTCOME MEASURES: Total and incremental life expectancy (LE) with each intervention strategy. RESULTS: Depending on the assumed penetrance of the BRCA mutation, compared with surveillance alone, 30-year-old early-stage breast cancer patients with BRCA mutations gain in LE 0.4 to 1.3 years from tamoxifen therapy, 0.2 to 1.8 years from PO, and 0.6 to 2.1 years from PCM. The magnitude of these gains is least for women with low-penetrance mutations (assumed contralateral breast cancer risk of 24% and ovarian cancer risk of 6%) and greatest for those with high-penetrance mutations (assumed contralateral breast cancer risk of 65% and ovarian cancer risk of 40%.) Older age and poorer prognosis from primary breast cancer further attenuate these gains. CONCLUSIONS: Interventions to prevent second cancers, particularly PCM, may offer substantial LE gain for young women with BRCA-associated early-stage breast cancer. Estimates of LE gain may help women and their physicians consider the uncertainties, risks, and advantages of these interventions and lead to more informed choices about cancer prevention strategies.

Adult↗

PubMed2006

An adjunctive preventive treatment for cancer: ultraviolet light and ginkgo biloba, together with other antioxidants, are a safe and powerful, but largely ignored, treatment option for the prevention of cancer.

Cancer has surpassed heart disease as the leading cause of death in the United States. The mortality rate for cancer is high (roughly 42%), and it increases dramatically with increasing age, especially in patients between the ages of 40 and 60 years old. Currently, the efforts at cancer prevention have been minimal. The drugs developed so far are expensive and have serious side effects. There are at least 18 vitamin D-sensitive cancers. Ultraviolet light, and specifically ultraviolet B (UVB), could reduce cancer by the limited exposure of suitable skin areas to UVB of an intensity and duration insufficient to produce skin cancer. An irrational fear of skin cancer is preventing this idea from being implemented. Though skin cancer incidence is significant, mortality from skin cancer is relatively rare. Roughly 1,000,000 Americans will be affected by skin cancer but only 10,000 deaths are expected in 2005 (a 1% mortality rate). Skin cancer is easily detected and often cured by excisional biopsy alone. Current practice among practicing clinicians is to use a prescription drug substitute for UV light, calcitriol (1-25 dihydroxycholcalciferol). However, high levels of (calcitriol) are dangerous, and there is no consensus on just what a high dose or a safe dose is. Apart from skin cancer, UV light exposure possesses few risks. Additionally, a number of botanical agents such as ginkgo biloba, vitamins E and C, carotenoids, selenium and proanthocyanidins can prevent the risk of skin cancer. Ginkgo biloba also possess the following additional cancer chemopreventive qualities: (1) promoting apoptosis of cancer cells; (2) an anti-clastogenic effect on chromosomes by repairing and reconstituting broken and damaged chromosomes; (3) a powerful therapeutic effect on the treatment of fibrosis-related cancer; (4) a therapeutic effect on free radical-induced cancer; (5) a therapeutic effect on the treatment of cancer incident to the result of numerous carcinogens; (6) a therapeutic effect on preventing free radical-induced cancer; (7) an enhancing effect on radiation therapy in the treatment of cancer; and (8) a therapeutic effect on reducing the size of cancer tumors. Ginkgo biloba is widely-used and has few adverse effects. The proposed preventive treatment for cancer consists of short intermittent exposure of the least sensitive areas of the body to sunlight and/or artificial ultraviolet light. The routine testing of plasma vitamin D levels help monitor the effectiveness of the treatment and periodic checkups with a dermatologist help monitor the safety.

Antineoplastic Agents↗