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Journal Article

Cancer mortality surveillance--United States, 1990-2000.

04 Jun 2004-Morbidity and Mortality Weekly Report (MMWR Surveill Summ)-Vol. 53, Iss: 3, pp 1-108
TL;DR: Although cancer remains the second leading cause of death in the United States, the overall declining trend in cancer mortality demonstrates considerable progress in cancer prevention, early detection, and treatment.
Abstract: Problem/condition Cancer is the second leading cause of death in the United States and is expected to become the leading cause of death within the next decade. Considerable variation exists in cancer mortality between the sexes and among different racial/ethnic populations and geographic locations. The description of mortality data by state, sex, and race/ethnicity is essential for cancer-control researchers to target areas of need and develop programs that reduce the burden of cancer. Reporting period covered 1990-2000. Description of system Mortality data from CDC were used to calculate death rates and trends, categorized by state, sex, and race/ethnicity. Trend analyses for 1990-2000 are presented for all cancer sites combined and for the four leading cancers causing death (lung/bronchus, colorectal, prostate, and breast) categorized by state, sex, and race/ethnicity. Death rates per 100,000 population for the 10 primary cancer sites with the highest age-adjusted rates are also presented for each state and the District of Columbia by sex. For males, the 10 primary sites include lung/bronchus, prostate, colon/rectum, pancreas, leukemia, non-Hodgkin lymphoma, liver/intrahepatic bile duct, esophagus, stomach, and urinary bladder. For females, the 10 primary sites include lung/bronchus, breast, colon/rectum, pancreas, ovary, non-Hodgkin lymphoma, leukemia, brain/other nervous system, uterine corpus, and myeloma. Results For 1990-2000, cancer mortality decreased among the majority of racial/ethnic populations and geographic locations in the United States. Statistically significant decreases in mortality among all races combined occurred with lung and bronchus cancer among men (--1.7%/year); colorectal cancer among men and women (--2.0%/year and--1.7%/year, respectively); prostate cancer (--2.6%/year); and female breast cancer (--2.3%/year). For 1990-2000, cancer mortality remained stable among American Indian/Alaska Native populations. Statistically significant increases in lung and bronchus cancer mortality occurred among women of all racial/ethnic backgrounds, except among Asian/Pacific Islanders. Interpretation Although cancer remains the second leading cause of death in the United States, the overall declining trend in cancer mortality demonstrates considerable progress in cancer prevention, early detection, and treatment. Public health action More effective tobacco-cessation programs are necessary to reduce lung and bronchus cancer mortality among women and sustain the decrease in lung and bronchus cancer mortality among men. Additional programs that deter smoking initiation among adolescents are essential to ensure future decreases in lung and bronchus cancer mortality. Continued research in primary prevention, screening methods, and therapeutics is needed to further reduce disparities and improve quality of life and survival among all populations.

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Journal ArticleDOI
04 Aug 2005-Nature
TL;DR: It is shown that conditional inactivation of Trp53 in the mouse prostate fails to produce a tumour phenotype, whereas complete Pten inactivation in the prostate triggers non-lethal invasive prostate cancer after long latency, and support a model for cooperative tumour suppression in which p53 is an essential failsafe protein of Pten-deficient tumours.
Abstract: Cellular senescence has been theorized to oppose neoplastic transformation triggered by activation of oncogenic pathways in vitro, but the relevance of senescence in vivo has not been established. The PTEN and p53 tumour suppressors are among the most commonly inactivated or mutated genes in human cancer including prostate cancer. Although they are functionally distinct, reciprocal cooperation has been proposed, as PTEN is thought to regulate p53 stability, and p53 to enhance PTEN transcription. Here we show that conditional inactivation of Trp53 in the mouse prostate fails to produce a tumour phenotype, whereas complete Pten inactivation in the prostate triggers non-lethal invasive prostate cancer after long latency. Strikingly, combined inactivation of Pten and Trp53 elicits invasive prostate cancer as early as 2 weeks after puberty and is invariably lethal by 7 months of age. Importantly, acute Pten inactivation induces growth arrest through the p53-dependent cellular senescence pathway both in vitro and in vivo, which can be fully rescued by combined loss of Trp53. Furthermore, we detected evidence of cellular senescence in specimens from early-stage human prostate cancer. Our results demonstrate the relevance of cellular senescence in restricting tumorigenesis in vivo and support a model for cooperative tumour suppression in which p53 is an essential failsafe protein of Pten-deficient tumours.

1,915 citations

Journal ArticleDOI
TL;DR: Age, geographic location, reproductive events, exogenous hormones, lifestyle risk factors, familial history of breast cancer, mammographic density, history of benign breast disease, ionizing radiation, bone density, height, IGF‐1 and prolactin levels, chemopreventive agents and genetic factors are summarized.
Abstract: Breast cancer is the most frequent cancer in women and represents the second leading cause of cancer death among women (after lung cancer). The etiology of breast cancer is still poorly understood with known breast cancer risk factors explaining only a small proportion of cases. Risk factors that modulate the development of breast cancer discussed in this review include: age, geographic location (country of origin) and socioeconomic status, reproductive events, exogenous hormones, lifestyle risk factors (alcohol, diet, obesity and physical activity), familial history of breast cancer, mammographic density, history of benign breast disease, ionizing radiation, bone density, height, IGF- 1 and prolactin levels, chemopreventive agents. Additionally, we summarized breast cancer risk associated with the following genetic factors: breast cancer susceptibility high-penetrance genes (BRCA1, BRCA2, p53, PTEN, ATM, NBS1 or LKB1) and low-penetrance genes such as cytochrome P450 genes (CYP1A1, CYP2D6, CYP19), glutathione S-transferase family (GSTM1, GSTP1), alcohol and one-carbon metabolism genes (ADH1C and MTHFR), DNA repair genes (XRCC1, XRCC3, ERCC4/XPF) and genes encoding cell signaling molecules (PR, ER, TNFalpha or HSP70). All these factors contribute to a better understanding of breast cancer risk. Nonetheless, in order to evaluate more accurately the overall risk of breast tumorigenesis, novel genetic and phenotypic traits need to be identified.

491 citations


Cites background from "Cancer mortality surveillance--Unit..."

  • ...Breast cancer is the most commonly occurring cancer among women (22% of all cancers in 2000 [1] and is second only to lung cancer as a cause of cancer death in women (15% of cancer deaths) [2]....

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  • ...3% per year due to multiple factors, including improvements in cancer screening and novel and more effective treatment regimens [2]....

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Journal ArticleDOI
TL;DR: African American patients with sex-specific cancers had worse survival than white patients, despite enrollment on phase III SWOG trials with uniform stage, treatment, and follow-up.
Abstract: BACKGROUND: Racial disparities in cancer outcomes have been observed in several malignancies. However, it is unclear if survival differences persist after adjusting for clinical, demographic, and treatment variables. Our objective was to determine whether racial disparities in survival exist among patients enrolled in consecutive trials conducted by the Southwest Oncology Group (SWOG). METHODS: We identified 19 457 adult cancer patients (6676 with breast, 2699 with lung, 1244 with colon, 1429 with ovarian, and 1843 with prostate cancers; 1291 with lymphoma; 2067 with leukemia; and 2208 with multiple myeloma) who were treated on 35 SWOG randomized phase III clinical trials from October 1, 1974, through November 29, 2001. Patients were grouped according to studies of diseases with similar histology and stage. Cox regression was used to evaluate the association between race and overall survival within each disease site grouping, controlling for available prognostic factors plus education and income, which are surrogates for socioeconomic status. Median and ten-year overall survival estimates were derived by the Kaplan-Meier method. All statistical tests were two-sided. RESULTS: Of 19 457 patients registered, 2308 (11.9%, range = 3.9%-21.6%) were African American. After adjustment for prognostic factors, African American race was associated with increased mortality in patients with early-stage premenopausal breast cancer (hazard ratio [HR] for death = 1.41, 95% confidence interval [CI] = 1.10 to 1.82; P = .007), early-stage postmenopausal breast cancer (HR for death = 1.49, 95% CI = 1.28 to 1.73; P < .001), advanced-stage ovarian cancer (HR for death = 1.61, 95% CI = 1.18 to 2.18; P = .002), and advanced-stage prostate cancer (HR for death = 1.21, 95% CI = 1.08 to 1.37; P = .001). No statistically significant association between race and survival for lung cancer, colon cancer, lymphoma, leukemia, or myeloma was observed. Additional adjustments for socioeconomic status did not substantially change these observations. Ten-year (and median) overall survival rates for African American vs all other patients were 68% (not reached) vs 77% (not reached), respectively, for early-stage, premenopausal breast cancer; 52% (10.2 years) vs 62% (13.5 years) for early-stage, postmenopausal breast cancer; 13% (1.3 years) vs 17% (2.3 years) for advanced ovarian cancer; and 6% (2.2 years) vs 9% (2.7 years) for advanced prostate cancer. CONCLUSIONS: African American patients with sex-specific cancers had worse survival than white patients, despite enrollment on phase III SWOG trials with uniform stage, treatment, and follow-up.

429 citations

Journal ArticleDOI
TL;DR: It is suggested that this ongoing antigen-antibody reaction may generate chronic inflammation, possibly contributing to the high frequency of diet-related carcinomas and other diseases in humans.
Abstract: Human heterophile antibodies that agglutinate animal erythrocytes are known to detect the nonhuman sialic acid N-glycolylneuraminic acid (Neu5Gc). This monosaccharide cannot by itself fill the binding site (paratope) of an antibody and can also be modified and presented in various linkages, on diverse underlying glycans. Thus, we hypothesized that the human anti-Neu5Gc antibody response is diverse and polyclonal. Here, we use a novel set of natural and chemoenzymatically synthesized glycans to show that normal humans have an abundant and diverse spectrum of such anti-Neu5Gc antibodies, directed against a variety of Neu5Gc-containing epitopes. High sensitivity and specificity assays were achieved by using N-acetylneuraminic acid (Neu5Ac)-containing probes (differing from Neu5Gc by one less oxygen atom) as optimal background controls. The commonest anti-Neu5Gc antibodies are of the IgG class. Moreover, the range of reactivity and Ig classes of antibodies vary greatly amongst normal humans, with some individuals having remarkably large amounts, even surpassing levels of some well-known natural blood group and xenoreactive antibodies. We purified these anti-Neu5Gc antibodies from individual human sera using a newly developed affinity method and showed that they bind to wild-type but not Neu5Gc-deficient mouse tissues. Moreover, they bind back to human carcinomas that have accumulated Neu5Gc in vivo. As dietary Neu5Gc is primarily found in red meat and milk products, we suggest that this ongoing antigen-antibody reaction may generate chronic inflammation, possibly contributing to the high frequency of diet-related carcinomas and other diseases in humans.

282 citations


Cites background from "Cancer mortality surveillance--Unit..."

  • ...While advanced cancer is most often fatal, early stage disease can have a good survival rate (Stewart et al. 2004)....

    [...]

  • ...D ow nloaded from https://academ ic.oup.com /glycob/article/18/10/818/1997766 by Tel Aviv U niversity user on 07 January 2021 While advanced cancer is most often fatal, early stage disease can have a good survival rate (Stewart et al. 2004)....

    [...]

Journal ArticleDOI
TL;DR: Improved data on American Indian and Alaska Native (AI/AN) ancestry is used to provide an updated and comprehensive description of cancer mortality and incidence among AI/AN populations from 1990 to 2009.
Abstract: Objectives. We used improved data on American Indian and Alaska Native (AI/AN) ancestry to provide an updated and comprehensive description of cancer mortality and incidence among AI/AN populations from 1990 to 2009.Methods. We linked the National Death Index and central cancer registry records independently to the Indian Health Service (IHS) patient registration database to improve identification of AI/AN persons in cancer mortality and incidence data, respectively. Analyses were restricted to non-Hispanic persons residing in Contract Health Service Delivery Area counties in 6 geographic regions of the United States. We compared age-adjusted mortality and incidence rates for AI/AN populations with White populations using rate ratios and mortality-to-incidence ratios. Trends were described using joinpoint analysis.Results. Cancer mortality and incidence rates for AI/AN persons compared with Whites varied by region and type of cancer. Trends in death rates showed that greater progress in cancer control was...

174 citations

References
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TL;DR: A joinpoint regression model is applied to describe continuous changes in the recent trend and the grid-search method is used to fit the regression function with unknown joinpoints assuming constant variance and uncorrelated errors.
Abstract: The identification of changes in the recent trend is an important issue in the analysis of cancer mortality and incidence data. We apply a joinpoint regression model to describe such continuous changes and use the grid-search method to fit the regression function with unknown joinpoints assuming constant variance and uncorrelated errors. We find the number of significant joinpoints by performing several permutation tests, each of which has a correct significance level asymptotically. Each p-value is found using Monte Carlo methods, and the overall asymptotic significance level is maintained through a Bonferroni correction. These tests are extended to the situation with non-constant variance to handle rates with Poisson variation and possibly autocorrelated errors. The performance of these tests are studied via simulations and the tests are applied to U.S. prostate cancer incidence and mortality rates.

3,950 citations

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3,888 citations

01 Jan 2004
TL;DR: The number of new cancer cases for 2010, excluding basal and squamous cell skin cancers and in situ carcinomas except urinary bladder, is estimated as a rough guide and should be interpreted with caution.
Abstract: Estimated number of new cancer cases for 2010, excluding basal and squamous cell skin cancers and in situ carcinomas except urinary bladder. Note: State estimates are offered as a rough guide and should be interpreted with caution. State estimates may not add to US total due to rounding.

2,269 citations

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TL;DR: Immediate androgen suppression with an LHRH analogue given during and for 3 years after external irradiation improves disease-free and overall survival of patients with locally advanced prostate cancer.

1,692 citations

Journal ArticleDOI
TL;DR: As compared with placebo, letrozole therapy after the completion of standard tamoxifen treatment significantly improves disease-free survival.
Abstract: background In hormone-dependent breast cancer, five years of postoperative tamoxifen therapy — but not tamoxifen therapy of longer duration — prolongs disease-free and overall survival. The aromatase inhibitor letrozole, by suppressing estrogen production, might improve the outcome after the discontinuation of tamoxifen therapy. methods We conducted a double-blind, placebo-controlled trial to test the effectiveness of five years of letrozole therapy in postmenopausal women with breast cancer who have completed five years of tamoxifen therapy. The primary end point was disease-free survival. results A total of 5187 women were enrolled (median follow-up, 2.4 years). At the first interim analysis, there were 207 local or metastatic recurrences of breast cancer or new primary cancers in the contralateral breast — 75 in the letrozole group and 132 in the placebo group — with estimated four-year disease-free survival rates of 93 percent and 87 percent, respectively, in the two groups (P ≤ 0.001 for the comparison of disease-free survival). A total of 42 women in the placebo group and 31 women in the letrozole group died (P=0.25 for the comparison of overall survival). Low-grade hot flashes, arthritis, arthralgia, and myalgia were more frequent in the letrozole group, but vaginal bleeding was less frequent. There were new diagnoses of osteoporosis in 5.8 percent of the women in the letrozole group and 4.5 percent of the women in the placebo group (P=0.07); the rates of fracture were similar. After the first interim analysis, the independent data and safety monitoring committee recommended termination of the trial and prompt communication of the results to the participants. conclusions As compared with placebo, letrozole therapy after the completion of standard tamoxifen treatment significantly improves disease-free survival.

1,538 citations