1,721,291 research outputs found
Racial/ethnic patterns of cancer in the United States, 1988-1992 /
No full text"Prepared by the Cancer Control Research Program, Division of Cancer Prevention and Control, National Cancer Institute"--Prelim. p.Mode of access: Internet
The researchers' toolbox.
No full textDescription based on: March 2000; title from caption."A newsletter of the Applied Sociocultural Research Branch of the National Cancer Institute"--March 2000.Mode of access: Internet.Issued by: Division of Cancer Control and Population Sciences,
SEER summary staging manual 2000 : codes and coding instructions /
No full textIncludes index.Shipping list no.: 2001-0259-P."July 2001"--P. [4] of cover.[Prepared by] "Cancer Statistics Branch, Surveillance Research Program, Division of Cancer Control and Population Sciences, National Cancer Institute, U.S. Department of Health and Human Services, Public Health Service, National Institutes of Health."Mode of access: Internet
Pink book
No full textPreface -- Why Use this Book? -- Introduction -- Overview -- Stage 1: Planning and Strategy Development -- Stage 2: Developing and Pretesting -- Stage 3: Implementing the Program -- Stage 4: Assessing Effectiveness -- Communication Research Methods -- Appendix A: Communication Planning Forms and Samples -- Appendix B: Selected Planning Frameworks, Social Science Theories, and Models of Change -- Appendix C: Information Sources -- Appendix D: Selected Readings and Resources -- Appendix E: GlossaryU.S. Department of Health & Human Services, National Institutes of Health, National Cancer Institute."Reprinted August 2004.""Revised December 2001.""This document was revised in coordination with the Centers for Disease Control and Prevention during development of CDCynergy--a program-planning tool on CD-ROM."Called also: the Pink book.Also available via the World Wide Web.Includes bibliographical references (p. 236-242)
Tumor Microenvironment of Metastasis in Human Breast Carcinoma: A Potential Prognostic Marker Linked to Hematogenous Dissemination
No full textPurpose: Multiphoton-based intravital imaging has shown that invasive carcinoma cells in mouse and rat mammary tumors intravasate when associated with perivascular macrophages, identifying a potential tumor microenvironment of metastasis (TMEM). We define TMEM as the tripartite arrangement of an invasive carcinoma cell, a macrophage, and an endothelial cell. The aim of this study was to determine if TMEM density in human breast carcinoma samples predicts the development of systemic, hematogenous metastases.
Experimental Design: A case-control study of 30 patients who developed metastatic breast cancer and 30 patients without metastatic disease was done. Cases were matched to controls based on currently used prognostic criteria. Paraffin-embedded primary breast cancer samples were stained using a triple immunohistochemical method allowing simultaneous identification of carcinoma cells, macrophages, and endothelial cells. Two pathologists, blinded to outcome, evaluated the number of TMEM per 20 high-power fields.
Results: No association was seen between TMEM density and tumor size or grade, lymph node metastasis, lymphovascular invasion, or hormone receptor status. TMEM density was greater in the group of patients who developed systemic metastases compared with the patients with only localized breast cancer (median, 105 versus 50, respectively; P = 0.00006). For every 10-unit increase in TMEM density, the odds ratio for systemic metastasis was 1.9 (95% confidence interval, 1.1-3.4).
Conclusions: TMEM density predicted the development of systemic, hematogenous metastases. The ability of TMEM to predict distant metastasis was independent of lymph node status and other currently used prognosticators. Quantitation of TMEM may be a useful new prognostic marker for breast cancer patients.National Institutes of Health (U.S.) (Grant GM58801)National Cancer Institute (U.S.). Integrative Cancer Biology Program (Grant 1-U54-CA112967
The Cancer Transition in Japan since 1951
Get PDFThe overall trend of cancer mortality in Japan has been decreasing since the 1960s (age-standardized death rates for ages 30-69), though trends differ enormously among various forms of the disease. Cancer mortality was heavily influenced by Japanese postwar economic recovery, which led to improved living conditions and better control of infectious agents known to cause some common forms of cancer (stomach, cervical). However, Japanese wealth and development have also been associated with risky personal behaviors (smoking, drinking) and other conditions, leading to increases in cancers with no known or else very weak links to infection. This shift away from infectious and toward non-infectious causes of prevalent forms of cancers is called the "cancer transition," by analogy to Omran's "epidemiologic transition." We suggest that the cancer transition described here in the case of Japan must be a part of efforts to revise and update the epidemiologic transition, which should incorporate new knowledge about the role of infection in chronic disease morbidity and mortality.cancer, cancer transition, epidemiologic transition, health, health and development, infectious diseases, Japan, mortality, non-infectious disease
Differences in Breast Cancer Diagnosis and Treatment:Experiences of Insured and Uninsured Patients in a Safety Net Setting
Get PDFTo explore how well the safety net performs at eliminating differences in diagnosis and treatment of insured and uninsured women with breast cancer, we compared insured and uninsured women treated in a safety net setting. Controlling for socioeconomic characteristics, uninsured women are more likely to be diagnosed with advanced disease, requiring more extensive treatment relative to insured women, and also experience delays in initiating and completing treatment. The findings suggest that, despite the safety net system, uninsured women with breast cancer are likely to require more costly treatment and to have worse outcomes, relative to insured women with breast cancer.
Bounds in Competing Risks Models and the War on Cancer
Get PDFIn 1971 President Nixon declared war on cancer and increased the federal funds allocated to cancer research dramatically. Thirty years later, many have declared this war a failure. Overall cancer statistics confirm this view: age-adjusted mortality in 2000 was essentially unchanged from the early 1970s. At the same time, age-adjusted mortality rates from cardiovascular disease have fallen quite dramatically. Since the causes underlying cancer and cardiovascular disease are likely to be correlated, the decline in mortality rates from cardiovascular disease may be somewhat responsible for the rise in cancer mortality. It is natural to model mortality with more than one cause of death as a competing risks model. Such models are fundamentally unidentified, and it is therefore difficult to get a clear picture of the progress in cancer. This paper derives bounds for aspects of the underlying distributions under a number of different assumptions. Most importantly, we do not assume that the underlying risks are independent, and impose weak parametric assumptions in order to obtain identification. The theoretical contribution of the paper is to provide a framework to estimate competing risk models with interval data and discrete explanatory variables, both of which are common in empirical applications. We use our method to estimate changes in cancer and cardiovascular mortality since 1970. The estimated bounds for the effect of time on the duration until death for either cause are fairly tight and we find that trends in cancer show much larger improvements than previously estimated. For example, we find that time until death from cancer increased by about 10% for white males and 20% for white women.
NPCR Public Use Research Data Standards and Data Dictionary
No full textThe National Program of Cancer Registries (NPCR), administered by the Centers for Disease Control and Prevention (CDC), was established by Congress in 1992. Through cooperative agreements, NPCR supports central cancer registries in 46 states, the District of Columbia, Puerto Rico, U.S. Pacific Island Jurisdictions, and the U.S. Virgin Islands (see map below).The Surveillance, Epidemiology, and End Results (SEER) Program, administered by the National Cancer Institute (NCI), has been funded since 1973 as a result of the National Cancer Act of 1971. SEER collects reportable cancer cases from 20 U.S. geographic areas, including 5 states (see map below). Together, CDC\u2019s NPCR and NCI\u2019s SEER Program cover the entire United States population. These combined data are the official source of federal statistics on cancer incidence and are referred to as the U.S. Cancer Statistics.The cancer registries funded by CDC and NCI routinely collect data on patient demographics, primary tumor site, tumor morphology, stage at diagnosis, first course of treatment, and outcomes. Medical facilities such as hospitals, doctor\u2019s offices, pathology laboratories, and other treatment centers send demographic and clinical information related to people with cancer to a central cancer registry, where the information is consolidated. On an annual basis, the central cancer registries submit demographic and clinical information about each cancer case to CDC and/or NCI. None of the information submitted to CDC or NCI contains personally identifiable information about individual patients.CS293113-CPublication date from document properties.npcr-seer-public-use-database-data-dictionary-2005-2015-508.pd
Risk determination and prevention of breast cancer
Get PDFBreast cancer is an increasing public health problem. Substantial advances have been made in the treatment of breast cancer, but the introduction of methods to predict women at elevated risk and prevent the disease has been less successful. Here, we summarize recent data on newer approaches to risk prediction, available approaches to prevention, how new approaches may be made, and the difficult problem of using what we already know to prevent breast cancer in populations. During 2012, the Breast Cancer Campaign facilitated a series of workshops, each covering a specialty area of breast cancer to identify gaps in our knowledge. The risk-and-prevention panel involved in this exercise was asked to expand and update its report and review recent relevant peer-reviewed literature. The enlarged position paper presented here highlights the key gaps in risk-and-prevention research that were identified, together with recommendations for action. The panel estimated from the relevant literature that potentially 50% of breast cancer could be prevented in the subgroup of women at high and moderate risk of breast cancer by using current chemoprevention (tamoxifen, raloxifene, exemestane, and anastrozole) and that, in all women, lifestyle measures, including weight control, exercise, and moderating alcohol intake, could reduce breast cancer risk by about 30%. Risk may be estimated by standard models potentially with the addition of, for example, mammographic density and appropriate single-nucleotide polymorphisms. This review expands on four areas: (a) the prediction of breast cancer risk, (b) the evidence for the effectiveness of preventive therapy and lifestyle approaches to prevention, (c) how understanding the biology of the breast may lead to new targets for prevention, and (d) a summary of published guidelines for preventive approaches and measures required for their implementation. We hope that efforts to fill these and other gaps will lead to considerable advances in our efforts to predict risk and prevent breast cancer over the next 10 years
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