Cancer epidemiology – Flashcards

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What is the basic term for cancer epidemiology?
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the study of patterns and determinants of cancer risk, outcome, and control in healthy or diseased populations
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What is cancer epidemiology?
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the study of the distributions and determinants of cancer in populations, seeking to: 1. discover deviations from randomness that offer clues to their explanations 2. assess the validity and strength of associations that are suspected causes 3. evaluate the effectiveness of preventive measures through continued monitoring of cancer incidence and mortality
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What happened in 1713?
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Bernardino Ramazzini, an Italian physician, reported the virtual absence of cervical cancer and relatively high incidence of breast cancer among nuns He hypothesized that these observations were related to their celibate lifestyle
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What happened in 1775?
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-Percivall Pott of Saint Bartholomew's Hospital in London described an occupational cancer -Cancer of the scrotum was shown to be caused by soot collecting in the skin folds of the scrotum of chimney sweeps -This research led to identification a number of occupational carcinogenic exposures and to public health measures to reduce a person's cancer risk at work
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What happened in 1761?
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1. John Hill wrote Cautions Against the Immoderate Use of Snuff, which discussed the risks of tobacco use 2. Observations from Hill (and Thomas Venner's book Via Recta, published in London in 1620) were the first to link tobacco and cancer; ultimately leading to the Surgeon General's 1964 report Smoking and Health
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The Early 20th century - the "cigarette epidemic"
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1. 1940s - tobacco use skyrocketed 2. 1950 - it was established that cigarette smoking caused lung cancer 3. 1971 - Fairness Doctrine 4. 1998 - Master Settlement Agreement, which led to the creation of the American Legacy Foundation
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modern perspective: 20th century - the "cigarette epidemic"
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1. Evidence from several case-control studies clearly showed an association between tobacco and lung cancer, which spurred two cohort studies for further confirmation 2. Doll & Hill, 1954 - cohort study of 40,000 British doctors was established; In 2004, after 50 yrs of follow-up, they reported that the excess mortality associated with smoking involved vascular and respiratory diseases and cancers 3. Thun et al, 1995 - similar findings from the American Cancer Society cohort 4. 1930-1990 - the epidemic was responsible for ~4 million deaths from lung cancer in the U.S. 5. Numerous studies demonstrated that cigarette smoking was associated with additional cancers, including cancers of the mouth, oral pharynx, esophagus, pancreas, liver, bladder, and possibly cancer of the kidney and myeloid leukemia
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Carcinogen
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any substance capable of causing cancer in living tissues
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International Agency for Research on Cancer
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(IARC), which is part of the World Health Organization (WHO) has the most widely used system for classifying carcinogens For the past 30 yrs, IARC has evaluated the cancer-causing potential of >900 substances
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Human papilloma viruses (HPVs)
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Cervical, penile, anal, vaginal, vulvar, oropharyngeal (head and neck) cancers
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Epstein-Barr virus (EBV)
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Nasopharyngeal, some types of lymphoma (including Burkitt lymphoma and Hodgkin lymphoma), some stomach cancers
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Hepatitis B and C viruses (HBV, HCV)
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Liver cancer
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Human immunodeficiency virus (HIV)
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Doesn't directly cause cancer but indirectly from weakened immune system
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Human Herpesvirus 8 (HHV-8)
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Kaposi sarcoma, some rare blood cancers (including primary effusion lymphoma)
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Lab and Epidemiologic studies
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Many types of studies are necessary for classification of a substance as a carcinogen lab- in cell cultures or in animal studies Epidemiologic studies - in people Ultimately the combination of these allow scientists to make assessments of a substance's carcinogenic ability
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Human T-lymphotrophic virus-1 (HTLV-1)
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Lymphocytic leukemia and non-Hodgkin lymphoma (Adult T-cell leukemia/lymphoma [ALT])
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Merkel cell polyomavirus (MCV)
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Merkel cell carcinoma (a rare type of skin cancer, also called neuroendocrine carcinoma of the skin)
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What land mark happened in 1950?
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epidemiological and experimental evidence shows cigarette and tobacco constituents responsible for lung cancer
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What land mark happened in the 1970s?
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Diethylstillbestrol (DES) assicauted with vaginal adenocarcinoma in daughters of DES-treated women
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What land mark happened in the 1981?
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Dietary factors may be related to 35% of cancer deaths -we believe this could be more
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What land mark happened in the 1994?
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BRCA1 mutations associated with increased risk of breast and ovarian cancer
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What land mark happened in the 2002?
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Estrogen-progestin hormone replacement therapy doesn't decrease heart disease, increases breast cancer risk
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What land mark happened in the 2003?
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Breast cancer incidence falls significantly after discontinuation of HRT
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What is a malignant tumor?
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Malignant tumors invade surrounding normal tissue, have more aggressive characteristics Metastasis is the highest degree of malignancy and frequently ends in the death of cancer patients due to rapid growth and spread to other organs
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What is a benign tumor?
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remain clustered in a single location, tend to be non-fatal Size and location of benign tumors can, however, be problematic
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Carcinoma
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originate in epithelial tissue, such as the cells lining the intestines, bronchi, or mammary ducts
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Sarcoma
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originate in mesenchymal tissue, such as bone, muscle, or connective tissue
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Hematopoietic and lymphoid malignancies
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spread throughout the bone marrow, lymphatic system, and peripheral blood (leukemias and lymphomas)
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Cancer is derived from?
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1. Cancer is derived from Greek words: "karkinos" (means crab) "-oma" (means growth) 2. Hippocrates used karkinoma to describe the radiating, appendage-like projections extending from some breast tumors 3. Cancers are solid growths or non-solid leukemias in the circulatory system
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Monoclonal origin of cancer
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A single normal cell is transformed into a cancer cell as a result of various genetic mutations, which allow the cancer cell to proliferate uncontrollably, forming a homogenous tumor
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Polyclonal origin of cancer
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Multiple normal cells are simultaneously transformed into cancer cells that are able to proliferate uncontrollably, forming a heterogeneous tumor
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Epigenetics
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the study of gene expression differences that do not directly involve DNA nucleotide modifications A major distinction between epigenetic and genetic alterations is that epigenetic changes can be more easily reversible with therapeutic applications Epigenetic regulation involves: Histone modification DNA methylation Genomic imprinting X inactivation
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CpG island hypermethylation
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Inactivation of TSGs such as p53, p16, and RB; and inactivation of DNA repair genes such
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Global hypomethylation
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Activation of oncogenes such as RAS, MYC, WNT; and chromosomal/genomic instability
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Cancer - A Genetic disease
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Cancer is a multistep process that involves progressive accumulation of genetic and epigenetic alterations which ultimately lead to the transformed phenotype. Regardless of whether a cancer occurs sporadically or is passed on as a hereditary trait, cancer is considered a genetic disease.
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Evading growth suppressors
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This capability allows cancer cells to avoid the powerful programs that negatively regulate cellular proliferation These regulators are tumor suppressor proteins (encoded by tumor suppressor genes) RB and TP53 proteins are the prototypical ones They operate as the central nodes within two complementary regulatory networks that govern the decisions of cells to either proliferate or activate senescence and apoptosis
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Tumor suppressor genes
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provide cancer-preventive effects (i.e., they suppress tumor growth) The presence of a single copy of a normal tumor suppressor allele is sufficient for the growth-controlling function Tumor suppressor genes therefore usually act as recessive genes at the cellular level, as a loss of both alleles are required for the loss of function of a tumor suppressor gene, "Loss of function" cancer genes
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Knudson's "two-hit" hypothesis
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The second "hit" may be due to a deletion, chromosome loss, other mutation, or epigenetic alteration, leading to inactivation of the tumor suppressor activity.
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Proto-oncogenes
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non-mutated alleles of genes that contribute to normal cellular replication and tissue maintenance Mutations and altered expression patterns of proto-oncogenes cause them to act as oncogenes, leading from regulated to unregulated cell growth, which ultimately drives the pathogenesis of human cancers "Gain of function" cancer genes
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oncogenes
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Oncogenes stimulate growth and proliferation, disturb normal cell cycle regulation, alter signal transduction pathways, or up-regulate transcription of growth related genes these functions promote the development of cancers
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Enabling replicative immortality
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This capability allows cancer cells to undergo unlimited successive growth and division cycles, ultimately leading to immortalization Telomeres are known to be important to the process of immortalization Telomeres protect the ends of chromosomes and therefore are involved in determining the capability of cells to proliferate in an unlimited manner The length of telomeric DNA shorten as cells undergo successive growth and division cycles, and once they have lost their protective functions (shortened to a certain length) the cell enters into senescence
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inducing angiogenesis
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This capability allows cancers cells to promote the development of new vasculature so that the tumor can obtain nutrients and oxygen as well as for removal of metabolic wastes and carbon dioxide The prototypical angiogenesis inducers are VEGF-A and TSP-1 They are involved in development of new blood vessels during embryonic and postnatal development; in homeostatic survival of endothelial cells; and in physiological and pathological situations in adults Gene expression of these angiogenic inducers can be upregulated by hypoxia and by oncogenic signaling in tumors Angiogenesis is of particular importance for invasion and metastasis
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Activating invasion and metastasis
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This capability allows cancers to spawn new cancer cells that move from the primary site and invade adjacent tissue, and then subsequently travel to distant site(s) and develop new tumors at these site(s) The best characterized alteration that promotes the activation of invasion and metastasis is the loss of function of E-cadherin, which is a molecule involved in cell-to-cell adhesion E-cadherin antagonizes invasion and metastasis, so the reduced expression of this protein would promote these activities
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Emerging hallmarks and enabling characteristics of cancer
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Emerging 1. Deregulating cellular energetics 2. Avoiding immune destruction Enabling 1. Genomic instability and mutation 2. Tumor-promoting inflammation
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Sustaining proliferative signaling
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This capability allows cancer cells to induce and sustain positively acting growth-stimulatory signals... Under normal circumstances, growth-promoting signals are under tight control, instructing cells to progress through cell growth and division cycles --> homeostasis of cell number In cancer cells, there is deregulation of these signals, whereby cells can sustain proliferative signaling --> increase in the number and size of cells without regulation
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Evading immune destruction
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Highly immunogenic cancer cells may evade immune destruction by immobilizing parts of the immune system that were supposed to eradicate them For example, cancer cells may: paralyze infiltrating cytotoxic T lymphocytes (CTLs) and natural killer (NK) cells, by secreting cytokines and other immunosuppressive factors recruit inflammatory cells that are actively immunosuppressive, such as regulatory T cells (Tregs) and myeloid-derived suppressor cells (MDSCs)
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Resisting cell death
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This capability allows cancer cells to evolve a variety of strategies that limit the pathways leading to programmed cell death (apoptosis) The most common cause of this is loss of function of the TP53 protein, which is a critical damage sensor that signals the apoptosis-inducing circuitry that a cell should undergo apoptosis When cells that are damaged don't undergo cell death, they are able to survive and continue proliferating, thereby leading to tumor growth
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Caretaker gene
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a gene responsible for keeping other genes healthy (i.e., through preventing mutations from occurring in other genes) Examples of caretaker genes include: p53, mlh1, and msh2
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Gatekeeper gene
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a gene responsible for controlling or inhibiting cell growth Examples of gatekeeper genes include: Rb, APC, BRCA1/2
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Tumor-promoting inflammation
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the inflammatory state of premalignant and malignant lesions is driven by immune cells, which serve to promote tumor progression through a variety of mechanisms
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causality
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A factor is considered the cause of a specific type of cancer when alterations in the frequency or intensity of the factor are followed by changes in the frequency of occurrence of the cancer, after the latency or induction period Causality is rarely characterized by a simple 1:1 correspondence between a single exposure and any one type of cancer If so, the exposure would be both necessary and sufficient for the occurrence of the cancer
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Deregulating cellular energetics
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Cancer cells compensate for the lower efficiency of energy production by glycolysis (relative to mitochondrial oxidative phosphorylation) partly by upregulating glucose transporters, which increase glucose import into the cytoplasm Additionally, some tumors have subpopulations of cells that generate energy through different pathways Hypoxic, glucose-dependent cells that secrete lactate (as waste) Oxygenated cells that preferentially import and utilize the lactate (produced by neighboring cells) for the production of energy Questions still remain as to whether this emerging hallmark is functionally independent from the six core hallmarks of cancer The redirection of energy production is largely determined by proteins involved in programming the core hallmarks Glycolytic fueling has been shown to be associated with activated oncogenes and tumor suppressor genes So, "aerobic glycolysis" may simply be an additional phenotype produced by proliferation-inducing mutations
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Inevitability
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Completion of a causal pie is synonymous with eventual occurrence (not necessarily diagnosis) of the disease
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Genomic instability and mutation
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generation of random mutations including chromosome rearrangements that orchestrate hallmark capabilities Defects of the DNA-maintenance machinery ("caretakers" of the genome) are central to this enabling characteristic These caretaker genes behave like tumor suppressor genes in that loss of function occurs throughout the course of tumor progression Inactivation of these genes involve inactivating mutations or epigenetic repression A diverse array of defects have been documented in caretaker genes including those whose gene products are involved in: Detecting DNA damage and activating the repair machinery Directly repairing damaged DNA Inactivating or intercepting molecules before they have damaged the DNA Another major source of tumor-associated genomic instability involves the loss of telomeric DNA in many tumors, which is associated with: Amplification of chromosome segments Deletion of chromosome segments Telomerase (the enzyme that helps to stabilize telomere length in human stem cells by adding TTAGGG repeats onto telomere ends) enables genomic instability by allowing cells to proliferate uncontrollably, escaping senescence and gaining immortalization In the past decade, many large-scale gene sequencing studies have been done to characterize recurrent alterations within cancer genomes 1000s of mutations have been identified, but few are recurrent when you compare tumor types TP53 is the most frequently mutated gene in all tumor types Other genes, encoding tumor suppressors and oncogenes, and involved in growth regulation have also been shown to be frequently mutated (CDKN2A, PTEN, EGFR, and RAS)
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Causality
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A component cause can involve presence of a detrimental exposure or absence of a preventive exposure
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Burden of disease
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The amount of disease caused by a causal pie depends on the prevalence of all component causes
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Temporality
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Component causes can act simultaneously or far apart in time
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Interaction
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Component causes in the same causal pie interact biologically to cause disease
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Attributable fraction
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Different component causes are responsible for more than 100% of disease cases
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Disease prevention
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Blocking the action of any component cause prevents completion of the respective sufficient cause and therefore prevents disease occurrence through that pathway
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Strength
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A strong association is more likely to be causal.
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Consistency
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An association is more likely to be causal when it is observed in different population groups.
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Specificity
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When an exposure is associated with a specific outcome only (one cancer site or histological type), then it is more likely to be causal.
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Temporality
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A cause should not only precede the disease, but also the time of exposure should be compatible with the latency period or incubation period.
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Gradient
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If there is a monotonic dose-response relationship between exposure dose and outcome, then there is strong evidence of causality.
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Sir Austin Bradford Hill in 1965 The Hill Criteria for inferring causation
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Criteria for inferring causation from epidemiological studies have been proposed by many scientists, but the most widely used
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Plausibility
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An association is more likely to be causal when it is biologically plausible.
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Coherence
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A cause and effect interpretation of an association should not conflict with what is known about the natural history and biology of the disease, or its distribution in time and place.
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Experimental evidence
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If experimental evidence exists, then the association is more likely to be causal.
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Analogy
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The existence of an analogy (for example, if a drug causes a type of cancer, then another similar drug could also have the same effect) could strengthen the belief that an association is causal.
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Limitations of hill's causal criteria
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The strength of an exposure-disease association depends on the prevalence of other causes There can be exceptions to consistency (in hindsight) Specificity can be limited (one exposure can cause many different outcomes) It may be difficult to establish temporality Threshold phenomena (e.g., U-shaped association) won't support a dose-response (gradient) Plausibility is too subjective Coherence may not be distinct from plausibility or consistency Experimental evidence is not always available Many analogies may be available
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Incidence
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defined as the number of new cases, often presented per 100,000 person-years, or as an absolute number of cases per year Incidence rates give the most obvious measure of the burden of cancer exposures at the population level
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Cancer incidence
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Data are available for only a small portion of the global population Limitations: Sophisticated infrastructure Census of the entire population Access to adequate diagnostic facilities Timely reporting of new cases Under- or overestimation of the true incidence The Surveillance, Epidemiology, and End Results (SEER) Program of the NCI works to provide cancer statistics in an effort to reduce the burden of cancer among the U.S. population
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What are some of the differences between the most commonly diagnosed cancers among women in the U.S. comparing 2015 and 2016?
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2015 breast lung ; bronchus colon and rectum uterine corpus (endometrial) thyroid non-hodgkin lymphoma melanoma pancreas leukemia kidney;renal pelvis 2016 breast lung ; bronchus colon and rectum uterine corpus (endometrial) thyroid non-hodgkin lymphoma melanoma leukemia pancreas kidney;renal pelvis
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What are some of the differences between the most commonly diagnosed cancers among men in the U.S. comparing 2015 and 2016?
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2015 Prostate lung;bronchus colon;rectum urinary bladder melanoma non-hodgkin lymphoma kidney;renal pelvis oral cavity; pharynx liver;intrahepatic duct 2016 Prostate lung;bronchus colon;rectum urinary bladder melanoma non-hodgkin lymphoma kidney;renal pelvis oral cavity; pharynx liver;intrahepatic duct
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Age-standardized incidence
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age-standardized rates allow the calculation of incidence rates as weighted averages of age-specific categories Age-standardized incidence rates give the summary rates that would be expected if each population in the comparison has the same age distribution
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Cumulative incidence
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defined as the proportion of people who develop cancer among those at risk over a specified time period Cumulative incidence is often more easily interpreted than incidence, and gives the probability that an individual will develop cancer during the time period in question Several assumptions are necessary to validly measure and estimate cumulative incidence rates No loss to follow-up No competing risks These assumptions are often unrealistic, and in those cases, the use of incidence rates (rather than cumulative incidence) is more appropriate
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Prevalence
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defined as the proportion of the population, often by gender and age category, with a past or current cancer diagnosis Prevalence can be difficult to estimate and therefore not widely used to measure cancer burden, but often gives information that is useful for planning healthcare resources
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Survival
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defined as the proportion of cancer patients surviving their disease for a specified time period after diagnosis As a measure, survival is considered the best measure for evaluating effectiveness of cancer care continuum (from screening through treatment)
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Observed survival
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describes the probability of surviving a specified time period, typically starting from the date of diagnosis All causes of death are considered
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Corrected survival
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provides a more valid estimate of the excess death rate attributable to the cancer under study Only cancer-specific causes of death are considered
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Relative survival
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based on a statistical methodology that allows the survival rate to be calculated without dependence on knowledge of the causes of death among individual cases Survival is relative to that expected in a group from the general population with the same age and gender distribution Requires 2 assumptions: Information about survival in the absence of cancer must be readily available Cancer cases must have the same "baseline" risk of death as the general population
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Mortality
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defined as the number of cancer deaths, often presented per 100,000 person-years, or as an absolute number of deaths per year Mortality rates are widely considered the most important indicator of cancer burden The preferred measure for evaluating secondary prevention
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Advantages of Cancer mortality rates
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More readily available than other measures No follow-up is required Death registries are well established in most developed countries
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Disadvantages of Cancer mortality rates
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Reliability is dependent on how accurately the causes of death are classified Mortality rates don't accurately reflect the burden of cancers with favorable prognosis For fatal cancers, mortality rates approximate incidence rates
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What cancers cause the most deaths among women in the U.S.?
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Lung & bronchus breast colon&rectum pancreas ovary uterine corpus (endometrial) leukemia liver&intrahepatic bile duct non-hodgkin lymphoma brain&other CNS
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What cancers cause the most deaths among men in the U.S.?
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lung&bronchus prostate colon&rectum pancreas liver&intrahepatic bile duct leukemia esophagus urinary bladder non-hodgkin lymphoma brain & other CNS
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What are the observable differences between the most commonly diagnosed cancers and those causing the most cancer deaths? Among women? Among men?
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The cancers most commonly diagnosed have screening programs and high 5-year survivals The cancers causing the most deaths have a very low 5-year survival with no screening and aggressive nature
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Years of life lost (YLL)
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defined as the number of years of life lost between the age at death and the expected age at death (in the absence of the cancer in question) Describes the difference between dying from cancer in childhood versus later in life This is not a widely used measure
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Disability adjusted life years (DALYs)
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combines the impact of cancer on both survival and the quality of life One DALY = one lost year of "healthy" life To calculate DALYs, two parameters must be available Total number of life years lost due to the disease The number of these years lived with a disability of known severity
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Global cancer burden
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World population in 2016: 7.4 billion Cancer incidence: 14.1 million 6.1 million in developed countries 8 million in developing countries Cancer deaths: 8.2 million >22,000 cancer deaths per day 2.9 million in developed countries 5.3 million in developing countries By 2030, the global burden is expected to grow to 21.4 million new cases and 13.2 million deaths
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Geographic variation
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the occurrence of types of cancer and overall cancer burden due to the following factors: Prevalence of the major risk factors for each specific cancer Availability and use of medical practices (i.e. screening) Availability and quality of treatment Age structure in the population
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HOT TOPIC - CHINA
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A new report estimates there were 4.3 million new cancer cases and .2.8 million cancer deaths in China in 2015, with lung cancer the most common cancer and the leading cause of cancer death in China. Cancer death rate is equivalent to >7500 cancer deaths occur per day in China With increasing incidence and mortality, cancer is the leading cause of death in China and is a major public health problem. Among men, the five most common cancers are: lung, stomach, esophagus, liver, and colorectal Among women, the most common cancers are: breast, lung and bronchus, stomach, colorectal, and esophagus Much of the cancer incidence and deaths in China could be prevented through reducing the prevalence of risk factors, while also increasing the effectiveness of clinical care delivery, particularly for those living in rural areas and in disadvantaged populations.
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Geographic variation, some examples Worldwide
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Breast cancer was the leading cancer among women (and the leading cause of cancer death) in 10 out of the 21 world areas Cervical and lung cancers were the leading causes of death in the remaining areas
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Geographic variation, some examples Developing countries
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In Africa, the most common cancers in men were prostate, lung, liver, esophageal, bladder, Kaposi sarcoma and non-Hodgkin lymphoma Two of the four leading cancers in men (stomach and liver) and women (stomach and cervix) were related to infection
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Geographic variation, some examples Developed countries
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Prostate cancer was the most common cancer in developed countries, except in Japan, where stomach cancer was the most common Only ~8% of incident cancers attributable to infection
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HPV in the US
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Screening can prevent cervical cancer by detecting precancerous lesions early enough to be treated and preventing their progression to cancer HPV test detects HPV infections associated with cervical cancer and can be used to predict a patient's future cervical cancer risk In the US, HPV tests are recommended to be used in conjunction with Pap tests In many low-resource settings there is a lack of availability of technical and public health infrastructure to support cervical cancer screening, which is related to the higher incidence and mortality in some countries
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overall incidence in U.S States
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digestive system cancers (18.09%), followed by genital system cancers (17.65%) and breast cancer (14.79%) imposed the largest burden Other ; unspecified primary cancers account for 2.03% of all incident cancers
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Cancer incidence are highest in U.S
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CA (10.28%), FL (7.19%), TX (6.92%), NY (6.54%), and PA (4.96%)
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Overall cancer incidence with men compared to women
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men (522.6 per 100,000) than women (419.0 per 100,000)
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Incidence rates among men are highest in...
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KY, LA, DE, MS, NY (NJ has the 6th highest rates)
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Incidence rates among women are highest in.....
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KY, MA, NH, PA, CT (NJ has the 9th highest rates)
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What states have the highest Breast cancer rates?
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D.C CT MA NH WA
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What states have the highest Prostate cancer rates?
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D.C LA NJ UT DE
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overall cancer deaths, states with highest numbers are...
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CA (9.91%) FL (7.32%), TX (6.62%), NY (5.86%), and PA (4.82%) (NJ has the 9th highest number of cancer deaths)
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Overall cancer mortality rate in the U.S. is
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higher among men (207.9 per 100,000) than women (145.4 per 100,000)
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Cancer mortality rates among men are highest in
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MS, KY, LA, AL, AR (NJ falls below the U.S. rate and ranks 36th)
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Cancer mortality rates among women are highest in
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KY, WV, DC, LA, OK (NJ falls below the U.S. rate and ranks 27th)
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The 5-year relative survival rate for all cancers diagnosed in the U.S. during 2005-2011 compared to 1975-1977
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was 69%, which reflects an increase from 49% Improvement in survival rates likely reflect: Earlier diagnosis of some cancers Improvements in cancer treatment and therapies Relative survival rates vary substantially by cancer type and stage at diagnosis
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The Agency for Healthcare Research and Quality (AHQR) estimates that the direct medical costs (total healthcare expenditures) for cancer in the U.S. in 2013 were
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$74.8 billion 44% ($32.9 billion) - attributed to outpatient or office-based care 40% ($29.9 billion) - attributed to inpatient hospital stays This is alarming given that 33 million Americans (~10%) remained insured during the 2014 calendar year This reflects ~9 million fewer uninsured Americans following implementation of the Affordable Care Act
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What causes Cancer disparities?
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Social factors Economic factors Cultural factors Health system factors Biological factors (not clearly understood)
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"Poverty is a carcinogen."
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- Dr. Samuel Broder, Former NCI Director (1989-1995) Inequities in work, wealth, income, education, housing, and overall standard of living, as well as social barriers to high-quality healthcare, including cancer prevention, early detection, and treatment services also are important factors.
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High SES vs Low SES
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Among those with lower SES, there is disproportionately higher cancer mortality rates than those with higher SES, irrespective of race/ethnicity This disparity is largest for lung cancer Mortality rates are 4-5 times higher in the least educated than most educated sub-groups
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Lower SES and behaviors
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Individuals of lower SES are more likely to engage in poorer health behaviors, known to increase cancer risk Tobacco use Physical inactivity Poor dietary habits Lower SES is also associated with financial, structural and personal obstacles to adequate and timely health care lack of health insurance The Affordable Care Act (ACA) is expected to substantially reduce these obstacles
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Cancer disparities by SES
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Individuals with no health insurance are more likely to be diagnosed with advanced disease and are less likely to receive standard treatment and survive their cancer Data from the U.S. Census Bureau indicate that in 2009, 1 in 4 African Americans and Hispanics/Latinos lived below the poverty line, compared to 1 in 11 non-Hispanic whites 1 in 5 AAs and 1 in 3 Hispanics/Latinos or American Indian/Alaska Natives were uninsured, compared to 1 in 8 non-Hispanic whites
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