Epidemiology of Cancer
(Environmental Biology of
Cancer)
Folder Title: Epidemio(NoTP)
Updated: Feb. 04, 2016,
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Epidemiology of Diseases
Distribution of patterns of health and disease.
Determination of potential causation that leads to the observed
distribution.
Observational vs Experimental Sciences:
• Observe episodes of disease appearance (e.g. geographic "hotspots" or occupational or familial patterns)
• Retrospective analysis of potential causative associations
• Prospective trials to determine causative sources
Determine "Relative Risk" or "Odds Ratio"
• Small vs large Relative Risk Values
Association or Correlation is not Causation
Complications in Epidemiological Observations
Reliable reproducible data and conclusions vs.
firmly held beliefs or "common sense" assumptions.
Problems with acquisition of data and data reliability:
• Time patterns of exposure vs appearance of disease
• Combinations of causative sources and sequences of
exposures
• High background appearance (non-rare diseases)
• Usually small impact of an agent on an individual or
population
• Retrospective data: recall bias and data reporting
• Prospective trials: Costs, ethical problems, subject
cooperation
Deducing Actual Causation from Epidemiological Data
Epidemiological data comparing high and low incidence rates based on
different population groups poses the questions:
1.
Why is one group presenting high risk for a given type of cancer?
2.
Why is another group presenting relatively low risk for that type of
cancer?
3.
What does that tell us about causation?
4.
Does that present possibilities for prevention and diagnosis?
Breast Cancer
Relative Risks
Epidemiological data comparing high and low
incidence rates based for different types of cancer
based on different countries poses the questions:
1. Why is a given cancer (e.g. liver cancer) high in
one set of countries?
2. Why is that same cancer very low in other
countries?
3. What does that tell us about causation?
4. Does that present possibilities for prevention and
diagnosis?
Specific Cancer Incidence
and Migratory Patterns:
Cancers and
Environmental Effects
Cancer Incidence Following Migration
Figure 2.20 The Biology of Cancer (© Garland Science 2007)
p. 45
Epidemiological Data can also sometimes
provide clues about the biological mechanisms
underlying certain types of cancers.
Malignant Melanoma
(Solar radiation exposure)
Burkitt’s Lymphoma
(Co-infection with virus transmitted by
mosquitos also transmitting malaria)
White Males
White Females
Black Males
& Females
MelRace
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Completed Question 1, Class 5, February 2, 2016
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Completed Question 1, Class 5, February 2, 2016
Cancer Incidence and Changes in Gene
Expression:
Reciprocal Translocation
9 to 22 Reciprocal Translocation:
Chronic Myelogenous Leukemia (CML)
8 to 14 Reciprocal Translocation:
Burkitts Lymphoma
Fluorescent in
situ
hybridization
(FISH) of
normal
metaphase
human
chromosomes
using
chromosome
specific DNA
probes with
different
fluorescent dyes
Figure 1.11b The Biology of Cancer (© Garland Science 2007)
Chromosome-specific Probe Analysis of Reciprocal Translocation (9 to 22)
in Chronic Myelogenous Leukemia
Chromosome 9 (White); Chromosome 22 (Purple)
Figure 2.23b The Biology of Cancer (© Garland Science 2007)
Reciprocal translocation between chromosomes 9 and 22
produces fusion of a cancer-inducing gene, the abelson or
abl gene with information on another chromosome.
This chromosome fusion is expressed as a fusion protein
involving the abl gene product.
This miss-expressed fusion protein drives cell division in
leucocytes leading to chronic myelogenous leukemia.
Other types of leukemia are supported by fusions proteins
involving the abl gene that are fused at different break points
and give fusion proteins of different molecular weights
Reciprocal Translocation (8 to 14) in Burkitt’s Lymphoma
Figure 4.13a The Biology of Cancer (© Garland Science 2007)
p. 109
Incidence of Burkitt’s Lymphoma in Relation to Infectious Disease Etiology:
Aedes simpsoni mosquito transmission vector for malaria
and Epstein Barr Virus co-infection
Figure 4.12 The Biology of Cancer (© Garland Science 2007)
Myc Oncogene (Chromosome 8) Expression Controlled by Fusion with
Immunoglobulin Heavy Chain Gene (Chromosme 14) in Burkitt’s Lymphoma
Figure 4.13b The Biology of Cancer (© Garland Science 2007
p. 109)
Epidemiology of Cancer
Based on Age
Incidence of Various Kinds of Cancers in Men and Women as a Function of Age
See Figure 11.1, Cancer incidence at various ages for men and women. p. 400. Weinberg.
Note maximum incidence per 100,000 population at about age 70, then drop off after that age.
Serious incidence begins around age 35 except for breast cancer which can have an earlier onset
depending on genetics and hormonal status.
Why do “super-old” seem to show cancer resistance?
Carcinogenic Agents,
the Story of Tobacco, Cancer,
and Government Regulation
Data from
1960’s:
DoseResponse
Effect
CigDose
p. 46
Table 2.6 The Biology of Cancer (© Garland Science 2007)
Cigarette Consumption and Lung Cancer: 1880 to 2000
Figure 11.2 The Biology of Cancer (© Garland Science 2007)
Recent Data on Trends in
Cigarette Consumption:
Centers for Disease Control
Under: What has the Government
Done for Me Lately?
“I’m from the Government and I
am trying to help”. (Reagan’s idea
of a statement to ridicule)
CDC Data: http://www.cdc.gov/mmwr/preview/mmwrhtml/mm4843a2.htm
Latest Data from Centers for Disease Control:
Smoking 2015: Less than 20%
Environmental and
Occupational Cancers
Effects from Nuclear
Plant Melt-Down
Journal of the
National Cancer
Institute,
July, 1996
Chernobyl nuclear powerplant melt-down, April 1986
Kids&Rad
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End Epidemiology
Presentation Here:
Older Data Follows
Cancer Incidence and Length of Time of Carcinogen Exposure
Mesothelioma in
human insulation
workers
Squamous cell
carcinoma in mice.
Figure 11.4 The Biology of Cancer (© Garland Science 2007)
CxCauses
WorkCx
Table 2.7 The Biology of Cancer (© Garland Science 2007)
p. 47
Cultural Associations
and Specific Cancers
Journal of the National
Cancer Institute
October, 1996
StomCxEthnic
Wake up Mom.
Time to Play!
Male Cancer Death Rates for Various Carcinomas, 1939 to 1947. Log-Log Plot
Figure 11.3 The Biology of Cancer (© Garland Science 2007)
Slope of 5 indicates a series of rate limiting steps
Table 2.5 part 1 of 2 The Biology of Cancer (© Garland Science 2007)
p. 44
Solar exposure & skin pigmentation
?
Epstein-Barr Virus Association
?
Hepatitis B Virus
Papilloma viruses
Papilloma viruses
Helicobacter pylori infection
Smoking
?
?
Table 2.5 part 1 of 2 The Biology of Cancer (© Garland Science 2007)
p. 44
AgeEffct
Incidence
IInteracting causative agents: Alcohol and cigarettes
See also Figure 7-6,
Biological Basis of Cancer,
p 191
Lifetime Melanoma Risk: 1935 to 1996
Figure 7-8, Biological Basis of Cancer, 1998, p 194
MelRisk