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Pathophysiology of Cancer

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Cancer Genetics. Tumor/Host Interactions. Clinical Application: Breast Cancer ... Differences in the incidence of breast, liver, gastric, colon and prostate ... – PowerPoint PPT presentation

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Title: Pathophysiology of Cancer


1
Pathophysiology of Cancer
2
  • Characteristics of Cancer
  • Molecular Mechanisms of Growth Control
  • Cancer Genetics
  • Tumor/Host Interactions
  • Clinical Application Breast Cancer

3
The Nature of Cancer
4
Neoplasia Unregulated accumulation of cells
5
  • Normal Tumor
  • Abnormal regulation of cell growth
  • Abnormal cell-cell interactions

6
Normal Tumor Normal stem cell
Cancer stem cell
7
Characteristics of Stem Cells
  • Unlimited capacity for self-renewal
  • Cellular immortality
  • But relatively low rate of proliferation
  • Capable of differentiation into the mature cells
    that constitute organ function
  • Proliferation can be dramatic once a cell has
    committed to differentiation
  • But differentiated cells have limited life-span

8
Normal
Cancer
Stem cell Compartment
Proliferative Compartment
Etc. Maturation Compartment
Cell loss (apoptosis)
Etc., Etc., Etc. Maturation Compartment
9
Lessons From Stem Cell Kinetics
  • The growth rate of cancer cells does not exceed
    that of normal cells
  • Abnormal differentiation of cancer cells results
    in a greater percentage of cells in the
    proliferative pool (at the expense of the
    maturation pool)
  • Tumor (mass) growth exceeds normal growth due to
    a higher proliferative fraction and a lower rate
    of cell loss (death)

10
Benign Malignant
pleomorphism abnormal nuclei
mitoses loss of polarity abnormal
differentiation
11
Invasion
12

Abnormal cell-substratum interaction
13

Invasion into adjacent structures

14
Dissemination (Metastases)
15
Penetration of vasculature Survival in
circulation Survival in a new organ
16
metastatic spread is not random but determined
by -pattern of venous blood flow -specific
receptors on tumor and endothelial
cells -metastatic fitness is genetically
determined
17
Cancer Epidemiology
  • Or,
  • Guilt by Association

18
Caveat epidemiology
  • Studies are observational and therefore do not
    establish cause and effect
  • Initial observations require confirmation and
    exclusion of confounding variables
  • However, well-performed studies can provide
    valuable insights into factors that contribute to
    cancer.

19
Cancer Incidence
  • Cancer is a disease of aging
  • Deaths increased 3x in the 7th decade compared to
    the 5th 6th decades combined
  • But, cancers differ in their age-related incidence

20
Cancer Incidence
  • Environment affects cancer incidence
  • Differences in the incidence of breast, liver,
    gastric, colon and prostate cancers in Japanese
    and US populations disappear following
    immigration (unknown factors)
  • Liver cancer incidence is related to incidence of
    Hepatitis B C incidence and afflatoxin exposure
  • Melanoma incidence is associated with UV exposure

21
Cancer Incidence
  • Toxins affect cancer incidence
  • Tobacco - lung, upper aerodigestive tract
    everything else
  • Asbestos - lung, mesothelioma
  • Alcohol - liver, upper aerodigestive tract
    esophagus,
  • Others - see table 7-3

22
Cancer Incidence
  • Infectious agents
  • H. pylori - gastric lymphoma adenoCA
  • Papillomavirus - cervical CA
  • HTLV - T-cell leukemia
  • Epstein-Barr virus - lymphomas and nasopharyngeal
    cancers

23
Cancer Incidence
  • Genetic factors
  • Specific cancer genes (addressed later)
  • Unidentified genetic factors (generally a low
    level familial risk)

24
Cancer Incidence
  • Obesity increases the risk of most cancers

25
Cancer Epidemiology Conclusions
  • Cancer is the result of the cumulative effects of
    living and the interplay of environmental
    exposures and genetic predisposition
  • It is likely that most risk factors act as either
    Initiators or Promoters of carcinogenesis.
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