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7/27/2019 Fisiopatologia Del Cancer [Modo de Compatibilidad]
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Physiopathology of cancer
Dr. Julio Hilario Vargas
Department of Physiology
School of Medicine
National University of Trujillo
Brain Cancer Cell
Source: http://www.alternative-cancer.net/Cell_photos.htm
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Is a class of disease in which a group of cells display
uncontrolled growth through division beyond normal
limits, invasion that intrudes upon and destroys
adjacent tissues, and sometimes metastasis, in which
cancer cells spread to other locations in the body vialymph or blood. These three malignant properties of
cancers differentiate them from benign tumors, which
are self-limited, and do not invade or metastasize.
CANCER
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By the type of cell that the tumor resembles and is thereforepresumed to be the origin of the tumor. These types include:
Carcinoma: Cancer derived from epithelial cells. This group
includes many of the most common cancers, including those of
the breast, prostate, lung and colon.
Sarcoma: Cancer derived from connective tissue, ormesenchymal cells.
Lymphoma and leukemia: Cancer derived from hematopoietic
(blood-forming) cells
Germ cell tumor: Cancer derived from pluripotent cells. In adults
these are most often found in the testicle and ovary, but are more
common in babies and young children
Blastoma: Cancer derived from immature "precursor" or
embryonic tissue. These are also commonest in children
Cancers classification
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Tipos comunes de cncer
- American Cancer Society: Cancer Facts and Figures for Hispanics/Latinos 2006-2008. Atlanta, Ga: American Cancer
Society, 2006. Disponible tambin en Internet.
- Lipworth L, Tarone RE, McLaughlin JK: The epidemiology of renal cell carcinoma. Journal of Urology 176(6 pt 1):2353-
2358, 2006
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Genomic Instability
An increased tendency of the GENOME to acquire MUTATIONS when
various processes involved in maintaining and replicating the genomeare dysfunctional
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Phenotypic Changes in the Progression of Neoplasia
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Phenotypic Changes in the Progression of Neoplasia
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Zitvogel L et al., Nat. Rev. Immunol., 2006, 6:715.
Cancer Immunoediting: The New
Surveillance Hypothesis
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Dunn GP et al., Nat. Immunol., 2002, 3:991.
Surveillance
At equilibrium immune selection develops leading to tumor escape
Cancer Immunoediting: Three Es
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The three Es of cancer immunoediting: host protective versus tumor
sculpting actions of immunity
Dunn GP, Old LJ, Schreiber RD. The immunobiology of cancer immunosurveillance and immunoediting. Immunity. 2004 Aug;21(2):137-48.
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Cancers are primarily an environmentaldisease with 90-95% of cases due
environmental factors such as lifestyle, and
5-10% directly due to heredity.
Common environmental factors leading tocancer include: tobacco (25-30%), diet and
obesity (30-35%), infections (15-20%),
radiation, lack of physical activity, and
environmental pollutants.
Some viruses and bacteria are included too.
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HTLV: Human T-cell leukemia-lymphoma virus; HHV-8: Human herpesvirus-8; KSHV: Kaposis
sarcoma herpesvirus
Oncogenic Human Viruses
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Is a normal gene that can become an oncogene due tomutations or increased expression. The resultant protein
may be termed an oncoprotein.
Proto-oncogenes code for proteins that help to regulate cell
growth and differentiation. Proto-oncogenes are often
involved in signal transduction and execution of mitogenic
signals, usually through their protein products. Upon
activation, a proto-oncogene (or its product) becomes a
tumor-inducing agent, an oncogene. Examples of proto-
oncogenes include RAS, WNT, MYC, ERK, and TRK
Proto-oncogene
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Biochim Biophys Acta 1602(2), M. Frame, Src in Cancer, 114-130, 2002
Src-induced signaling from membrane/adhesions that controls cell behaviour
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Is a gene that has the potential to cause cancer
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Representative Oncogenes Activated in Human Tumors
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Representative Tumor Suppressor Genes Inactivated in
Human Tumors or the Human Germline
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Rescuing the function of mutant p53
Alex N. Bullock & Alan R. Fersht. Nature Reviews Cancer1, 68-76 (October 2001)
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Retinoblastoma : the tumor suppressor gene paradigm
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DNA damage, repair mechanisms, and consequences
2001 Nature Publishing Group Hoeijmakers, J. H. J. Genome maintenance mechanisms for
preventing cancer. Nature 411, 366374 (2001)
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DNA repair mechanisms
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Loca l symp toms:Are restricted to the site of the primary cancer. They
can include lumps or swelling (tumor), hemorrhage (bleeding from the
skin, mouth or anus), ulceration and pain. Although local pain commonly
occurs in advanced cancer, the initial swelling is often painless.
Metastat ic symptom s:are due to the spread of cancer to other locations
in the body. They can include enlarged lymph nodes (which can be felt or
sometimes seen under the skin), hepatomegaly (enlarged liver) orsplenomegaly (enlarged spleen) which can be felt in the abdomen, pain
or fracture of affected bones, and neurological symptoms.
Systemic symptoms:occur due to distant effects of the cancer that are
not related to direct or metastatic spread. Some of these effects can
include weight loss (poor appetite and cachexia), fatigue, excessivesweating (especially night sweats), anemia (low blood count) and other
specific conditions termed paraneoplastic phenomena. These may be
mediated by immunological or hormonal signals from the cancer cells
Signs and symptoms