CANCER

Sarcomas

Leukemias

Lymphomas

Carcinomas, which account for about 90% of all cancers,

Cell differentiation

hyperplasiadysplasiametaplasia y anaplasiametastasis

Cell Differentiation

Density independent growth

Anchorage independent growth

Cell Aging and telomerase activity

Metastasis

E-Cadherin &

Plasminogen activatoractivates plasmin

Plasmin cleaves ECM andactivates MMPs

Sites of Metastasis 1/1000 will survive

Clones

Failure of Adequate Immune Response:Evading immune systemTGF-B resistant and secreting

Epidemiology of Cancer andCauses of Cancer

inducible on exposure to non-polar aromatic molecules such as dioxin

P450pre-carcinogenscarcinogen activation

2-naphtylamine(cigarettes)*Sólo en la dieta, directo a la vejiga no induce el cancer

Benzopyrene en cigarrillo

P450 (liver homogenate) Carcinogen activation

tar DMBA (dimethylbenz-anthracene)

Croton oils a Phorbol Ester (Protein Kinase C)

InitiationPromotionTumor Progression

UV and p53 mutations

Epstein-Barr– Burkitt lymphoma

Hb & Hc,

HTLV-I (Human T-cell Lymphotropic virus)

Helicobacter pylori

Prevalence of HPV in 90% of cervical cancers

Proto-oncogenes to oncogenesOncogenes

Fusión de genesTropomiosina con Fragmento de Receptor cinasa de tirosina

Tumor supressor genes

RB tumor suppressor gene

RB tumor suppressor gene

10 million people diagnosedwith cancer each year willhave tumors with p53mutations

Colon carcinoma

Most hereditary forms of breastcancer arise in women who inherit a mutant copy of either the BRCA1 or BRCA2 gene, both of whichcode for proteins involved in repairing double-strand DNA breaks

Most cancers are not hereditary, they exhibit genetic instability

Genetic instability can also arise from defects in mitosis that cause disruptions in chromosome sorting during cell division, resulting in broken chromosomes and aneuploidy

xeroderma pigmentosum

Multiple mutations are usually required to convert a normal cell into a cancer cell.