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Hanahan & Weinberg: The hallmarks of cancer. Cell 100:57-70, 2000

Hanahan & Weinberg: The hallmarks of cancer. Cell 100:57-70, 2000. ONCOGENE ACTIVATION. ONCOGENE ACTIVATION. TUMOR SUPPRESSOR INACTIVATION. 1) Point mutation. p53. TUMOR SUPPRESSOR INACTIVATION. 1) Point mutation : p53, BRCA1 etc. 2) Deletion 3) Epigenetic silencing. Locus 9p21.

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Hanahan & Weinberg: The hallmarks of cancer. Cell 100:57-70, 2000

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  1. Hanahan & Weinberg: The hallmarks of cancer. Cell 100:57-70, 2000

  2. ONCOGENE ACTIVATION

  3. ONCOGENE ACTIVATION

  4. TUMOR SUPPRESSOR INACTIVATION 1) Point mutation p53

  5. TUMOR SUPPRESSOR INACTIVATION 1) Point mutation: p53, BRCA1 etc. 2) Deletion 3) Epigeneticsilencing

  6. Locus 9p21

  7. TUMOR SUPPRESSOR INACTIVATION 1) Point mutation: p53, BRCA1 etc. 2) Deletion 3) Epigeneticsilencing 4) Protein-proteininteractions

  8. TUMOR SUPPRESSOR INACTIVATION Protein-protein interactions

  9. Cellula normale PTEN Cellula tumorale PTEN effetti lievi attività PI3K/Akt/mTOR INIBITORI DI mTOR attività PI3K/Akt/mTOR

  10. Table 1 Examples of oncogene addiction: studies in mice Weinstein IB and Joe AK (2006) Mechanisms of Disease: oncogene addiction—a rationale for molecular targeting in cancer therapy Nat Clin Pract Oncol 3: 448–457 10.1038/ncponc0558

  11. Table 2 Examples of oncogene addiction: studies in human cancer cell lines Weinstein IB and Joe AK (2006) Mechanisms of Disease: oncogene addiction—a rationale for molecular targeting in cancer therapy Nat Clin Pract Oncol 3: 448–457 10.1038/ncponc0558

  12. Table 3 Clinical evidence of oncogene addiction Weinstein IB and Joe AK (2006) Mechanisms of Disease: oncogene addiction—a rationale for molecular targeting in cancer therapy Nat Clin Pract Oncol 3: 448–457 10.1038/ncponc0558

  13. MODELS OF ONCOGENE ADDICTION

  14. MODELS OF ONCOGENE ADDICTION

  15. MODELS OF ONCOGENE ADDICTION

  16. Twogenes (‘A’ and ‘B’) are said to be synthetic lethal if mutation of either gene alone is compatible with viability but simultaneous mutation of both genes causes death.

  17. Cellula normale Rb Cellula tumorale Rb SOPRAVVIVENZA blocco attività E2F VELENI DELLA TOPO II  espressione gene A  espressione gene topoisomerasi II  attività E2F  espressione gene B  espressione gene C

  18. B is an extragenicsuppressorof A if mutation of B suppresses the phenotype observed when A is mutated.

  19. % B inhibition % B inhibition

  20. HOW CAN WE SELECTIVELY TARGET TUMOR RELEVANT DEFECTS? INIBIT GENE EXPRESSION INIBIT PROTEIN FUNCTION Small molecule inhibitors AS-ODN mAbs siRNA

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