Neoplasia: Molecular Basis Of Cancer Flashcards
Acquired mutations caused by
Exogenous agents (viruses, chemicals) Endogenous of cellular metabolism
Principal targets of cancer causing mutations
Growth promoting proto oncogenes
Growth inhibiting tumor suppressor genes
Genes that regulate programmed cell death
Genes involved in DNA repair
Growth promoting proto oncogenes
Gain of functions
Excessive function
Complete new function
Dominant in normal cells
Tumor suppressor genes
Loss of function
Both genes must be damaged in most
Only one gene damaged but still it caused tumor suppressor genes
Haploid insufficiency
Apoptosis
Less death that enhances survival a of cells
Gain of function - suppress apoptosis
Loss of function - promote cell death
DNA repair
Loss of function
Contribute to the development of malignant phenoyptype
Driver mutations
First driver mutation
Initiating mutations
Ang mga iniated cells ay mag acquire ng? Nag mag co contribute sa development ng cancer at ito ay matagal
Additional driver mutations
Cancers arise from cells with stem cell like properties
Cancer stem cells
Common early step on the road to malignancy
Loss of function mutations
Increase the frequency of mutations but no phenotypic consequences
Passenger mutations
More common than driver mutations
Passenger mutations
Competition among tumor cells for access to nutrient and micro environmental riches
Darwinian contest or selection
Pernicious tendency of tumors to become more aggressive over time
Tumor progression
Two types of mutation in DNA sequencing
Present in all tumor site
Unique to a subset of tumor sites
Present in the founding cell at the moment of transformation
Present in all tumor site
Unique to a subset of tumor sites
During after the transformation
During outgrowth and spread of tumor
Family trees
Galápagos Islands
Explain natural history of cancer
Changes in tumor behavior therapy
Selection of the fittest cells
Selective pressures that cancer cells face
Chemotherapy or radiotherapy
Pero pag nag recur ang tumor resistant na ito sa chemotherapy
Nice to know
Also contribute to the malignant properties of cancer cells. Except DNA mutations
Epigenetic aberrations
Epigenetic aberrations includes
DNA methylation
Histone modifications
Silence gene expression
DNA. Methylation
Enhance dampen gene expression
Histone modifications
Unlike DNA mutations, Epigenetic are
Potentially reversible by drugs
DNA mutations
Epigenetic
Passed to daughter cells
DNA methylation
Silencing effect
Histone modification
Far ranging effects
Cellular and molecular hallmarks of cancer
Oncogene activation
Self sufficiency in growth signals
Inactivation of tumor suppressor gene
Insensitivity to growth inhibitory signals
Warburgs effects
Altered cellular metabolism
Metabolic switch to aerobic glycolysis
For rapid cell growth
Warburg effects
Resistant to programmed cell death
Evasion apoptosis
Immortality
Stem cell like property
Limitless replicative potential
Kahit walang vascular supply
Sustained angiogenesis
Accelerated those hallmarks of cancer
Genomic instability
Cancer promoting inflammation
Genes that promotes autonomous cell growth in cancer cells
Oncogenes
Un mutated cellular counter part of oncogene
Proto oncogene
Encode proteins by oncogene
Freed from normal checkpoints
Oncoproteins
Most frequently mutated oncogenic pathway
Tyrosine kinase pathway
Accelerators of DNA replication
Once proteins
Slow or brakes
Tumor suppressors
Physiologic conditions of growth factor
- Growth factor bind ps to receptor
- Activate cytoplasmic signal transducing proteins
- Transmits to nucleus via: cytoplasmic receptor proteins or 2nd messenger
- DNA transcription
- Cell division
Nonlethal genetic damage lies at the heart of
Carcinogenesis
