1223636
Molecular Basis of Neoplasm
- General
- Nonlethal genetic damage
- clonal expansion from precursor cell
- 4 types of regulatory genes
- proto-oncogenes
- tumor suppressor genes
- apoptosis genes
- DNA repair
- proto-oncogenes
- accumulation of complementary mutation
- driver mutations allow for other mutations to accumulate
- passenger mutations
- driver mutations allow for other mutations to accumulate
- evolve and progress under Darwinian selevtion
- changes tumor behavior and history of the cancer
- changes tumor behavior and history of the cancer
- epigenetic aberrations cause problems too
- Nonlethal genetic damage
- Cellular and Molecular
Hallmarks of Cancer
- 8 fundamentals of changes
- self-sufficiency in growth signals
- insensitivity to growth-inhibitory signals
- altered cellular metabolism
- evasion of apoptosis
- limitless replicative potential (Immortality)
- sustained angiogenesis
- ability to invade and metastasize
- ability to evade host immune response
- self-sufficiency in growth signals
- accelerated by genomic instability and cancer-promoting inflammation
- 8 fundamentals of changes
- Self-Sufficiency in Growth
Signals: Oncogenes
- mutations in proto-oncogenes
- oncogenes
- promote cell growth in the absence of growth-promoting signalling
- promote cell growth in the absence of growth-promoting signalling
- Mutations in...
- G protein coupled
- JAK/STAT
- WNT
- Notch
- TGFb/SMAD
- Hedgehog
- NF-kB
- G protein coupled
- oncogenes
- mutations in proto-oncogenes
- Proto-oncogenes, Oncogenes, Oncoproteins
- drive proliferation
- Mutations of...
- Growth Factors
- can synthesize GF on their own
- can synthesize GF on their own
- Growth Factor Receptors
- become constitutively active
- become constitutively active
- Down stream components of TK signaling pathway
- RAS mutations
- signal transmitting protein
- reduced GTPase activity
- signal transmitting protein
- BRAF and PI3K
- BRAF
- serine/threonine kinase
- stimulate downstream kinases
- serine/threonine kinase
- PI3K
- activates AKT
- PTEN mutation removes regulation
- activates AKT
- BRAF
- Nonreceptor Tyrosine Kinases
- ex: BCR-Abl
- same function as receptor TK
- ex: BCR-Abl
- Transcription Factors
- disregulation of mitotic pathways
- disregulation of mitotic pathways
- MYC oncogene
- activates with other cell growth genes
- sometimes upregulates telomerase
- can be used to reprogram somatic cells backwards
- activates with other cell growth genes
- Cyclins and CDK
- stop having cell cycle checkpoints
- promotes progression
- promotes progression
- stop having cell cycle checkpoints
- Growth Factors
- drive proliferation
- Insensitivity to Growth Inhibition:
Tumor Suppressor Genes
- normally stop growth
- two-hit hypothesis
- two mutations are required to cause symptoms
- sporadic or familial
- two mutations are required to cause symptoms
- RB: governs proliferation
- negative regulation on G1/S transition
- hyper/hypophosphorylated
- negative regulation on G1/S transition
- TP53
- regulates cell cycle progression, DNA repair, cellular senescence and apoptosis
- Enter text here
- regulates cell cycle progression, DNA repair, cellular senescence and apoptosis
- normally stop growth
- Growth-Promoting Metabolic
Alterations: The Warburg Effect
- Evasion of Programmed
Cell Death (Apoptosis)
- Limitless Replicative Potential: The Stem
Cell-Like Properties of Cancer Cells
- Angiogenesis
- Invasion and Metastases
- Evasion of Host Defense
- Genomic Instability
- Cancer-Enabling Inflammation
- Dysregulation of
Cancer-Associated Genes
- Molecular Basis of
Multistep Carcinogenesis
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