Molecular Basis of Neoplasm

Jeff Amos
Mind Map by Jeff Amos, updated more than 1 year ago
Jeff Amos
Created by Jeff Amos over 5 years ago
16
1

Description

step 1 Pathology Mind Map on Molecular Basis of Neoplasm, created by Jeff Amos on 09/01/2014.
Tags

Resource summary

Molecular Basis of Neoplasm
1 General
1.1 Nonlethal genetic damage
1.2 clonal expansion from precursor cell
1.3 4 types of regulatory genes
1.3.1 proto-oncogenes
1.3.2 tumor suppressor genes
1.3.3 apoptosis genes
1.3.4 DNA repair
1.4 accumulation of complementary mutation
1.4.1 driver mutations allow for other mutations to accumulate
1.4.2 passenger mutations
1.5 evolve and progress under Darwinian selevtion
1.5.1 changes tumor behavior and history of the cancer
1.6 epigenetic aberrations cause problems too
2 Cellular and Molecular Hallmarks of Cancer
2.1 8 fundamentals of changes
2.1.1 self-sufficiency in growth signals
2.1.2 insensitivity to growth-inhibitory signals
2.1.3 altered cellular metabolism
2.1.4 evasion of apoptosis
2.1.5 limitless replicative potential (Immortality)
2.1.6 sustained angiogenesis
2.1.7 ability to invade and metastasize
2.1.8 ability to evade host immune response
2.2 accelerated by genomic instability and cancer-promoting inflammation
3 Self-Sufficiency in Growth Signals: Oncogenes
3.1 mutations in proto-oncogenes
3.1.1 oncogenes
3.1.1.1 promote cell growth in the absence of growth-promoting signalling
3.1.2 Mutations in...
3.1.2.1 G protein coupled
3.1.2.2 JAK/STAT
3.1.2.3 WNT
3.1.2.4 Notch
3.1.2.5 TGFb/SMAD
3.1.2.6 Hedgehog
3.1.2.7 NF-kB
4 Proto-oncogenes, Oncogenes, Oncoproteins
4.1 drive proliferation
4.2 Mutations of...
4.2.1 Growth Factors
4.2.1.1 can synthesize GF on their own
4.2.2 Growth Factor Receptors
4.2.2.1 become constitutively active
4.2.3 Down stream components of TK signaling pathway
4.2.4 RAS mutations
4.2.4.1 signal transmitting protein
4.2.4.2 reduced GTPase activity
4.2.5 BRAF and PI3K
4.2.5.1 BRAF
4.2.5.1.1 serine/threonine kinase
4.2.5.1.2 stimulate downstream kinases
4.2.5.2 PI3K
4.2.5.2.1 activates AKT
4.2.5.2.2 PTEN mutation removes regulation
4.2.6 Nonreceptor Tyrosine Kinases
4.2.6.1 ex: BCR-Abl
4.2.6.2 same function as receptor TK
4.2.7 Transcription Factors
4.2.7.1 disregulation of mitotic pathways
4.2.8 MYC oncogene
4.2.8.1 activates with other cell growth genes
4.2.8.2 sometimes upregulates telomerase
4.2.8.3 can be used to reprogram somatic cells backwards
4.2.9 Cyclins and CDK
4.2.9.1 stop having cell cycle checkpoints
4.2.9.1.1 promotes progression
5 Insensitivity to Growth Inhibition: Tumor Suppressor Genes
5.1 normally stop growth
5.2 two-hit hypothesis
5.2.1 two mutations are required to cause symptoms
5.2.2 sporadic or familial
5.3 RB: governs proliferation
5.3.1 negative regulation on G1/S transition
5.3.2 hyper/hypophosphorylated
5.4 TP53
5.4.1 regulates cell cycle progression, DNA repair, cellular senescence and apoptosis
5.4.2 Enter text here
6 Growth-Promoting Metabolic Alterations: The Warburg Effect
7 Evasion of Programmed Cell Death (Apoptosis)
8 Limitless Replicative Potential: The Stem Cell-Like Properties of Cancer Cells
9 Angiogenesis
10 Invasion and Metastases
11 Evasion of Host Defense
12 Genomic Instability
13 Cancer-Enabling Inflammation
14 Dysregulation of Cancer-Associated Genes
15 Molecular Basis of Multistep Carcinogenesis
Show full summary Hide full summary

Similar

Fluid and Electrolyte Imbalances
D R
Infectious diseases
Clare Yu
Malignancies
Mark George
Bowel (Colorectal) cancer
Mark George
Molecular cell biology of cancer
Alyssa B
Drugs used to treat lung cancer & staging system
Alyssa B
Breast Pathology I
Matthew Coulson
GCSE AQA Biology - Unit 1
James Jolliffe
Physics 1
Peter Hoskins
GCSE AQA Physics - Unit 1
James Jolliffe
Business Studies Unit 1
kathrynchristie