4361376
Beschreibung
Mindmap von Nikhil Dhall, aktualisiert more than 1 year ago
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Erstellt von Nikhil Dhall
vor fast 9 Jahre
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Cancer Biochemistry
- proliferation, evade suppression,
immune, telomerase, angiogenesis,
inflammation, genome instability,
avoid apoptosis, metastasis,
metabolism
- ras - oncogene to make
RAF active --> 30% all
cancer, 90% pancreatic
cancer
- myc- oncogene -->
burrito lymphoma;
convert cell to use
glycolysis with RAS
- FOS - dimerize with
JUN to make AP-1
(TF) -->
osteosarcoma
- tumor suppressors
- Rb - normally
bound to E2F to
prevent activity
when cyclin D is
low - is
hyperphosphorylated
by
CDK4/6+cyclinD
- P53 - made in response to
cancer caused cell damage
to regulate transcription of
GADD45 and P21
- p21 is
a CKI
that
inhibits
CDK/cyclin
- P53 will cause
apoptosis if P21
doesnt work, will
block telomerase, and
will stimulate an
angiogenesis inhibitor
- p21 is
a CKI
that
inhibits
CDK/cyclin
- E-Cadherin -
normally causes
cells to stick
together but if
mutated will allow
tumor cells to break
off and metastasize
- APC - B-Catenin separated from
E-cad is degraded by APC; if
APC is gone, B-catenin will
stimulate MYC which will allow
for the tumor to use glycolysis
- BRCA-1: double
stranded break
repair --> 80% of
breast cancer
- Rb - normally
bound to E2F to
prevent activity
when cyclin D is
low - is
hyperphosphorylated
by
CDK4/6+cyclinD
- Cancers Caused
- Myc - burkitt lymphoma
- FOS/JUN - osteosarcoma
- BRCA1/2 - breast
cancer
- Also Her2 & ERB-B2
- Also Her2 & ERB-B2
- Rb - sarcoma
- APC - Familial Adenomatus polyposis
- Myc - burkitt lymphoma
- HIF - with normal O2, is modified with ROS and destroyed
- with cancer, not degraded and goes to
nucleus to stimulate VAGF and recruit
endothelial cells along with PDGF to make
platelets for blood vessels
- with cancer, not degraded and goes to
nucleus to stimulate VAGF and recruit
endothelial cells along with PDGF to make
platelets for blood vessels
- Glycolysis - GLUT 1 stimulators
- HIF
- RAS
- Mac
- HIF
- SHH binds PTCH which
alleviates suppression of SMO
(GPCR) in fetuses - this is not
necessarily related to cancer
- activates Ga-i
- cAMP down regulated
- activation of GLI (TF)
- activation of GLI (TF)
- cAMP down regulated
- activates Ga-i
- Other Ideas & Definitions
- Tumor suppressor: Both alleles must be knocked out to allow unchecked growth (like brakes of a car)
- Oncogene: 1 allele knocked out leads to accelerated growth (like adding NOS to a car)
- 4 possible mutations leading to cancer
- radiation / chemical carcinogen (mutation is most
likely in the promoter, through it could be in the
structural gene also)
- Gene rearrangement -
putting a porto-oncogene
onto a strong promoter
- Virus - oncogene is
inserted to genome
behind a strong
promoter
- Gene amplification
- radiation / chemical carcinogen (mutation is most
likely in the promoter, through it could be in the
structural gene also)
- Tumor suppressor: Both alleles must be knocked out to allow unchecked growth (like brakes of a car)
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