Cancer Biochemistry

Nikhil Dhall
Mind Map by Nikhil Dhall, updated more than 1 year ago
Nikhil Dhall
Created by Nikhil Dhall over 5 years ago
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Description

brief overview of cancer from biochemical perspective

Resource summary

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