Lecture notes

Essential Molecular Biology (BIOC0007) Notes - Cancer

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Module
Essential Molecular Biology (BIOC0007)

Institution
University College London (UCL)

Explore Essential Molecular Biology at UCL. Delve into the complex world of cancer, unraveling oncogenic transformation, understanding oncogenes, exploring metastatic growth, and dissecting redox regulation and metabolic reprogramming. Tailored for Year 1 students, these notes provide a humanized a...

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Uploaded on December 1, 2023
Number of pages 18
Written in 2021/2022
Type Lecture notes
Professor(s) Dr eleni makrinou
Contains All classes

sujansathiendran Member since 3 year 5 documents sold

Cancer – Summary
Basis of Oncogenic Transformation
 Terminology
o Oncogene
 Mutated gene that has potential to cause cancer
 In tumour cells – these genes are often mutation or expressed at high levels
o Oncogenic transformation
 Process of successive acquisition of genetic and epigenetic alterations affecting cell growth,
proliferation, and survival
o Oncogenesis (tumorigenesis)
 Formation of a cancer – whereby normal cells are transformed into cancer cells
o Tumorigenic factors
 Factors which can result in a cell undergoing oncogenesis
o Progenitor cell
 Descendent of stem cells that can further differentiate to create specialised cell types – can
only differentiate into cells that belong to the same tissue or organ
o Metastasis
 Spread of cancer cells from the place where they first formed to another part of the body
o Quiescence
 Inactivity or dormancy
o Constitutive signalling
 Spontaneous isomerisation of a receptor into an active state in the absence of ligand 
resulting in an increased in the basal level of the system
o Mitogenic signal
 Triggers signal transduction pathways leading to mitosis
 Gene expression governs cellular functions
o Same genes – expression defines mRNAs  defines proteins  defines life of cells
 Proliferation
 Process that results in an increase of the number of cells
 Apoptosis
 Programmed cell death
 Growth
 Cell growth
 Differentiation
 Cell differentiation
 Transformation
 If exposed to tumorigenic factors
 Oncogenic transformation
o Mutational targets of oncogenic transformation are genes which effect cell growth, proliferation,
and death
 Two types of genes associated with malignant growth = oncogenes + tumour suppressors
o Main tumorigenic factors – cause DNA damage  induces malignant growth
 Chemical carcinogens
 Harmful irradiation
 Tumorigenic viruses = virus integrates into cell  during replication integrates viral DNA into
DNA  can result in gain-of-function mutation
o DNA repair mechanisms and oncogenic transformation
 Mechanisms work efficiently is damage is not extensive
 Extensive and continuous exposure of cells to carcinogens or radiation  damage is too
much for efficient repair = mutations accumulate – resulting in start of malignant growth
o Theory of malignant transformation

,Cancer – Summary
 Cancer is a stepwise accumulation of oncogenic mutations that affect growth,
differentiation, and cell survival
 Progressive transformation of normal human cells into highly malignant descendants
o Driver mutation = mutation that can lead to oncogenic transformation
o Passenger mutation = mutation that can help cancer grow faster
o Stem cells  progenitor cells  differentiated cells
 Environmental factors  progenitor cells  cancer
stem cell  tumour progression
 Differentiated cells cannot immediately
form cancer stem cells
o Need to first be de-differentiated
into proliferative cells
o Further mutations can form cancer
stem cells
 Initiation and progression of cancer
o Only proliferating cells can initiate oncogenic growth
o Tumours initiate as a result of a single mutation in a single progenitor or stem cell
 Cells gradually change from normal  malignant  highly malignant
o Mutations in offspring of mutated cell are necessary for the progression of malignant phenotype
o Clonal selection and expression of cells with growth advantage cause tumour’s heterogeneity
 Mutations occur in genes controlling cell growth, proliferation, and survival  leading to cancer
o Oncogenes
 Mutation results in gain of function
 C-erbB2
 Ras
 PI3-K
 Myc
o Tumour suppressors
 Mutation results in loss of function
 p53
 Rb
 APC
 Oncogenes and proto-oncogenes
o Oncogene
 Gene that can induce cancer formation when activated by mutations or overexpression
o Proto-oncogene
 Normal gene with a potential to function as an oncogene – via hot-spot mutations =
deletions, insertions, DNA amplification, re-arrangements
 Main classes of oncogenes
o Growth factors (mitogens)
 Induce cell proliferation
 c-Sis
 Receptor tyrosine kinases
 Transduce signals for cell growth and differentiation
o EFGR
o PDGFR
o VEGFR
 Cytoplasmic tyrosine kinases
 Mediate responses to and activation of receptor of cell proliferation, migration,
differentiation and survival
o Src

, Cancer – Summary
o Syk
o MTK
 Cytoplasmic serine/threonine kinases
 Involved in organism development, cell cycle regulation, differentiation, cell survival
and apoptosis
o Raf
 Regulatory GTPases
 Involved in signalling a pathway leading to cell proliferation
o Ras protein
 Transcription factors
 Regulate transcription of genes that induce cell proliferation
o myc
 Multistage model of tumorigenesis
o Gain of function of loss of function mutation inactivates suppressor gene
o Leading to proliferation
o Benign tumour cells grow locally
o Further mutations inactivate DNA repair genes
o Proto-oncogenes mutate to oncogenes
o More mutations – more genetic instability  metastatic disease
o Malignant cells invade other cells  metastasize to different sites
 Two types of tumours
o Benign
 Unrestrained growth
 Increase in size and mass
 Easy to be removed surgically
 Does not invade organs
o Malignant
 Unrestrained growth
 Increase in size and mass
 Further mutations – allow invasiveness  resulting in metastatic potential
 Properties of transformed cells
o Reduced requirement for growth supplement
 Serum, growth factors, hormones
 Normal cells need more growth supplement for growth
 Cancer cells don’t need as much – as they produce their own growth factors
o Loss of the capacity to go into quiescent (inactive) state
 Growth arrest
 Normal cells divide and the go into quiescence
 Cancer cells are unable to go into quiescence – as they overexpress telomerase
o Altered morphology
 Look different from precursors
 Tumour cells are rounded – do not need to spread as wide to induce proliferative
signalling
o Loss of contact inhibition
 Tumour cells grow on top of each other
 Normal cells grow as a monolayer
 Cancer cells grow on top of each other
o Loss of anchorage dependence
 Tumour cells grow in soft agar
 Normal cell cannot adhere to agar = does not grow
 Cancer cells grow in agar

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