Lecture notes

Oncogenes: Tumour Suppressor Genes

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Module
CANCER BIOLOGY LECTURE NOTES

Institution
University Of East Anglia

Tumour Suppressor genes: * Loss of functions * Familial cancer * Tumour Suppressor *NF1,PTEN,APC *Khudson's Two-Hit Hypothesis *FRAUMENI SYNDROME

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Uploaded on October 29, 2024
Number of pages 5
Written in 2022/2023
Type Lecture notes
Professor(s) Dr helen james
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Cancer Biology Lecture Notes 1-5

£ 50.12 £ 20.54 7 items

1. Lecture notes - Introduction to cancer biology
2. Lecture notes - The neoplastic phenotype
3. Lecture notes - Oncogenes: tumour suppressor genes
4. Lecture notes - Oncogenes: tumour suppressor genes 2
5. Lecture notes - Cell cycle
6. Lecture notes - Programmed cell death: apoptotic process
7. Lecture notes - Programmed cell death: apoptotic process
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L4: ONCOGENES I [03/10/2022]

I. CANCER IS A GENETIC DISEASE

Oncogenes:

 PRESENCE in altered or excessive forms contributes to cancer
 Mutated forms lead to over-active or too much protein
 Involved in growth control

Tumour Suppressor Genes:

 ABSENCE can contribute to cancer
 Restrain cell growth and division
 Often involved n inherited predisposition to cancer

II. HOW ARE ONCOGENES INDENTIFIED?
 Knock in and knock out

Oncogenes: “A gene that causes the transformation of normal cells into cancerous tumour cells”,
also defined as “Mutated and/or over-expressed version of normal gene, that in a dominant
fashion releases the cell from normal growth restraints”

 Oncogenes gains a function:
- A proto-oncogene is the wild-type allele (normal gene) of an oncogene
- Activating mutation of proto-oncogene creates the oncogene
- One allele usually only affected = DOMINANT

III. HISTORICAL EVIDENCE
 1911: Rous isolated virus from spontaneous chicken sarcomas
 1914: Theodore Boveri experimented on the development of double-fertilised sea-urchin
eggs and later suggested that malignant tumours might be result of a certain abnormal
condition of chromosomes, which may arise from the multipolar mitosis.
 1960: Nowell & Hungerford – evidence form casual role for genomic rearrangement
 1969: Huebner & Todaro – proposed viral genes: integrated into genome; dominant
/activated; malignant transformation
 Stehelin et al., - demonstrated the RSV contained sequence not found in related, but non-
transforming retrovirus. Viral sequence was related to sequence in DNA of normal chicken

IV. MECHANISMS OF TRANSFORMATION BY RETROVIRUSES

,  We can identify oncogenes through retroviruses
 Humans do not have many viruses that cause cancers but more in animals and other species

V. DNA TUMOUR VIRUSES: ‘viral oncogenes’
 SV40 Large T antigen: binds and inactivates p53 – growing evidence of SV40 in brain cancers,
NHL, lymphoma, and mesothelioma
 Adenovirus E1A: binds pRb and immortalises cells

E1B (55K) inactivates p53

 HPV E6: interacts with p53 and activates telomerase
E7: interacts with pRb
- HPV 16, 18, 31, 33, 45 found in >99% of all cervical cancer
- Vaccination for HPV to prevent cervical carcinoma
VI. CANCER HALLMARKS

Q&A: Which of the following statements are true of oncogenes?

a. Proto-oncogenes are the result of mutations in oncogenes
b. Both alleles need to be mutated for oncogenic function to be acquired
c. Mutations causing oncogenes usually result in dominant activities

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