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Tumour Associated Antigen

Antigen present on normal cells, magnified in tumour cells

Oncofetal Antigens

Antigens present in embryonic developments

Tumour Specific Antigens

Antigens unique to tumour cells
Point mutation of DNA

macrophage activation

Activation via T cell dervied IFN- G
02 free radical

NK cells

Lymphocyte that do not need to recognise a specific antigen before releasing toxin.
Tumour cells still susceptible.

Tumour evasion of CTL

lack of co stim
lack of adhesion molecules
lack of class 1 MHC

Tumour evasion of the CTL response

Increased expression of TGF-B and PGE2
Endocytosis of antigen
Fas and FasL

Stimulate patients immune response

Active immunotherapy
DNA vaccines
Stimulate CTL growth

Transfer of cells/ antibodies

Passive immunotherapy
Inject CTL into patient

Tumour Infiltrating Lymphocytes

WBC's loaded with IL-2

Monoclonal Antibodies

Conjugated to radionucleide
Conjugated to toxin
Bind to cancer and activate NK cells
Passive immunotherapy

Invasion factors

Loss of cell to cell adhesion by E cadherin
Attachment to matrix component- laminin
Degradation of ECM
Motility of tumour cells.

Degradation- proteolytic enzymes break away the ECM
Amoeboid movement
Attachment- involvement of intergrin.

How do cells move within the stroma


inhibit E caherin in breast cancer (no cell to cell adhesion)


Methods of spread of tumour

Lymphatic spread

Spread commonly used by carcinomas

Haemotogenous spread

Spread commonly used by sarcomas


Local effects of tumour


Type 16 and 18- cervical cancer
DNA intergrated into host genome and E1 and E2
Inhibit E1 and E2 which usually inhibit E6 and E7
E6 and E7 not stopped-uncontrolled growth.
E6 and E7 bind onto pRb and separate it from the E2F (more cell growth)


Nasopharyngeal Carcinoma
Hodgkins Lymphoma
B cell lymphoma
Burkitts Lymphoma


Signalling molecule released by cells and act locally


Signalling molecule released by cells and through blood

Growth factor promoters

Tumours need this in order to start growing after intiation

Breat carcinoma

Increased oestrogen exposure
Due to:
Increased age, long space between menaupause, high fat diet

Endometrial carcinoma

Prolonged oestrogen exposure causes endometrial hyperplasia
Risk: obesity, oestrogen replacement therapy

Prostate cancer

Prolonged exposure androgens, dihydrotestosteron (testosterone metabolite)

Insulin, Gonadotrophin, calcitonin, glucagon, serotonin

Hormones released by tumours

Bronchogenic squamous cell carcinoma

PrTHP paraneoplastic syndrome

Small cell lung cancer

Cancer causes Cushings syndrome
Release of ACTH, ADH

Renal cell carcinoma/hepatocellular carcinoma

Release of erythropoeitein

Lung cancer
Breast cancer
Cervical cancer
Stomach cancer
Oral cancer
Liver Cancer

Opportunity for primary cancer prevention

Identification of unrecognized cancer


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