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Flashcards in Oncology Deck (67)

All retroviruses carry viral oncogenes. True or false?


Retroviruses can carry oncogenes or switch on the host's proto-oncogenes. 

Some retroviruses carry viral oncogenes, which are genes that code for proteins that can transform a host cell.

Others don't have oncogenes but integrate into the host genome NEXT TO a proto-oncogene, using the retrovirus's long terminal repeat (LTR) to switch on the proto-oncogene.

LTR is a section of the virus's genome that codes for polymerase, capsid & envelope


Name two types diseases that affect domestic animals or pets that are caused by retroviral infection.

FeLV - Feline Leukemia

Ovine Pulmonary Adenocarcinoma


Describe the pathogenesis of feline leukemia virus.

transmitted oronasally via biting, mutual grooming, sharing of feeding bowls

starts at tonsils → viraemia in bloodstream → bone marrow → GIT epithelial cells

about 60% of cats clear infection, 30% become persistently infected & develop disease


What oncogenic mechanism does FeLV use? Oncogene or LTR to switch on proto-oncogenes in host?

It switches on a proto-oncogene.

FeLV is an enveloped retrovirus with RNA oncogene that inserts into c-myc gene in host genome, leading to uncontrolled expression of myc → cell proliferation (lymphocytes)
causes tumours of lymphocytes (lymphoma)


Describe the pathogenesis of RETROVIRUSES.

Adsorption to receptor on target cell → Membrane fusion → uncoating → reverse transcription of RNA strand to DNA (RNA to RNA-DNA hybrid to DNA) → enters host nucleus → integrates into host genome → protein synthesis in cytoplasm → capsid assembly → budding → maturation, reinfection




Describe the structure of Retroviruses.

Family Retroviridae
- RNA virus
- enveloped
- carry reverse-transcriptase enzyme that transcribes RNA into DNA
- each virus gene has a long-terminal repeat section (LTR) that code for polymerase, capsid & envelope
- oncogenes (v-onc) carried by retroviruses lead to cell transformation aka tumours

- retroviruses without oncogenes use their LTR to integrate into host genome next to protooncogene, switching it on for cell proliferation



What is the pathogenesis of Ovine Pulmonary Adenocarcinoma?

- caused by Jaagsiekte sheep retrovirus with env (a structural gene) as oncogene
- malignant tumour of glandular epithelial cells in lung
transmitted via respiratory route
- Type II pneumocytes that produce surfactant proliferate and the lungs become filled with surfactant


What is Papillomavirus & how does its structure differ from Retrovirus?

Family Papillomaviridae
- dsDNA virus
- Non-enveloped
- species specific except for Bovine PV


Family Retroviridae
- RNA virus
- Enveloped
- carry reverse-transcriptase enzyme that transcribes RNA into DNA


How do Papillomaviruses & Retroviruses differ in their oncogenic mechanisms? 

Papillomaviruses use E5, a viral protein, to cause skin tumours (papillomas) & sarcoids. 

- E5 inhibits formation of gap junctions between cells, reducing communication & growth inhibitory signals

- E5 downregulates MHC Class I expression (for Killer T cells), evading host immunosurveillance

E5 binds to receptor for platelet-derived growth factor (PDGF) → cell proliferation

Retroviruses use oncogenes (v-onc) to cause cell-proliferation/transformation, or they insert themselves in the host's genome & use their long-terminal-repeats (LTRs) to switch on nearby host proto-oncogenes, causing tumours of lymphocytes (lymphomas) or glands (adenomas).



Describe the pathogenesis of Papillomaviruses.

Virus enters at base & moves up:

Enter via damaged skin or mucosa epithelium at basal layer → infect dividing basal-membrane cells → expression of “early proteins” initiates proliferation of cells → “late” or “structural genes” & virus particles are expressed in upper layers of epithelium, where epithelium finally differentiate from basal cells into keratinocytes



Which is the only papillomavirus that is not species-specific?

Bovine Papillomavirus (BPV). 

There are 10 different types & they can infect other species, including horses, in which they cause sarcoids. 


What are the clinical signs of Bovine Papillomavirus (BVP) in cattle?

Mostly affects calves & yearlings.

Usually benign tumours on head, neck ("angleberries"), shoulders & udder, as well as rumen. Secondary infection can lead to harmful infection.

Most regress spontaneously after six months.

Malignant tumours require co-factors such as mutagens & immunosuppressants from eating bracken fern - cancer in upper GIT & bladder can develop this way.


What are the clinical signs of disease caused by Canine Papillomavirus?

Usually oral papillomatosis: benign tumours on lips, tongue & palate that spontaneously regress.


What are the clinical signs of disease caused by Equine Papillomavirus?

Don't confuse this with Bovine Papillomavirus that causes usually benign sarcoids in horses.

Equine Papillomavirus causes benign skin tumours around nose and mouth, usually self-limiting.


What virus causes sarcoids in horses?

Bovine Papillomavirus

Sarcoids are locally invasive skin tumours (don't metastasize)

Sarcoids frequently reoccur after surgical removal.

Described as verrucous (covered with warts), fibroblastic (hyperplasia in connective-tissue cells), occult (early form, usually hairless area), or mixed

Transmission likely to involve biting flies that inject BPV deep into basal layer



Retroviruses carry their own RNA polymerase to transcribe DNA into mRNA. True or false?

False. Retroviruses use HOST RNA pol. 

Retroviruses carry their own reverse transcriptase, which reverse transcribes viral DNA from viral RNA (first making a DNA-RNA hybrid). The viral DNA, carrying LTRs that include envelope, capsid & reverse transcriptase, integrates into the host genome, and is then transcribed into mRNA by the host's own RNA pol. 

This mRNA is then translated in the cytoplasm on ribosomes, assembled with capsid, then buds out to mature into another retrovirus and reinfect other cells.


Feline leukemia virus (FeLV) causes tumours of lymphocytes. True or false.

True. It causes lymphoma.


How many types of FeLV are there?

Three: A, B & C. 

We are only interested in A.


FeLV can originate in any organ. True or false.


May be multicentric, involving lymphoid tissues at various sites.

It can also involve predominantly only one site, such as the thymus, alimentary tract or more rarely the skin or kidney.


What is the most common cause of death in cats with FeLV?

Secondary infections caused by immunosuppression, causd by malfunction of lymphocytes


How is FeLV diagnosed?

Detection of FeLV virus in blood by immunochromatography.

FeLV viral proteins can be detected with SNAP test that uses labelled anti-FeLV antibodies to capture virus, forming virus-antibody complexes.



What are the differences between hereditary lesions, congenital lesions & malformations?

Hereditary lesions: 

Genetically transmitted diseases
eg., viral diseases

Congenital lesions:

Disorders of growth detected at birth
NB not all congenital defects have an hereditary basis


Disorders of growth occurring during gestation
If early in gestation & sufficiently severe →  foetal death & resorption
If late in gestation → malformation limited & foetus usually survives


List some causes of hereditary lesions.

Viral diseases - some viruses cross to foetus via placenta.
Eg., Bovine Diarrhoea Virus (BVD) and Feline Panleukopenia (FPL) can result in calves & kittens, respectively, with cerebellar hypoplasia



List some examples of congenital lesions. 

Nutritional deficiencies: Copper deficiency in pregnant ewe can lead to degeneration of prenatal & neonatal lamb’s white matter & spinal cord:

Swayback - congenital form: more severe lesions in lambs affected prenatally, destruction of subcortical white matter in brain, lambs weak, ataxic, born dead

Enzootic ataxia -  delayed onset up to 6 months, demyelination of dorsolateral & ventromedial tracts in white matter of SC, varying ataxia


List some causes of malformations (occurring during gestation) that are not necessarily hereditary (can be congenital, ie., detected at birth).

Chromosomal defects - often result in early abortion or resorption
Eg. trisomy, XX true hermaphrodite

Toxins - plants, pesticides.
Eg., Veratrum californicum ingested by ewe in early pregnancy might produce cyclopia in lambs as it interferes with neural-tube development 

Drugs, hormones, antibiotics - similar to toxins, cross via placental blood supply, to cause growth defects in foetus.
Griseofulvin (ringworm treatment) given to pregnant queen can result in cleft palate in her kitten
Oestrogens & Actinomycin D (antibiotic) 

Ionising radiation - foetus very susceptible because of high rate of cell division. Eg. X-rays

Physical factors - Eg. adhesions between foetal membranes or umbilical cord, esp. around limbs, can result in amputation of skeletal segments

Anoxia - lack of O2 in gestation


What is atrophy & what are the causes?

Decrease in size of cells & organ, AFTER organ has reached normal size - Reversible if inciting cause can be corrected

- inadequate cellular nutrition eg., PSS (portosystemic shunt) in liver

- pressure: compression by nearby lesion (tumour) can compromise blood supply

- ↓ work load: eg. broken leg leads to muscle atrophy

- denervation: eg., CN V (trigeminal) damage → temporal-muscle atrophy in cat

- ↓ endocrine stimulation: eg. prolonged steroid therapy → atrophy of zona fasiculata in adrenal gland


What is the gross appearance of atrophied kidneys?

Kidneys appear smaller & paler. 



What is the appearance of adipose atrophy in skeletal muscle (skeletal muscle atrophy)?

Progressive mobilisation of fat, deposits severely depleted, clear, gelatinous material remains, occurs following severe illness & weight loss.



What is the microscopic appearance of skeletal-muscle atrophy?

- smaller cells
- inactive-looking cells
- relative ↑ in supportive connective tissue maybe



What is hypertrophy? 

↑ in SIZE of cells & ∴ organ, ↑ in organ weight


What are the four main reasons cells undergo hypertrophy?

in response to ↑ physiological need eg., exercise
in response to ↑ demand due to organ dysfunction eg. cardiac hypertrophy due to valvular deficiency

when one of paired organs is damaged or lost eg., kidneys

hollow organs become thickened around an obstruction eg., intestine, gall bladder, bladder

due to anabolic steroids (think of Gold’s Gym)


What is hypoplasia?

Lack of cell growth ie., organ fails to grow


Can range from mildly hypoplastic to complete absence of organ aka vestigial/rudimentary

Aplasia & Agenesis = complete absence of tissue


What is pituitary dwarfism?

It's a form of hypoplasia due to pituitary cysts and a resulting lack of trophic hormones. Result is smaller animal, seen in German Shepherds.



What is hyperplasia?

Increase in NUMBER of cells, ∴ ↑ in size of organ


What are some causes of hyperplasia?

1. Hormonal stimulation

eg. Parathyroid hyperplasia in chronic renal failure & prostatic hyperplasia in older dogs:

↓ in GFR → K+-Ca++ imbalance → PTH ↑ to cause more Ca++ absorption

2. Response to irritation, cell loss or injury; regenerative response


How could a pituitary-gland tumour (pituitary adenoma) lead to hyperplasia?

It could produce more ACTH, stimulating the adrenal glands to become hyperplastic.

Eg., Adrenocortical nodular hyperplasia.


What is metaplasia?

Cells morph into different type of cells
Occurs solely in connective tissue & epithelium

eg. connective tissue: cartilage changes to bone in damaged tissue

eg. epithelium: in smokers, ciliated epithelial cells can undergo metaplasia to become squamous epithelial cells, unable to move mucous out of lungs.


What is dysplasia?

Cells become disorganised, dysplastic
Normal arrangement & pattern of tissue may be lost


What is anaplasia?

Loss of structure or function of normal cells


Irreversible reversion to a more primitive state

Feature of highly malignant tumours (micro):
- Cells & nuclei of different sizes
- Prominent nucleoli in some nuclei
- Mitotic figures may we weird shapes


What are growth disorders during life versus malformations & congenital defects?

Growth disorders during life: 

Atrophy & Hypertrophy

Hypoplasia (Incl. Aplasia & Anagenesis)





Malformations & Congenital Defects:

Chromosomal defects eg. trisomy

Cerebellar hypoplasia in calves infected with BDV

Cerebellar hypoplasia in kittens infected by feline parvovirus

Cyclopia in lambs when dam ingested toxins

Cleft palate in kittens when queen treated with Griseofulvin for ringworm

Hypomyelination & Demyelination in pre-natal & neotal lambs' CNS due to copper deficiency in ewes: swayback & enzootic ataxia



How do tumours arise?


Tumours arise with genetic mutation that result in stimulation/up-regulation of proto-oncogenes and/or down-regulation of tumour-suppressor genes.

In this process, the cell loses its ability to differentiate (anaplasia), as the mutation has caused the gene to lose its ability to restrict genome expression.

Since the brakes on cellular growth, such as p53 protein and Rb-1 protein, have been suppressed, and/or proto-oncogenes such as Ras and E2F protein are activated constitutively, the cell loses its ability to control proliferation, so uncontrolled proliferation of the tumour cell take place to form a tumour, which contains 109 cells (ie., one billion).

Initiation → Promotion → Progression


Initiation → Promotion → Progression

Describe the first, initiation step in malignant-tumour growth / carcinogenesis. 

Step 1:  Initiation:

Irreversible genetic change/mutation occurs in the cell, introduced by a mutagenic initiator (aka carcinogenic initiator):

Non-acquired: Hereditary genetic damage, Age

Acquired: Chemicals, Radiation, Hormones, Bacteria, Parasites, Viruses, Immunological Factors, Chronic Inflammation or Irritation

Cell can appear morphologically normal & remain quiescent (eg., in G0 phase of cell cycle), but has growth advantage & can respond quickly & vigorously to mitogenic signals or are resistant to apoptosis-inducing stimuli. 


Initiation → Promotion → Progression

Describe the second, promotion step, in the multistep process of neoplastic tumour growth / carcinogenesis.

Step 2: Promotion

Initiated cells become exposed to certain stimuli such as promoting agents or promoters, such as the LTR of a retrovirus. The initiated cells grow, potentially leading to pre-neoplastic lesion or a benign tumour.

NB Promoters are NON-MUTAGENIC, & thus their effects can be reversible. 


Initiation → Promotion → Progression

Describe the final, progression step, in the multistep process of neoplastic tumour growth / carcinogenesis.

Step 3: Progression

Conversion of benign tumour to an increasingly malignant & ultimately metastatic tumour in an IRREVERSIBLE process.

Increasing tumour-cellular heterogeneity occurs with progression (ie., they become different sizes, in anaplasia)


What modifications do neoplastic growths (tumours) use to survive in local tissue?


Neoplastic growths in benign and malignant cases can lead to angiogenesis and lymphangiogenesis in local tissue, as the tumour needs blood supply & lymphatic drainage as it grows.
In fact, a tumour can’t grow beyond 1 or 2 mm in diameter without angiogenesis, which stimulates cell proliferation. The tumour induces host blood-vessel cells via TAFs (tumour angiogenesis factor) to supply it with vascular branches.
Similarly, tumour lymphangiogenesis induces the development of lymphatic vessels throughout the tumour. The lymphatic branches become essential for the spread of tumours.
NB: Tumour blood vessels are torturous, irregular, leaky, less efficient & tend to lead to necrotic areas around the tumour.


How do you distiguish between benign & malignant tumours microscopically (histology, cytology)?

Benign tumours:

Uniform cell appearances
May have capsule (ring of connective tissue)

Malignant tumours:

Non-uniform cell appearances
Variable cellular & nuclear size & shape
Can also include giant nucleolus & multinucleated tumour cells
Lack defined capsule or border
Mitoses: use of mitotic index = count of mitoses per 10 under random high-power (40x) microscope fields


This is a cytological sample of canine round-cell tumour (cutaneous histiocytoma). Is it benign or malignant? 


Uniform cell appearances
May have capsule (ring of connective tissue)


This is a cytological sample of canine round-cell tumour (cutaneous histiocytoma). Is it benign or malignant? 


Non-uniform cell appearances
Variable cellular & nuclear size & shape
Note multinucleated tumour cells
Lack defined capsule or border 

Mitotic cells


Describe the clinical course of a benign tumour.

Do not metastasize

Growth by expansion, putting pressure on other organs and ulcerating on body surface, but not necrotic
Do not penetrate capsule or surrounding tissues
“Shell out” easily at surgery


Describe the clinical course of a malignant tumour.

Metastasize starting with Primary Tumour

Growth is invasive & infiltrative
Surgery requires removal of wide margin of surrounding tissue
Necrosis centrally, ulcerates

Local invasion:

1. Intravascular: in blood vessels or lymphatic vessels' tumour bolus via haematogenous spread will enter venous drainage; must complete metastatic cascade

Eg. preferential sites include bone, mammary, thyroid, prostate, ovary lung & brain

2. Serosal or transcoelomic spread - coelomic surfaces ideal such as peritoneum, pleura, pericardial sac, often with protein-rich exudate, cells in aspirates.

Eg. carcinomas of pancreas, lung, kidney

3. Intra-organ seeding (uncommon) - via airways or local blood/lymph


  1. What is the metastic cascade?

The series of events leading to metastasis, starting with detachment of neoplastic cells from the primary site through to attachment and tumor growth at a distant site.

CTCs are circulating tumour cells.


Outline the steps of the Metastic Cascade, which describes metastasis via vessels (blood, lymph).


1. Primary tumour forms

2. Detachment & migration of malignant cells - release of proteases to degrade basement membrane

3. Adhesion to vessel wall

4. Invasion of vessel

5. Transport of micrometastasis (circulating tumour cells, CTCs)

6. Evasion of host defenses & platelet clumping (in blood vessels)

7. Exit from vessel & migration to site of metastasis

8. Formation of secondary tumour


What are DIRECT EFFECTS malignant tumours have on tissues to cause life-threatening disease?

1. Replacement of functioning cells
2. Compression
3. Invasion
4. Organ rupture
5. Embolus formation (infarction)
5. Ulceration - eg. gastric ulceration with carcinoma
6. Haemorrhage - eg. abdominal haemorrhage from ruptured splenic tumour (ie., haemoangiosarcoma)
7. Cachexia - ie., loss of muscle & fat, inappetance (also occurs as a systemic effect of cytokines & hormones)


What are INDIRECT, PARANEOPLASTIC EFFECTS malignant tumours have on the host to cause life-threatening disease?

These are areas of complications in the host remote from the primary tumour, usually due to tumour products:

Blood: Anaemia, thrombocytopaenia, disseminated intravascular coagulation (DIC)

Hypertrophic osteopathy in dogs & cats - symmetrical lameness & lots of periosteal new bone
Hypercalcaemia of malignancy - parathyroid hormone analogue produced by certain tumour cells stimulates Ca++ absorption

Neurologic effects: metabolic - hypercalcaemia, hypoglycaemia, seizures
myasthenia gravis - associated with thymoma

GIT: ulceration, abdominal pain, vomitting, haemorrhage, malaena (blood in stool)

Immune responses: Expression of tumour antigens that could be viral proteins, altered cell product or re-expressed molecules eg. embryonic antigens

- presence of lympocytes around many tumour types suggests immunosurveillance

- NK cells, cell-mediated immunity via cytotoxic lymphocytes, & humoral response via complement, are anti-tumour effector mechanisms


Discuss the species & breed predilections for common tumours in animals - give dog examples.

Hereditary neoplastic (tumour-causing) diseases are usually autosomal dominant. If recessive, the affected gene is inherited from both parents.

Eg. Certain dog breeds are susceptible to cancers:


Lymphoma, various brain, cutaneous mast cell tumours (MCT), mammary tumours, thyroid carcinoma, osteosarcoma, testicular tumours


Malignant Histiocytosis aka Histiocytic medullary reticulosis

Characterized by histiocytic infiltration of the lungs & lymph nodes. The liver, spleen & CNS can also be affected. Histiocytes are tissue macrophages or dendritic cells - components of the immune system that proliferate abnormally in this disease.


MCT, mammary tumours, thyroid carcinoma


Haemangiosarcoma, osteosarcoma, testicular tumours


Mammary tumours


Most tumours increase in incidence with age of host. Why?

Young animals, pre-natal and neo-natal, may be more prone to tumour growth due to the rapid cell-division occurring systemically.

Older animals, too, can become prone to tumours because of accumulated genetic damage. 

Accumulation of genetic damage
Decreasing immune function
Lag between cell transformation & clinically detectable tumour (slow growth)

Eg. Ovine sheep retrovirus - in younger animals, the tumour grows at much quicker stage than in older animals




List  reversible, acquired genetic damage / mutagenic initiators of neoplasia. 

Chemicals: Most are procarcinogens that require metabolic activation in vivo → ultimate carcinogen. eg. Bracken fern toxin can lead to bladder cancer in cows

Radiation - eg. UVB can lead to squamous cell carcinoma in white cats' ears & Hereford cattle eyelids

Hormones: e.g. steroid hormones, GH; eg. Spayed & neutered domestic animals may be less prone to tumour growth because they no longer have the receptors for  GH that enhance or stimulate cell proliferation. 

Bacteria, parasites: e.g. Spirocerca sp.

Viruses: affect young animals esp., eg. FeLV & Papillomaviruses

 Immunological Factors: Immunosuppression has role in genesis of certain tumours (e.g. FeLV)

Chronic Inflammation or Irritation: Associated with tumour development esp. in skin & other epithelial surfaces

• Possibly related to resultant hyperplasia


List irreversible, non-acquired mutagenic initiators of cancer.

1. Hereditary genetic damage

- usually autosomal dominant; if recessive, inherited from both parents

- early age of tumour development

- family history

Eg. In dogs: haematopoietic, brain, skin, MCT; in cats,  lymphoid

2. Age

- Accumulation of genetic damage
- Decreasing immune function
- Lag between cell transformation & clinically detectable tumour (slow growth)

Eg. Ovine sheep retrovirus 


Discuss the tissue predilections for common tumours in animals.

Fast-growing cells and those turning over quickly, such as the epithelial cells in the GIT (crypt cells) are more prone to tumours than lung epithelium, where there are many terminally differentiated cells.

In lungs, high turnover only occurs if there’s damage to the cells, rather than a regular process of regeneration as in the intestinal epithelium.

That said, Clara cells in the lung and hepatocytes surrounding the central vein of the liver can become active in the initiation stage of carcinogenesis.


What is the definition of neoplasia?

• uncontrolled purposeless cell proliferation

• cell proliferation continues without the inciting cause

• form from single mutated cell

• neoplastic cells exhibit altered differentiation (anaplasia, metaplasia) - eg. Clara cells in lungs lose their cilia

• rate of growth exceeds normal for the tissue - increase in number of mitoses

• tumours classified as 'benign' or 'malignant’


How are benign tumours named?

The suffix -oma in most cases denotes a benign tumour:
fibroma - fibroblasts
lipoma - fat cells
haemangioma - vascular endothelium
histiocytoma - neoplasm of histiocytes, which are phagocytic monocytes

Other benign tumours:
sarcoid - low-grade fibrosarcoma in skin of horses & cats; has viral involvement  (Bovine Papilloma Virus; can become malignant)
melanoma - tumour of melanocytes; can be benign or malignant


How are malignant tumours named?

Exceptions with -oma are malignant:

Carcinoma - malignancy of cells that are epithelial (endodermal or ectodermal) in origin, eg., squamous-cell carcinoma or gastric adenocarcinoma (gastric glands).

Sarcoma - malignancy of mesenchymal origin eg.,  fibrosarcoma in connective tissue, osteosarcoma in bone, haemangiosarcoma in blood vessels (cells are much more undifferentiated than in haemoangioma), histiosarcoma & lymphosarcoma.

Also malignant:
lymphoma, lymphosarcoma (leukosis) - lymphoid tissue
leukemia - when malignant lymphoid cells circulate in blood
myeloma, plasma-cell tumour, plasmacytoma - plasma cell tumours
melanoma, melanocytoma - melanocytes. Tumours can be melanotic or amelanotic (especially if very anaplastic)


What are the two "losses" fundamental to neoplasia development?

1. Loss of control of cell proliferation 
2.  Loss of normal cell differentiation, i.e. cells are

• Anaplasia = lack of differentiation.


How do fully differentiated cells differ from neoplastic cells?

Fully differentiated cell: Expresses only small % of genetic information of fertilized ovum because differentiation involves restriction of genome expression

Neoplastic cell: Show altered differentiation i.e. they are anaplastic. Generally, the poorer the differentiation (the more anaplastic), the poorer the prognosis

Well-differentiated tumours (not very anaplastic) may retain architecture, or function of normal tissue

Poorly differentiated tumours show inappropriate behaviour e.g. growth patterns, inappropriate hormone/protein production


p53 is:

A. Proto-oncogene

B. Tumour-suppressor gene

C. Viral oncogene

D. Viral capsid gene


p53 is a tumour-suppressor gene. When it is disabled, uncontrolled cellular proliferation can occur. p53 has been associated with these cancers in DOGS:

Thyroid carcinoma 

Lymphoid tumours


Mammary tumour

Colorectal tumour


What are the general features of the molecular basis of cancer?

1. Genetic injury

Genetic injury may be:
Inherited in germ cell line
Acquired in somatic cells (i.e. effects of
environmental agents)

2. Carcinogenesis

Multistep process: initiation → promotion
• Attributes of malignancy acquired in step-wise fashion (progression); the accumulation of successive mutations


How do tumours evade the immune system? Four ways.

1. Failure to display antigenic (or costimulatory) molecules by tumour cell - leads to lack of recognition of tumour by T lymphocyte; some tumours downregulate MHC I also (MHC I triggers Killer T cells)

2. Antigen masked by tumour cell - also leads to lack of recognition of tumour by T lymphocyte; tumour antigens might be complexed with fibrin

3. Tolerance - tumour antigen (or costimulatory) molecule shared with normal tissue leads to lack of recognition of tumour, or recognition but lack of activation of T lymphocyte

4. Immunosuppression by tumour cells or their products - leads to lack of response by immune system or apoptosis of T cells

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