List some different pathologies that cancer can be considered to be.

What percentage of MORTALITY in the DEVELOPED world does cancer account for?

What percentage of MORTALITY does cancer account for WORLDWIDE?

Each year, how many millions of cases of cancer are there worldwide?

Each year, how many millions of deaths is cancer responsible for worldwide?

What property is attributed to the word 'tumour' which means it cannot be used for general description in the way that 'neoplasm' can?

List the tissue types that neoplasms can occur in.

Which tissue is the most common for neoplasia and is also the most fatal when it occurs?

By who, in which journal, and when, was 'The Hallmarks of Cancer' published?

What two influences are the hallmarks of cancer acquired through?

List the six initial hallmarks of cancer set out by Hanahan and Weinberg in 2000.

List the additional four hallmarks of cancer than Hanahan and Weinberg added to the originals in 2011.

What are oncogenes?

Which of Hanahan and Weinberg's hallmarks of cancer do oncogenes affect?

What are oncogenes called before they are mutated into causing neoplastic change?

What are the two ways in which a protooncogene may be 'activated' that causes neoplastic change?

What two related cell processes do many common oncogenes promote (or promote the evasion of)?

Which four processes that affect the genetic code or genetic expression tend to be the cause of activation of an oncogene?

Is mutation in only one allele significant enough for an oncogenic effect?

What may point mutations result in the production of?

ras oncogenes code for a group of cytoplasmic proteins called 'ras proteins'. When activated, what do these proteins, and the cascade that they are involved in, do? Describe the steps.

What is the result of a point mutation in the ras protein gene?

To what extent must a deletion occur in order for the function of a whole protein to be changed?

What is v-erbB and what effect does it have on cell division?

Gene amplification can result in excessive production of an oncogene product. Describe one way in which a gene may be amplified in its expression.

What is HER-2 and what effect does it have on cell division/growth?

What happens to an oncogene in a chromosomal translocation?

Describe the effect of the chromosomal translocation of the myc region.

What specific cancer does the translocation of the myc region from chromosome 8 to the promoter region of chromosome 14 lead to?

What consequence does deletion of the negative regulatory region have for transcription?

What consequence might deletion of the entire regulatory region have for the expression of a gene?

What consequence might there be if the coding region for a gene is translocated from being adjacent to a weak gene promoter to a strong gene promoter?

What is the name of the neoplasm and the actual effect of the translocation from chromosome 9 to chromosome 22?

What is the name of the neoplasm formed when, and what is the actual effect of, translocation from chromosome 14 to 18 occur(s/ing)?

What is the neoplasm formed, and what is the cellular effect, when there is translocation from chromosome 11 to chromosome 22?

Normal cell growth is controlled by growth factors binding to receptors on the exterior membrane and initiating the signal transduction pathway which instructs the nucleus to produce proteins that cause cell proliferation. With this in mind, what might the activation of oncogenes affect?

What do the proteins of tumour suppressor genes do? Consequently, what might their mutation result in?

What is Knudson's two-hit hypothesis?

What was the first tumour suppressor gene to be identified?

What does the normal retinoblastoma (Rb) gene do? How is the gene usually disrupted?

Given its prevalence, what cancers is the disrupted retinoblastoma (Rb) gene found in?

What proportions of retinoblastoma (Rb) cases are inherited and sporadic?

Which gene, nicknamed 'the guardian of the genome', is probably the most common genetic abnormality in neoplasia?

Why is the p53 gene nicknamed the guardian of the genome?

List 3 ways in which normal function of the p53 gene may be lost.

What is the result of impairment to the normal function of the p53 gene?

What is the APC gene? What condition occurs if this is abnormal? What is the main feature of this condition?

Why must familial adenomatous polyposis be the result of the inheritance of ONE mutated/inactive copy of the APC gene?

What does the APC protein that is the product of the tumour-suppressor APC gene do?

What is the initial development in the loss of both copies of the APC gene in an individual?

By their early 30s, what might the progress of the disease be in an individual who has lost both copies of their APC gene?

By their 40s, what will almost all adenomatous polyposis coli patients have? What is the treatment?

In what percentage of cases of colorectal cancer is the APC gene mutated in?

Disruption of the APC gene is similar to disruption of the p53 gene in that normal senescence of a cell is prevented. Describe the changes to a cell with disruption of the APC gene.

What are the three stages of carcinogenesis?

Which stages of carcinogenesis do carcinogens tend to be responsible for?

Polycyclic hydrocarbons tend to be carcinogenic. In which sources might they be found? What neoplasms are they related with?

Aromatic amines are chemical carcinogens. In which sources might they be found? Which neoplasms are they associated with?

Nitrosamines are chemical carcinogens. In which sources might they be found? Which neoplasms are they commonly associated with?

Vinylchlorides are chemical carcinogens. Which source and which neoplasm are they commonly associated with?

Alkylating agents are potent chemical carcinogens. They are extremely cytotoxic. Name two sources in which they are found.

How do chemical carcinogens act?

Most carcinogens require metabolic activation before they can react with cell constituents. Why is this significant?

Polycyclic aromatic hydrocarbons generally produce cancers at the site of application (e.g. the skin and lungs). What are they metabolised to and what do these react with?

Describe the metabolism of aromatic amines.

Which chemical process are nitrosamines activated by? This is followed by the formation of which type of ion in the liver?

Chemotherapeutic agents act on rapidly dividing cells. As well as neoplastic cells, which normal tissues do they act on?

Why is there debate over whether to give a young person chemotherapy?

Alkylating agents are a chemotherapeutic agent. What effect do they have on DNA?

Topoisomerase inhibitors are chemotherapeutic agents. What effect do they have on DNA?

Taxanes and vinca alkaloids are chemotherapeutic agents. What effect do they have on cell division?

Anti-metabolites are chemotherapeutic agents. What effect do they have on cell division?

What type of cancers is a high fat diet associated with?

Which types of cancers are nitrates in the diet associated with?

Which types of cancers are red and processed meats associated with?

Which types of cancers are associated with alcohol?

Why can a high fat diet and obesity lead to adenocarcinoma of the oesophagus?

Why can a high fat diet and obesity lead to the development of breast cancer?

How can hormones potentially contribute to neoplasia (general)?

Oestrogens stimulate the proliferation of which tissues (and can therefore predispose to cancer in them)?

Suggest mechanisms for the relationship between higher levels of oestrogens and the development of breast/endometrial cancers.

Tumours can also be dependent on hormones for their growth so drugs which block oestrogen receptors, for example, can be used to suppress their growth. Name a drug which is effective in the suppression of breast cancers.

Prostate carcinomas can be treated by the removal of stimulation by which hormone?

What are growth factors?

What is the normal function of epidermal growth factor (EGF)? How is its function changed in cancer? What are the usual therapeutic target tissues associated with EGF change?

Transforming growth factor-β (TGF-β) is involved in which processes in its normal function? How are these changed in cancer?

What is the normal role of insulin-like growth factor (IGF)? How is this changed in cancer? Which tissues are most commonly affected by this change (and are therefore a therapeutic target)?

What is the normal function of fibroblast growth factor (FGF)? How is this changed in cancer?

What is the normal function of vascular endothelial growth factor (VEGF)? How is this altered in cancer? Which tissues are most commonly affected by this (and are therefore therapeutic targets)?

Which stage in carcinogenesis do growth factors tend to be involved in?

Can viruses cause cancer?

Which cancers is the Epstein-Barr virus associated with? What cellular effects does it have which promote/permit this?

Which cancer is the hepatitis B virus associated with? What is the mechanism?

Which cancers is the hepatitis C virus associated with? What is the mechanism?

Which cancers is the human papilloma virus associated with? What is the mechanism?

Which cancers is the human immunodeficiency virus (HIV) associated with? What is the mechanism?

Which cancers is the human T-cell lymphotrophic virus (HTLV-1) associated with? What is the mechanism?

What do the products of the human papilloma virus (HPV) do?

Cervical cancer was the leading cancer in women of child-bearing age until what was introduced?

Approximately how many cases of cervical cancer are there per year in the UK?

Approximately how many deaths from cervical cancer are there per year in the UK?

What is asbestos?

What were the common uses of asbestos and why?

What are the most pre-eminent forms of asbestos?

Which diseases is crocidolite (blue asbestos) indicated in?

Give that it is chemically inert, what property of asbestos is related to its toxicity?

Other than shape, what is the toxicity of asbestos related to?

What is the characteristic tumour associated with asbestos exposure?

Other than the chronic inflammatory response to asbestos, what is another mechanism for its carcinogenesis?

What is the general mechanism for ionising radiation in carcinogenesis?

How does radiation interact with DNA?

What types of DNA lesions are caused by the interaction of ionising radiation with DNA?

What type of neoplasm does ionising radiation usually cause and who does it usually affect?

Prolonged exposure to which type of ionising radiation increases the risk of skin tumours?

What is the mechanism for the development of skin tumours as a result of over-exposure to UV radiation in sunlight?

Why is UV light seen as specifically carcinogenic to the skin?

Name some neoplasms associated with UV radiation.

What has to be true of initiation, promotion and progression for cancer to develop?

What does an initiator and a promoter result in?

What does the continual effect of a promoter result in?

What is epidemiology?

What is the epidemiology of cancer in childhood?

What is the epidemiology of cancer in young people?

What is the epidemiology of cancer in middle to old age people?

Describe the 'multi-step' causation of neoplasia?

According to Cancer Research UK, what are the most commonly occurring cancers?

According to Cancer Research UK, which cancers cause the most deaths?