Carcinogenesis

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List some different pathologies that cancer can be considered to be.	Unregulated proliferation of cells resulting in a mass of abnormal cells; a malignant neoplasm; a homeostatic disease; prolonged cell life; 'evolution in microcosm'; an uncontrolled proliferation of cells that express varying degrees of fidelity to their precursors; diseases characterised by the uncontrolled and abnormal division of eukaryotic cells; 'cancers arise from violations of the basic rules of social cell behaviour'; new and poorly controlled growth of cells; the abnormal and continuous growth of cells which are no longer subject to the homeostatic controls which maintain the appropriate number of cells in normal tissues; or a group of diseases characterised by unregulated cell growth and invasion and spread of cells, from the site of origin to other sites in the body.
What percentage of MORTALITY in the DEVELOPED world does cancer account for?	~29%
What percentage of MORTALITY does cancer account for WORLDWIDE?	13%
Each year, how many millions of cases of cancer are there worldwide?	12.7 million cases
Each year, how many millions of deaths is cancer responsible for worldwide?	7.6 million deaths worldwide
What property is attributed to the word 'tumour' which means it cannot be used for general description in the way that 'neoplasm' can?	A tumour refers to a SOLID growth, whereas neoplasm just refers to new growth.
List the tissue types that neoplasms can occur in.	Epithelial cells, blood cells and the lymphatic system, germ cells, connective tissue cells, and neural cells.
Which tissue is the most common for neoplasia and is also the most fatal when it occurs?	Epithelial cells (e.g. the intestinal lining, lungs, mouth, nasal cavity etc).
By who, in which journal, and when, was 'The Hallmarks of Cancer' published?	Hanahan and Weinberg, Cell, 2000.
What two influences are the hallmarks of cancer acquired through?	The action of genes (oncogenes and tumour-suppressor genes), and the impact of the environment (carcinogenesis).
List the six initial hallmarks of cancer set out by Hanahan and Weinberg in 2000.	Self-sufficient in growth signals; insensitivity to anti-growth signals; tissue invasion and metastasis; limitless replicative potential; sustained angiogenesis; and evading apoptosis.
List the additional four hallmarks of cancer than Hanahan and Weinberg added to the originals in 2011.	Deregulating cellular energetics (metabolism changed to promote neoplasm survival); avoiding immune destruction; tumour-promoting inflammation (promotes growth and survival in solid tumours); and genome instability and mutation (apoptosis avoided when DNA changes).
What are oncogenes?	Any mutated gene that contributes to neoplastic transformation. They are activated in cancer, often promote cell growth, often repress cell death (senescence) and differentiation, and prevent normal tissue homeostasis.
Which of Hanahan and Weinberg's hallmarks of cancer do oncogenes affect?	Oncogenes affect potentially ALL of the hallmarks of cancer given how varied the characteristics are e.g. promoting continued angiogenesis etc.
What are oncogenes called before they are mutated into causing neoplastic change?	Protooncogenes.
What are the two ways in which a protooncogene may be 'activated' that causes neoplastic change?	There is altered gene expression, so that either the protein produced functions differently and contributes towards neoplastic change, or so that the protein is produced constantly (the gene is 'switched on').
What two related cell processes do many common oncogenes promote (or promote the evasion of)?	They promote mitosis/progress through the cell cycle, and the evasion of death signals.
Which four processes that affect the genetic code or genetic expression tend to be the cause of activation of an oncogene?	Point mutation of the triplet code, deletions of the triplet code, chromosomal translocations of entire loci, and amplification of gene expression.
Is mutation in only one allele significant enough for an oncogenic effect?	Yes :(
What may point mutations result in the production of?	Abnormally functioning protein products.
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.	ras proteins, when activated, recruit raf, another protein. Once raf is activated, it stimulates the mitogen-activated pathway, which ultimately leads to phosphorylation and activation of transcription factors fos and jun. fos and jun regulate the expression of growth control genes by binding to specific DNA sequences.
What is the result of a point mutation in the ras protein gene?	A substitution in the amino acid sequence of ras can lock it into its 'active state' by changing its structure so that it cannot interact with inhibitory proteins and downstream ras signalling is prolonged, ultimately stimulating the activation of transcription factors.
To what extent must a deletion occur in order for the function of a whole protein to be changed?	Given the specificity of protein shape, deletions may start from only a couple of base pairs, and go into deletion of an entire chromosome, and in either case change the function of the protein(s) involved.
What is v-erbB and what effect does it have on cell division?	v-erbB is a truncated form of the epidermal growth factor receptor (EGFR), in which the extracellular domain of the protein is not present due to deletion of this portion of its gene. As a result, the mutated receptor triggers cell division in the absence of epidermal growth factor (EGF).
Gene amplification can result in excessive production of an oncogene product. Describe one way in which a gene may be amplified in its expression.	The chromosome region may be duplicated so that there are more copies of the DNA template.
What is HER-2 and what effect does it have on cell division/growth?	HER-2 is protooncogene that codes for a transmembrane protein which closely resembles the epidermal growth factor receptor (EGFR). When it is duplicated (and it is a commonly duplicated gene) there are more receptor sites for epidermal growth factor (EGF) which promotes transcription and growth.
What happens to an oncogene in a chromosomal translocation?	It is inappropriately activated by another promoter region.
Describe the effect of the chromosomal translocation of the myc region.	Chromosomal translocation of myc (chromosome 8) to a location that falls within the regulation of the strong promoter region of immunoglobulin genes (chromosome 14) increases the expression of the myc gene. The increase in the myc protein results in an inappropriate increase in the transcription of myc-regulated genes, thus promoting growth.
What specific cancer does the translocation of the myc region from chromosome 8 to the promoter region of chromosome 14 lead to?	Burkitt's lymphoma.
What consequence does deletion of the negative regulatory region have for transcription?	Deletion of the negative regulatory region results in growth promoters only being positive/proliferative and only being able to bind to positive regulatory regions to direct RNA polymerase to start transcription.
What consequence might deletion of the entire regulatory region have for the expression of a gene?	Deletion of the regulatory domain prevents an enzyme from binding to this area to prevent replication - it is 'switched on'.
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?	Amplification of gene expression tends to occur as the coding region is receiving higher stimulation for transcription.
What is the name of the neoplasm and the actual effect of the translocation from chromosome 9 to chromosome 22?	This is involved in chronic myeloid leukaemia, and results in the formation of the bcr-abl protein which has tyrosine kinase activity.
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)?	This tends to result in follicular lymphoma, in which bcl-2 (an anti-apoptotic protein) is formed.
What is the neoplasm formed, and what is the cellular effect, when there is translocation from chromosome 11 to chromosome 22?	Ewing's sarcoma tends to be the result, and the EWS/FLI fusion protein is formed.
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?	They may increase the production of a growth factor, increase the expression of receptors for a growth factor (or multiple), result in mutant transcription factor production, and/or result in over-production of factors that prevent senescence. These can affect ALL of the hallmarks of cancer.
What do the proteins of tumour suppressor genes do? Consequently, what might their mutation result in?	They have a down regulatory effect on cell proliferation. Their inactivation may produce a neoplastic cell in which the effect of a growth-promoting factor goes unopposed.
What is Knudson's two-hit hypothesis?	Knudson proposed that a cell can only initiate a neoplasm when it contains TWO mutant alleles. This may be sporadic, in which both copies of an allele mutate randomly or are affected by a mutagen, or one copy of the allele may be inherited as mutated and only the second copy is sporadically mutated.
What was the first tumour suppressor gene to be identified?	The retinoblastoma (Rb) gene, which was discovered in a malignant tumour of the retina in childhood.
What does the normal retinoblastoma (Rb) gene do? How is the gene usually disrupted?	Normal Rb inhibits cell cycle progression from G1 to S phase. The Rb gene is usually disrupted by deletion or point mutation, and although it exists in all other tissues, only retinoblastoma and a few other rare cancers occur. The mutation blocks Rb function, so the cell cycle is not inhibited, and this results in uncontrolled cell growth.
Given its prevalence, what cancers is the disrupted retinoblastoma (Rb) gene found in?	Almost ALL cancers.
What proportions of retinoblastoma (Rb) cases are inherited and sporadic?	~40% inherited, and ~60% sporadic. Sporadic cases usually affect one eye whereas inherited cases can be bilateral.
Which gene, nicknamed 'the guardian of the genome', is probably the most common genetic abnormality in neoplasia?	The p53 gene.
Why is the p53 gene nicknamed the guardian of the genome?	Because it can elicit cell cycle arrest, apoptosis, DNA repair, and inhibition of angiogenesis, in response to stimuli such as radiation, drug or carcinogen induced DNA damage, cell stress, hypoxia and/or oncogene activation. In this way it protects the genome against mutation which may be harmful, and stops these from being transmitted to daughter cells.
List 3 ways in which normal function of the p53 gene may be lost.	Deletion of one or both of the alleles which reduces the concentration of p53 below that required for normal function; missense mutations in the region that allows p53 to interact with DNA (p53 is a tetramer protein); or inactivation of p53 through binding to other proteins such as those possessed by the E6 gene of human papilloma viruses.
What is the result of impairment to the normal function of the p53 gene?	This leaves a cell unable to repair itself or undergo apoptosis following further damage done to it, resulting in uncontrolled cell growth of cells with harmful DNA (e.g. that damaged by radiation or a virus).
What is the APC gene? What condition occurs if this is abnormal? What is the main feature of this condition?	The APC, or adenomatous polyposis coli, gene is responsible for controlling cell growth in the colon, and an abnormality in the gene may result in the development of familial adenomatous polyposis, the glandular formation of polyps in the colon.
Why must familial adenomatous polyposis be the result of the inheritance of ONE mutated/inactive copy of the APC gene?	The inheritance of two mutated/inactive copies of the APC gene is not viable with life and the foetus will not develop properly. As a result, familial adenomatous polyposis is a result of one inherited and one somatic mutated gene.
What does the APC protein that is the product of the tumour-suppressor APC gene do?	It is a multi-functional protein involved in cell division, signal transduction, apoptosis, cell-cell adhesion, and cell motility.
What is the initial development in the loss of both copies of the APC gene in an individual?	The formation of benign polyps (tumours). By their early 20s, a patient will have thousands of polyps in their colon, particularly in the rectosigmoid region.
By their early 30s, what might the progress of the disease be in an individual who has lost both copies of their APC gene?	The development of a malignant cancer in several/many of the previously benign polyps in their colon.
By their 40s, what will almost all adenomatous polyposis coli patients have? What is the treatment?	Carcinoma of the colon. By this age, the cancer is probably fatal without treatment. The treatment is a total colectomy which can result in dramatic weight loss, malnutrition and dehydration - hugely debilitating.
In what percentage of cases of colorectal cancer is the APC gene mutated in?	~90%
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.	It evades apoptosis, has an insensitivity to anti-growth factors, is self-sufficient in growth signals, and is likely to invade tissues and metastasise.
What are the three stages of carcinogenesis?	Initiation (an irreversible alteration of an oncogene or a tumour-suppressor gene), promotion (clonal expansion of the initiated area - stimulation of growth), and progression (stable alteration of an initiated cell; gaining ability to invade and metastasise).
Which stages of carcinogenesis do carcinogens tend to be responsible for?	Carcinogens tend to be responsible for initiation and promotion, but don't tend to be responsible for progression.
Polycyclic hydrocarbons tend to be carcinogenic. In which sources might they be found? What neoplasms are they related with?	They tend to be found in tars, cigarette smoke, barbecued food, and car exhausts. They are associated with neoplasms of the skin and lungs.
Aromatic amines are chemical carcinogens. In which sources might they be found? Which neoplasms are they associated with?	Aromatics amines are found in the rubber and dye industries, as well as in cooked meats. They are associated with neoplasia of the bladder, amongst others.
Nitrosamines are chemical carcinogens. In which sources might they be found? Which neoplasms are they commonly associated with?	They are found in tobacco and smoked foods, and are particularly associated with stomach and colorectal cancers.
Vinylchlorides are chemical carcinogens. Which source and which neoplasm are they commonly associated with?	Vinylchlorides are found in the manufacture of food packaging, and are associated with angiosarcoma of the liver.
Alkylating agents are potent chemical carcinogens. They are extremely cytotoxic. Name two sources in which they are found.	Mustard gas and chemotherapeutic agents.
How do chemical carcinogens act?	They act by causing damage to DNA and so mutating oncogenes and tumour-suppressor genes (as well as inevitably damaging other regions).
Most carcinogens require metabolic activation before they can react with cell constituents. Why is this significant?	Firstly, it explains why inert chemicals can be carcinogens - they are converted once they enter the body. Secondly, it explains why some people are more susceptible to developing cancers as a result of exposure to carcinogens than others exposed to the same level - a genetic difference in their metabolisms.
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?	Polycyclic hydrocarbons are metabolised to electrophilic epoxides which react with proteins and nucleic acids as these are electron dense.
Describe the metabolism of aromatic amines.	Aromatic amines are primarily metabolised in the liver and undergo N-hydroxylation to form the hydroxyl amino derivatives which are then detoxified by glucuronic acid. In the bladder, glucuronide is hydrolysed and this releases the reactive hydroxylamine.
Which chemical process are nitrosamines activated by? This is followed by the formation of which type of ion in the liver?	Hydroxylation activates nitrosamines. In the liver, this is followed by the formation of a reactive alkyl carbonium ion.
Chemotherapeutic agents act on rapidly dividing cells. As well as neoplastic cells, which normal tissues do they act on?	Hair, bone marrow, and gastrointestinal tissues.
Why is there debate over whether to give a young person chemotherapy?	Because the chemotherapeutic agent is toxic to healthy tissues as well as neoplasms, so the person is likely to develop cancer later on - and this is likely to be resistant to chemotherapeutic agents.
Alkylating agents are a chemotherapeutic agent. What effect do they have on DNA?	They interfere with base pairing of DNA, resulting in strand breaks so that the DNA cannot readily be transcribed for growth and replication.
Topoisomerase inhibitors are chemotherapeutic agents. What effect do they have on DNA?	They prevent DNA from uncoiling (uncoiling is done by topoisomerase) and therefore being transcribed for growth and replication.
Taxanes and vinca alkaloids are chemotherapeutic agents. What effect do they have on cell division?	They interfere with microtubule formation and mitosis, which disturbs/prevents cell division and the production of mutant daughter cells.
Anti-metabolites are chemotherapeutic agents. What effect do they have on cell division?	They block DNA synthesis and replication.
What type of cancers is a high fat diet associated with?	Breast and colon cancers.
Which types of cancers are nitrates in the diet associated with?	Stomach and nasopharyngeal cancers.
Which types of cancers are red and processed meats associated with?	Colon and stomach cancers.
Which types of cancers are associated with alcohol?	Oral, pharyngeal, laryngeal, oesophageal, breast, colon and liver cancers.
Why can a high fat diet and obesity lead to adenocarcinoma of the oesophagus?	This is a result of damage to the epithelial cells of the oesophagus caused by the acid reflux that is associated with obesity.
Why can a high fat diet and obesity lead to the development of breast cancer?	Because high fat deposits in adipose cells may be used for the synthesis of oestrogen from androgen by aromatase, and oestrogen stimulates the proliferation of breast tissue which can predispose to breast cancer due to increased growth.
How can hormones potentially contribute to neoplasia (general)?	By promoting the growth of certain tumour cells.
Oestrogens stimulate the proliferation of which tissues (and can therefore predispose to cancer in them)?	Breast and endometrium.
Suggest mechanisms for the relationship between higher levels of oestrogens and the development of breast/endometrial cancers.	This may be a result of the high division rate caused by oestrogens which allows less time for DNA repair and creates more opportunities for errors to occur. It may also be a result of the mutation of BRCA genes. BRCA genes produce nuclear tumour suppressor proteins which inhibit oestrogen signalling. Given that oestrogen signalling initiates proliferating effects, BRCA proteins therefore regulate transcription, the cell cycle and DNA repair. Loss or dysfunction of the BRCA genes could lead to uncontrolled proliferation dictated by oestrogen.
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.	Tamoxifen.
Prostate carcinomas can be treated by the removal of stimulation by which hormone?	Testosterone.
What are growth factors?	These are usually proteins capable of stimulating cellular growth, proliferation and/or differentiation. Expression and balance of growth factors is crucial in controlling cell behaviour and, therefore, cancer.
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?	EGF is normally responsible for cell proliferation and gastrointestinal function. In many cancers the receptor is overexpressed, resulting in cell proliferation occurring at a higher rate. The tissues usually affected are breast, colon and lung.
Transforming growth factor-β (TGF-β) is involved in which processes in its normal function? How are these changed in cancer?	TGF-β is involved in growth regulation and differentiation normally, and its signalling is lost in some tumours.
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)?	IGF is a mitogen (stimulates mitosis) which is over produced by tumour cells, resulting in a higher rate of cell growth and division. This most commonly affects breast and prostate tissues.
What is the normal function of fibroblast growth factor (FGF)? How is this changed in cancer?	FGF is a mitogen, as well as being angiogenic and involved in tissue repair. These pathways are frequently altered in cancer, resulting in a higher rate of cell division, angiogenesis occurring which supports tumour cell growth by providing nutrients, and growth encouragement as occurs in tissue repair.
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)?	VEGF stimulates angiogenesis, so its increased production in cancer can support the growth of a tumour as all solid tumours need a blood supply. Tissues commonly affected include the lungs, colon, kidneys, ovaries and liver.
Which stage in carcinogenesis do growth factors tend to be involved in?	Growth factor roles as carcinogens tend to be as promoters once the neoplasm has been initiated.
Can viruses cause cancer?	Only a few viruses are known to be implicated in human neoplasia and the molecular mechanism whereby they cause neoplastic transformation varies.
Which cancers is the Epstein-Barr virus associated with? What cellular effects does it have which promote/permit this?	The Epstein-Barr virus is associated with nasopharyngeal neoplasia, as well as Burkitt's, Hodgkin's and other β-cell lymphomas. It increases the rate of cell proliferation, as well as genomic instability and cell migration, while decreasing the rate of apoptosis.
Which cancer is the hepatitis B virus associated with? What is the mechanism?	The hepatitis B virus is associated with liver cancer. This is a result of the cell damage caused by inflammation and cirrhosis usually associated with chronic hepatitis.
Which cancers is the hepatitis C virus associated with? What is the mechanism?	The hepatitis C virus is associated with liver cancer and non-Hogkin's lymphoma. This is a result of the damage caused by inflammation, cirrhosis and fibrosis.
Which cancers is the human papilloma virus associated with? What is the mechanism?	The human papilloma virus is most often associated with cervical cancer, though it can be involved in others. It causes 'immortalisation' by increasing genomic instability and decreasing the DNA damage response and apoptosis.
Which cancers is the human immunodeficiency virus (HIV) associated with? What is the mechanism?	HIV is associated with Kaposi's sarcoma, non-Hodgkin's lymphomas, and cervical cancer. The mechanism is indirect, through immunosuppression enough cell damage can be done to increase genetic instability.
Which cancers is the human T-cell lymphotrophic virus (HTLV-1) associated with? What is the mechanism?	HTLV-1 is associated with adult T-cell leukaemias, and lymphomas. It does this through immortalisation and transformation of T cells.
What do the products of the human papilloma virus (HPV) do?	These protein products inactivate products made by tumour suppressor genes. This allows cells to escape normal regulation of growth.
Cervical cancer was the leading cancer in women of child-bearing age until what was introduced?	Screening.
Approximately how many cases of cervical cancer are there per year in the UK?	~9000
Approximately how many deaths from cervical cancer are there per year in the UK?	~3-400
What is asbestos?	Asbestos is a group of relatively inert forms of silica which exist as fibres 5-100µm long and 0.5-2.5µm in diameter.
What were the common uses of asbestos and why?	Asbestos was commonly used in roofing, vehicle brakes, insulation in housing, and firefighters' suits due to their ability to withstand heat and provide insulation.
What are the most pre-eminent forms of asbestos?	Chrysolite (white asbestos, biologically inert), and crocidolite (blue asbestos, biologically dangerous).
Which diseases is crocidolite (blue asbestos) indicated in?	It is indicated as the causative agent for bronchial carcinoma (through inhalation during manufacture of asbestos products), gastrointestinal tumours (through ingestion due to contaminated water filters), and malignant haematological disease (through inhalation and/or ingestion).
Give that it is chemically inert, what property of asbestos is related to its toxicity?	Its physical shape. There is a chronic inflammatory response as the asbestos fibres are recognised as foreign by macrophages but cannot be phagocytosed. The macrophage membranes are broken by the fibres and there is leakage of hydrolytic enzymes into the tissue, commonly the lung, which leads to aggregation of lymphoid tissue and stimulation of collagen synthesis - fibrosis of the lung.
Other than shape, what is the toxicity of asbestos related to?	It is dose related, and depends on exposure for a considerable period of time.
What is the characteristic tumour associated with asbestos exposure?	Mesothelioma.
Other than the chronic inflammatory response to asbestos, what is another mechanism for its carcinogenesis?	The production of reactive oxygen species (ROS) which can react with DNA to produce oxidised products e.g. 8-oxoguanine which would not be able to produce functioning oncogenes/tumour-suppressor genes, or may not be able to produce any at all.
What is the general mechanism for ionising radiation in carcinogenesis?	Ionising radiation causes DNA damage which, if not adequately repaired, can lead to mutations and these mutations can lead to cancer if in the right places.
How does radiation interact with DNA?	Particulate radiation (e.g. α and β particles) can react with DNA directly whereas electromagnetic radiation (e.g. x-rays, γ-rays) are indirectly ionising by releasing energetic electrons when these rays are absorbed. This absorption can be by DNA or other molecules e.g. H2O.
What types of DNA lesions are caused by the interaction of ionising radiation with DNA?	Base damage, inter-molecular cross-linking, and strand damage.
What type of neoplasm does ionising radiation usually cause and who does it usually affect?	Ionising radiation usually causes leukaemias, and most affects children if exposed (e.g. Chernobyl, Nagasaki, Hiroshima).
Prolonged exposure to which type of ionising radiation increases the risk of skin tumours?	UV radiation.
What is the mechanism for the development of skin tumours as a result of over-exposure to UV radiation in sunlight?	The conjugated double bonds in the rings of nitrogenous bases of DNA absorb UV radiation - the most carcinogenic is USB (290-320nm). The UV causes photoproducts such as pyrimidine dimers which cause a kink in the DNA so that DNA polymerase cannot read it. Under these conditions, DNA polymerase tends to add an adenine base which results in transitions of base pairs and consequent mutations in genes.
Why is UV light seen as specifically carcinogenic to the skin?	Because it cannot penetrate any deeper. UV radiation is seen as causative in the mutation of the p53 tumour-suppressor gene and the consequent neoplasia.
Name some neoplasms associated with UV radiation.	The cancer caused depends on the skin cell affected: squamous cell carcinoma, basal cell carcinoma, melanoma etc.
What has to be true of initiation, promotion and progression for cancer to develop?	These events must occur sequentially and within a certain time period.
What does an initiator and a promoter result in?	Neoplasia.
What does the continual effect of a promoter result in?	Invasive carcinoma.
What is epidemiology?	The study of the distribution and determinants of health-related states or events (including disease).
What is the epidemiology of cancer in childhood?	There are a small number of tumours that occur in childhood, primarily in embryonal tissues (blastomas), and leukaemias.
What is the epidemiology of cancer in young people?	Tumours are uncommon, but those that occur are usually of the bone, lymphoma and germ-cell tumours.
What is the epidemiology of cancer in middle to old age people?	There is an increasing incidence in epithelial neoplasms, probably as a result of an accumulation of events required for the 'multi-step' causation of neoplasia.
Describe the 'multi-step' causation of neoplasia?	The development of most cancers is a stepwise process involving an accumulation of mutations in a number of genes. It appears that perhaps 6 or 7 independent mutations are needed over several decades of life for cancer to be induced e.g. Bert Vogelstein's molecular model of multiple mutations leading to hereditary familiar adenomatous polyposis (FAP).
According to Cancer Research UK, what are the most commonly occurring cancers?	Breast and prostate cancers.
According to Cancer Research UK, which cancers cause the most deaths?	Lung and bowel cancers.

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