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Oncology Notes

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1. Introduction A neoplasm is the abnormal proliferation of cells. It can be defined as a new growth of cells, originally derived from normal tissues, which have undergone heritable genetic changes that have made them relatively unresponsive to growth controls and to expand beyond their normal anatomic boundaries. Neoplasms may be benign or malignant. Whilst a tumour may be either benign or malignant, cancer always refers to malignant neoplasms. Oncology is the study of neoplasia. Benign tumours do not invade the surrounding tissue or spread around the body and so are usually curable. Malignant tumours, if left untreated, can invade the site of location and spread to new sites around the body - metastasis. Pre-neoplastic changes can be diagnostically important. These include hyperplasia (increased cell number in a tissue), metaplasia (transformation of one differentiated cell type to another) and dysplasia (abnormal pattern of cell growth).Hyperplasia must be differentiated from hypertrophy, which is an increase in size of individual cells. Pre-neoplastic changes are usually reversible and are physiological responses to injury, irritation or increased demands.

2. Nomenclature Most tumours consist of a single cell type. The name of the neoplasm reflects the cell type from which the tumour has arisen. Benign tumours that have arisen from mesenchymal cells are given the suffix - oma. Malignant tumours of mesenchymal origin are -sarcomas. A prefix indicates the tissue of origin. For example, a lipoma is a benign tumour derived from a lipocyte, whereas a liposarcoma is a malignant tumour derived from a lipocyte. The cells of the haematopoietic system are mesenchymal. Tumours arising from blood cells or their precursors are called leukaemia. Neoplastic haematopoietic cells are usually found in large numbers in the blood stream, but may also form solid masses. Benign tumours arising from nervous tissue also are given the suffix -oma, for example astrocytoma arising from astrocyte cells. The word malignant is added to describe malignant tumours. Benign tumours arising from glandular epiethelium are termed adenomas. This term is also used to describe tumours that have not arisen from glandular epithelium but that have a tubular appearance, such as renal adenomas. Malignant tumours arising from the glandular epithelium are adenocarcinomas.

Benign tumours arising from protective epithelium are termed papillomas. Malignant tumours of epithelial origin are called carcinoma. Prefixes may be added to further describe the tumour. Carcinomas or adenocarcinomas that cause excessive collagen formation in the surrounding tissue are called scirrhous. For BSAVA full list of tumour nomenclature see: file:///C:/Users/user/Documents/Year%203/Principles%20of%20Clinical

3. Tumour grading Grading schemes indicate how similar or dissimilar a neoplasm is to normal tissue. Tumour grade is strongly linked to prognosis and response to therapy. Grading schemes evaluate the degree of differentiation of tumour cells. Grade I is well differentiated, Grad II is moderately differentiated and Grad III is poorly differentiated. The TMN system classifies tumours according to the size of the primary tumour (T), the degree of lymph node involvement (N) and the extent of metastasis (M). It is as follows:

T0 indicates carcinoma in situ T1-4 the indicate size of the primary tumour. The characteristics of this description vary depending on the type of tumour.

N0 indicates no lymph node involvement. N1 indicates regional lymph node involvement N2 indicates distant lymph node involvement.

M0 indicates there is no detectable metastasis. M1 indicates there is a secondary tumour in the same organ or cavity. M2 indicates there is distant metastasis.

4. Benign versus malignant tumours Characteristic Differentiation

Benign Well differentiated. Similar to tissue of origin. Little or no anaplasia.

Growth rate

Local invasion

Slow. Rare mitotic figures. Normal mitotic figures. No invasion.

Malignant Lack of differentiation. Atypical structure, dissimilar to tissue of origin. Variable anaplasia. Slow to rapid growth. Many mitotic figures. Abnormal mitotic figures. Local invasion.

Metastasis Host consequences

Cohesive growth. Capsule often present. No metastasis. Space occupying lesion (effect depends on location).

Infiltrative growth. Usually no capsule. Frequent metastasis. Life threatening.

Anaplastic cells are poorly differentiated cells that exhibit notable cellular and nuclear pleomorphism (variation in size and shape). Anaplastic nuclei are often:

Hyperchromatic (very dark staining) because of increased DNA content. Disproportionately large compared to cell size Have prominent nucleoli.

Mitotic figures appear as darkly staining figures histologically.

5. Tumour growth The latent period is the time before the tumour becomes clinically detectable. Masses become detectable at around 1cm in size and contain around 10 9 cells, a result of around 30 rounds of replication. This means by the time tumours are clinically detectable they have been developing the host for many years in the latent form. Many neoplastic cells no longer respond to extrinsic cell signals directing them to G0 (the quiescent state of the cell cycle) or express functional p53 (tumour suppressor gene product that gives cells time to repair damaged DNA by initiating cell-cycle arrest). As such they are insensitive to anti-growth signals, and are self-sufficient in growth signals. They have limitless replicative potential. Many cancer cells are also resistant to apoptosis. Genomic instability is a classic characteristic of cancer. Tumour growth begins with inititation, the introduction of an irreversible genetic change in cells by the action of a mutagenic agent or initiator. Mutagenic agents or initiators are physical or chemical carcinogens that damage DNA. The second stage is promotion. This is the outgrowth of initiated cells in response to selective stimuli that drive proliferation. Promotor stimuli are non-mutagenic, and so their effects are generally reversible. Progression of the tumour is the final stage. This includes the conversion of a benign tumour to an increasingly malignant and ultimately metastatic tumour. Malignant conversion is non-reversible. Tumours must undergo angiogenesis to continue to support growth. Tumours induce angiogenesis by releasing angiogenic factors such as vascular endothelial

growth factor (VEGF). Tumour blood vessels are unstable, disorganised and more permeable than those of normal tissue.

6. Metastasis 90% of deaths from cancer are as a result of secondary tumours at body locations distant to the primary tumour. These are metastases that are formed by cancer cells that have left the primary tumour and travelled through the blood and lymphatic vessels. Some tumours are more metastatic than others. Metastasis is a feature of malignant tumours only, but it should be noted that not all malignant tumours metastasise. Most carcinomas metastasise via the lymphatic system. The lymph nodes closest to the tumour are usually colonised first. It was traditionally thought that cancers spread from the local site to regional lymph nodes and then to distant lymph nodes, however recent evidence suggests this is not the case, and regional lymph node involvement indicates neoplastic disease is already widely systematic. Sarcomas tend to metastasise via the haematogenous system. Tumours generally invade veins instead of arteries, as arterial walls are thicker and much harder to penetrate. Ultimately, tumour cells that enter the veins enter the vena cava and lodge in the lungs, or enter the portal system and lodge in the liver. Cancers that arise on the surface of abdominal and thoracic structures undergo transcoelomic metastasis. Different types of tumour cells colonise different metastatic sites more or less readily. This depends on the ability of tumour cells to adapt to the microenvironment of distant tissues and the layout of the circulation. Metastasis begins by adhesion. Tumour cells must detach from the main tumour mass, penetrate the basement membrane and enter the extra-cellular matrix (ECM). For the cells to separate from each other, intercellular adhesion structures such as desmosomes and adherens junctions must be destroyed. Contact with ECM components must also be established, such as fibronectin, laminin, collagen and vitronectin. Invasion and intravasation then occurs. Tumour cells actively degrade the basement membrane and ECM by secreting matrix metalloproteinases (MMPs).

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