Fig. 12.1
Schematic representation of features of dysplasia as would be seen under the microscope
Neoplasms, Tumour and Cancer
Neoplasm (new growth): an abnormal mass of tissue, formed due to the uncontrolled proliferation of cells. Cells continue to divide after the cessation of growth signals. The word tumour (swelling) is often used synonymously.
Neoplasia: the process by which a neoplasm is formed
Cancer: a malignant neoplasm
In order to describe a neoplasm, the nature of the tumour (benign or malignant) and its histological origin must be known.
Tumour Behaviour: Benign/Malignant
All solid neoplasms are composed of neoplastic cells. However, neoplasms can be classified as either benign or malignant. Although there are several differences between the two (see Table 12.1), the key distinguishing criterion is the ability of malignant neoplasms to invade and metastasise.
Table 12.1
Benign and malignant neoplasms
Benign | Malignant |
|---|---|
No local invasion or metastasis | Local tissue invasion and metastasis |
Usually slow rate of growth | Usually erratic or rapid growth |
Well circumscribed | Poorly circumscribed |
Good prognosis but can compress vital organs | Often poor prognosis |
Histologically well-differentiated | Histologically poorly-differentiated |
Often encapsulated | If encapsulated, invasion through capsule is seen |
Histogenesis
Microscopic examination and staining are used to assess the tissue of origin of tumours. The four main tissues from which tumours can arise are epithelial, connective, lymphoid/haematopoietic and germline tissue. The majority of tumours arise from epithelial tissue as epithelial cells line the internal and external body surfaces and are thus the most exposed to carcinogens. Epithelial tissue can be further subdivided mainly into either glandular or squamous.
Nomenclature
Some broad rules govern the naming of neoplasms. Benign tumours are usually named by adding the suffix –oma to the name of the tissue. For example, a lipoma is a benign tumour of adipose tissue. Malignant tumours from mesenchyme and epithelia are distinguished by the terms carcinoma and sarcoma, respectively. For example, an osteosarcoma is a malignant bone tumour. Prefixes indicate the tissue type. Commonly used nomenclature is shown in Table 12.2. Some important exceptions to the above rules are melanomas, neuroblastomas and glioblastomas, which are all malignant tumours.
Table 12.2
Nomenclature of epithelial and connective tissue tumours
Tissue of origin | Benign | Malignant |
|---|---|---|
Epithelium | ||
Glandular epithelium | Adenoma | Adenocarcinoma |
Squamous epithelium | Squamous papilloma Acanthoma | Squamous cell carcinoma |
Connective tissue | ||
Adipose tissue | Lipoma | Liposarcoma |
Smooth muscle | Leiomyoma | Leiomyosarcoma |
Skeletal muscle | Rhabdomyoma | Rhabdomyosarcoma |
Bone | Osteoma | Osteosarcoma |
Fibrous tissue | Fibroma | Fibrosarcoma |
Blood vessel | Angioma | Angiosarcoma |
Tumour Biology
A basic understanding of tumour biology helps in the management of patients with cancer.
Neoplasia: Aetiology and Mechanisms
Fundamentally, cancer is caused by DNA mutations. The overall effect is an increase the activity of oncogenes and/or a decrease the activity of tumour suppressor genes. These mutations can occur as a result of complex interactions between environmental and genetic factors. For example, inherited genetic makeup may enhance or decrease susceptibility to the DNA-damaging effects of environmental toxins, radiation, infection or hormonal imbalances. Thus, cancer is multifactorial.
Hallmarks of Cancer
A widely accepted model of cancer development is the “multistep process” which suggests that multiple genetic changes need to take place in a stepwise manner for a cell to become cancerous. These mutations lead to the cells acquiring key characteristics called the hallmarks of cancer ([1]; see box below), which offer them a selective growth advantage over their neighbours.
Hallmarks of Cancer
- 1.
Resisting cell death
- 2.
Sustaining proliferative signalling
- 3.
Evading growth suppressors
- 4.
Limitless replicative potential
- 5.
Inducing angiogenesis
- 6.
Activating invasion and metastasis
- 7.
Reprogramming of energy metabolism
- 8.
Evasion of the immune system
Invasion and Metastasis
Metastasis of primary tumours to secondary sites, and the subsequent loss of organ function is the major cause of morbidity and mortality in cancer patients.
Metastatic Cascade
Metastasis is a highly complex process involving several stages, which remain to be fully understood. Despite the complexity of the process, cancer cells regularly metastasise. While the rates and sites of metastasis may differ between cancers, there are core similarities in the mechanism of the process. Briefly, cells reduce the expression of cell-adhesion molecules allowing them to break free from their neighbours. The subsequent release of enzymes (such as matrix metalloproteinases) permits local tissue destruction and invasion by malignant cells. Intravasation into nearby blood vessels allows spread to a distant site, though cells in the blood stream must avoid detection by the immune system. A secondary focus is set up after extravasation.
Routes of Metastasis
There are two main routes of metastasis:
Lymphatic spread is the main route for carcinomas and typically follows the arterial supply.
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