Intro to cancer Flashcards
Main types of cancer and features
Carcinoma: most common, arises from embryonic, endoderm, or ectoderm cells. can cover external or internal body surfaces
Sarcoma: cancer arising from embryonic mesoderm cells, supported by bone, cartilage, fat, connective tissue, or muscle
Lymphoma: cancer in the lymph nodes and immune system tissues
Leukaemia: cancer of immature white blood cells in the bone marrow, and accumulates in large numbers in the blood
Causes and symptoms
Diet/weight/physical activity
Tobacco/drugs
hormones
carcinogens/pollution
infective agents
radio/chemo therapy
genetic factors
disease specific symptoms, e.g.,
lung: coughing up blood, chest pain, breathlessness
pancreatic: weight loss, stomach/back pain, jaundice, DM
breast: lump or thickening, change in breast size, discharge, bleeding, weight loss
Mutations that occur in cancerous cells
Protooncogens encode the signalling pathways that play a role in regulating proliferation. Loss of function
Tumour suppressor genes mutate to lose function, leading to dysregulation of cell cycle and proliferation
DNA repair enzymes lose function, preventing repair to cancerous DNA
A cell will become cancerous after accusing several genetic mutations over time.
Metastasis cascade
Migration of cancerous cells leads to invasion of neighbouring tissue.
The cancer undergoes intravasation, crossing the vessel wall and enters the systemic circulation.
Only a small number of the cancer cells that have entered the blood will survive, completing metastasis. Platelets can aid in the metastasis.
Will arrest at the target location on the endothelial lining of the target.
Extravasation will occur, where the cells leave the blood and enter the target. Here growth of a secondary tumour can occur. This is all enhanced by chronic inflammation and increased permeability
Physiology and pathology of angiogenesis
It is the development of blood vessels from preexisting vasculature. Utilised in bodily development, menstrual cycle, wound healing, continual exercise, and response to ischaemic diseases.
In cancer, angiogenesis can become dysregulated. Produces poorly designed and distributed vessels that tend to be leaky, with poor SM tone. Formed from a mix of endothelial and tumour cells.
Mechanism of angiogenesis
Primarily mediated by activity of VEGF and VEGFR2.
Tumours release VEGF, which leads to the formation of a tip cell at the VEGFR2’s on the blood vessel. It stimulates the proliferation of endothelial cells, to produce a stalk cell that lengthens and forms a lumen of the new blood vessel.
PDGF acts at PDGFRbeta to recruit pericytes, which wrap around the new blood vessels, providing it structure and size. The pericytes recruit the formation of SM around the vessel, and mediate maturation of the blood vessel. This is not done as organised as in normal angiogenesis.
