Outline of Disease Processes in Cancer Flashcards
<p>What are most cancers (in terms of how many cells they arise from)?</p>
<p>Monoclonal (arise from a single cell)</p>
<p>What does monoclonal mean?</p>
<p>Arise from a single cell</p>
<p>How do cancer cells divide?</p>
<p>Using the mitosis stages just like normal cells</p>
<p>What are the stages of mitosis in cancer cells?</p>
<p>1) Interphase</p>
<p>2) Prophase</p>
<p>3) Metaphase</p>
<p>4) Anaphase</p>
<p>5) Telophase</p>
<p>6) Daughter cells</p>
<p>Why do cancer cells have uncontrollable growth?</p>
<p>They have no regulation</p>
<p>What are some properties of cancer cell that is different to normal cells?</p>
<p>Loss of contact inhibition</p>
<p>Increase in growth factor secretion</p>
<p>Increase in oncogene expression</p>
<p>Loss of tumour suppresor genes</p>
<p>What can you say about tumour suppresor genes in relation to cancer?</p>
<p>Cancer is caused by a loss of tumour suppresor genes</p>
<p>What can you say about cancer and oncogene expression?</p>
<p>Increase in oncogene expression leads to cancer</p>
<p>What are properties of normal cells that are different to cancer cells?</p>
<p>Oncogene expression is rare</p>
<p>Intermittent or co-ordinated growth factor secretion</p>
<p>Presence of tumour suppressor genes</p>
<p>What is carcinogenesis?</p>
<p>The initiation of cancer formation</p>
<p>What are the 2 stages of carcinogenesis?</p>
<p>Pre-clinical cancer</p>
<p>Clinical cancer</p>
<p>What are the steps of pre clinical cancer in carcinogenesis?</p>
<p>Initiation</p>
<p>Promotion</p>
<p>Tumour growth</p>
<p>What happens during clinical cancer in carcinogenesis?</p>
<p>Tumour progression</p>
<p>When are cancers detectable?</p>
<p>Only after a certain amount of cells are present</p>
<p>What are the causes of cancer seperated into?</p>
<p>Initiation</p>
<p>Promotion</p>
<p>Progression</p>
<p>What can initiate cancer?</p>
<p>Chemical</p>
<p>Physical</p>
<p>Viral</p>
<p>What is related to the promotion of cancer?</p>
<p>Growth factors</p>
<p>Oncogenes</p>
<p>What is related to the progression of cancer?</p>
<p>Metastasis</p>
<p>What are some chemicals that can initiate cancer?</p>
<p>Hydrocarbons such as soot and tarts</p>
<p>Analine dyes (cause bladder cancer)</p>
<p>Aflatoxin (causes liver cancer)</p>
<p>Nitrogen mustard (causes leukaemia)</p>
<p>Alcohol and smoking (causes lung, head and neck, and gastrointestinal cancers)</p>
<p>What are physical causes of cancer?</p>
<p>Ionising radiation</p>
<p>Mechanisms (chromosome translocation, gene amplification, oncogene activation)</p>
<p>What are some mechanisms that are considered a physical cause of cancer?</p>
<p>Chromosome translocation</p>
<p>Gene amplification</p>
<p>Oncogene activation</p>
<p>What are some virus causes of cancer?</p>
<p>Herpes virus (causes Burkitt's lymphoma-cervical cancer)</p>
<p>Hepatitis B (causes liver cancer)</p>
<p>Papilomavirus (causes adult T cell leukaemia/lymphoma)</p>
<p>What do oncogenes do?</p>
<p>Promote cells to become cancerous</p>
<p>How do oncogenes promote cells to become cancerous?</p>
<p>Transformation genes</p>
<p>Positive regulators of growth</p>
<p>What are growth factors that promote cancer growth?</p>
<p>Peptide molecules that:</p>
<p>Regulate cell growth and function<br></br>Bind to cell membrane receptors<br></br>Stimulate activation of intracellular signal transduction pathways</p>
<p>What do polypeptide molecules that are growth factors promoting cancer do?</p>
<p>Regulate cell growth and function</p>
<p>Bind to cell membrane receptors</p>
<p>Stimulate activation of intracellular transduction pathways</p>
<p>What do oncogenes cause in the surrounding cells?</p>
<p>The cells to undergo growth by paracrine stimulation</p>
<p>What does not happen in oncogene expression that normally happens?</p>
<p>The feedback loop that stops growth at a certain point</p>
<p>What is the most common altered tumour suppresor gene?</p>
<p>P53</p>
<p>What is the normal function of P53?</p>
<p>Transcriptional regulator</p>
<p>Promotes DNA repair</p>
<p>Apoptosis</p>
<p>Differentiation</p>
<p>What induces P53 to become altered?</p>
<p>DNA damage</p>
<p>Hypoxia</p>
<p>What is hypoxia?</p>
<p>Deficiency in the amount of oxygen reaching the tissues</p>
<p>Why is metastasis not random?</p>
<p>It is a cascade of tumour-host interactions in sequential steps</p>
<p>What is the process of invasion and metastasis?</p>
<p>1) Tumour invades through basement membrane</p>
<p>2) Moves into extracellular matrix/connective tissue/surrounding cells</p>
<p>3) Invades blood vessels</p>
<p>4) Spreads to distant tissues/organs</p>
<p>What are some enzymes involved in metastasis and what do they do?</p>
<p>Matrix metalloproteinases (MMPs which degrade the extracellular matrix)</p>
<p>Cahedrinks, integrins and CD44 (stop cell ahesion so the cancer cell can break away)</p>
<p>What is matrix metalloproteinases (MMPs)?</p>
<p>Enzymes that degrade the extracellular matrix</p>
<p>What are cahedrins, integrins and CD44?</p>
<p>Enzymes which stop cell adhesion so the cancer cell can break away</p>
<p>What is angiogenesis?</p>
<p>The formation of new blood vessels</p>
<p>What is angiogenesis a key factor in?</p>
<p>The maintanance and progression of malignant tumours</p>
<p>What must happen for a tumour to exceed 2mm in diameter?</p>
<p>New blood vessels must form</p>
<p>What is required for new blood vessels to form?</p>
<p>Degradation of the extracellular matrix</p>
<p>What are clinical correlations seen in relation to angiogenesis and cancer?</p>
<p>Vessel density</p>
<p>Tumour malignancy</p>
<p>Metastasis</p>
<p>What can prevent tumour growth?</p>
<p>Drugs that can inhibit growth factors</p>
<p>What is an example of a growth factor which can be inhibited by drugs?</p>
<p>Vascular endothelial growth factor (VEGF)</p>
<p>How does the inhibition of growth factors like vascular endothelial growth factor (VEGF) work?</p>
<p>Drugs block receptors on epithelial cells and prevent binding of VEGF</p>
<p>Prevents formation of new blood vessels so the tumour cannot grow</p>
<p>Why do immune cells not recognise cancer cells?</p>
<p>They are self</p>
<p>In terms of receptors, why do immune cells not kill cancer cells and how can we change this?</p>
<p>PD1 (programmed cell death receptor) is present on T cells</p>
<p>Ligand (PDL-1) is on tumour cells</p>
<p>Interaction of these two suppreses T cell activation, therapeutic opportunity to block either receptor</p>
