Pathology of Neoplasia

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  • Created by: LBCW0502
  • Created on: 14-01-20 09:47
What is the definition of neoplasia? (1)
New growth. Tumour (swelling). A neoplasm is an abnormal mass of tissue, the growth of which exceeds and is uncoordinated with that of the normal tissue and persists in the same manner after cessation of the stimuli which evoked the change
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What is the definition of neoplasia? (2)
Cell division without control.
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State features of the nomenclature
Oma (tumour). Carincoma (hard tumour). Sarcoma (soft tumour in connective/supportive tissue). Leukaemia (in blood forming tissues, abnormal number of blood cells). Lymphoma and myeloma. Brain and spinal cord
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State features of the cancer types
Carcincomas (in layers of cuboid epithelium). Bone carcinoma (less common). Lymphomas (cancer starts in lymphocytes in lymphatic system). Myeloma (cancer in plasma cells). Leukaemia (WBC cancers). Brain and spinal cord
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State the histogenetic classification of malignant tumours (1)
Epithelium (carincoma). Connective tissue (sarcoma). Bone marrow (leukaemia). Glandular epithelium (adenocarcinoma). Squamous epithelium (squamous carcinoma). Striated muscle (rhabdomyosarcoma). Smooth muscle (leiomyosarcoma). Bone (osteosarcoma)
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State the histogenetic classification of malignant tumours (2)
Liver (hepatocellular carcinoma). Skin (melanoma). Myeloid stem cells (myeloid leukaemia). Plasma cells (multiple myeloma). Lymphoid tissue (lymphoma). Gonad/male (seminoma). Gonad/female (dysgerminoma). Germ cells (malignant teratoma)
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What are the two types for mode of growth?
Benign and malignant (non-cancerous vs cancerous)
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Describe features of benign growth
Contained as a mass, doesn't spread, location may cause issues e.g. pressure on nerves/arteries, cause pain, infections
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Describe features of malignant growth
Cancerous, multiplies, invades surrounding tissue, unstable, abnormal cells, spreads in circulation
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What is a pre-cancerous mode of growth?
In between benign and malignant, not detected
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Describe features of the cell cycle (1)
Process to duplicate DNA to produce new cells. G1 phase (cellular contents, excluding the chromosomes are duplicated). G1 check point. S phase (each of the 46 chromosomes is duplicated by the cell, quick phase, base pairs exposed/sensitivity
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Describe features of the cell cycle (2)
G2 phase (cell double checks the duplicated chromosomes for error, making any needed repairs). G2 check point. Mitosis (cell growth stops). Metaphase check point (ensure cell can complete cell division) and cytokinesis (2 nuclei)
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Describe features of the cell cycle (3)
G0 phase (cell cycle arrest)
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What are the steps in mitosis? (1)
G2 (nuclear membrane broken down, loosely coiled replicated chromosomes, sister chromatids and centromere). Prophase (spindle fibres appear, chromosomes condense). Prometaphase (spindle fibres attach to chromosomes, chromosomes condense)
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What are the steps in mitosis? (2)
Metaphase (chromosomes align). Anaphase (centromeres divide, sister chromatids move to opposite poles). Telophase (nuclear membrane reforms, chromosomes de-condense, spindle fibres disappear)
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What are the steps in mitosis? (3)
Cytokinesis (cytoplasm divides, parent cell becomes 2 daughter cells with identical genetic information)
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What are cell cycle check points?
The cell has several systems for interrupting cell cycle if there is a problem. Checkpoints are biological traffic lights telling the cell when it can safely go or when to stop and fix a problem
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Where are the cell cycle checkpoints?
G1 checkpoint (G1/S transition). G2 check point (G2/M transition). Spindle checkpoint (transition from metaphase to anaphase)
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Describe features of the G1 checkpoint
Checks for: cell size, nutrients, growth factors, mechanical damage, DNA damage
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Describe features of the G2 checkpoint
Checks for: DNA damage and DNA replication completeness
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Describe features of the spindle checkpoint
Checks for: chromosome attachment to spindle at metaphase plate
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State the cytotoxics which can affect the cell cycle
Alkylating agents (whole cycle). Vinca alkaloids and mitotic inhibitors (M). Taxoids (M, G1). Antimetabolites (S). Cytotoxic antibiotics (G1, S, G2)
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What are the causes of cancer?
Multifactorial (environmental and lifestyle factors, genetic susceptibility)
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What are the causes of cancer? - genetic
Inherited predisposition in some cancers. No strong positive family history in most cancers. Certain cancers have genetic link. Nephroblastomas (run in families). Down's Syndrome and leukaemia. Breast cancer (BRCA1) - sister/daughter (2x chance)
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Mutations in DNA lead to changes in what?
Protein content/activity
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How can mutations arise? (1)
Copying errors during replication. Spontaneous cleavage of DNA synthesis. Reaction which chemicals. Introduction of viral DNA. UV or ionising radiation. Most cancers require multiple mutations (stepwise process/years)
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How can mutations arise? (2)
Accumulated damage to multiple genes. Many cancers have >5 independent mutations
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How do DNA mutations lead to cancer? (1)
DNA mutations changes protein content/activity (cancer). Some cancers form because a protein has a different activity. Gain of function mutation. Activation of oncogenes (normal function - cell growth, gene transcription)
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How do DNA mutations lead to cancer? (2)
Some cancers form due to a protein losing activity. Loss of function mutation. Inactivation of tumour suppressor genes (normal function - DNA repair, cell cycle control, cell death)
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Describe features of oncogenes (1)
Most human oncogenes are mutant forms of normal proteins. The normal gene is called a proto-oncogene. Most human oncogenes cause defects in growth signalling. Some are hyperactive versions of the normal protein
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Describe features of oncogenes (2)
Others have normal activity, but abnormally high expression
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Describe features of tumour suppressor genes (1)
Normal cells contain factors that suppress tumour development. Normal proteins regulate cell division and promote DNA repair
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Describe features of tumour suppressor genes (2)
Provide checkpoints during cell division. Negatively regulate signalling by growth factors. Positively regulate signalling by inhibitory growth factors. Contribute to DNA repair. Induce apoptosis
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Defects in tumour suppressor genes leads to what?
Unregulated cell division. Reduced ability to repair DNA. Failure to induce apoptosis. (Need balance of tumour suppressor genes and oncogenes. Cancer - more activity from oncogenes, less activity from tumour suppressor genes)
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Describe environmental and lifestyle factors can cause cancer? (1)
Chemicals (mutagens) - smoking, dietary factors (excess fat, alcohol, low fruit/vegetable intake, gut/breast/prostate), food additives), drugs (cytotoxics, oral contraceptives, HRT, NSAIDS)
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What is the effect of oral contraceptives, HRT and NSAIDs on cancer?
Oral contraceptives (reduce risk of ovarian cancer by increases risk of endometrial and breast cancer). HRT (increases risk of ovarian and endometrial cancer). NSAIDs (reduce risk of colorectal cancer)
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Describe environmental and lifestyle factors can cause cancer? (2)
Organochlorines (pesticides, plastics). Radiation (ionising, UV radiation, sun, phones, power lines). Obesity/lack of physical activity (oesophageal, colon, prostate, breast cancer)
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Describe environmental and lifestyle factors can cause cancer? (3)
Infection (viruses - Epstein-Barr virus/Burkitts, nasopharyngeal, HPV/cervix, hepatitis/hepatocellular, HIV/kaposi's sarcoma, lymphoma, H.pylori/stomach)
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Describe environmental and lifestyle factors can cause cancer? (4)
Immunological/immunosurveillance (AIDS patients developing some form of cancer). Endocrine (hormone dependent tumours e.g. breast, prostate). Trauma (chronic irritation/chronic inflammation)
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Describe environmental and lifestyle factors can cause cancer? (5)
Psychological (stress/repress emotions, also affects management and outcome/QOL). Treatment - psychological therapy
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Is cancer a signalling disease?
Yes
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Describe the emergence of a cancer cell (1)
Cancers originate from a single cell. Genetic mutations (changes in normal base sequence of DNA, contribute to the emergence of a cancer cell). A series of mutations accumulate in successive generations of the cell (clonal evolution)
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Describe the emergence of a cancer cell (2)
Eventually, a cell accumulates enough mutations to become cancerous
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What must cancerous cells do in order to develop and form into a tumour?
Mutations/alterations need to occur for the cell to acquire a succession of biological capabilities to occur (needs to overcome barriers to survive)
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What are the hallmarks of cancer? (6)
Sustaining proliferative signalling, evading growth suppressors. Activating invasion and metastasis. Inducing angiogenesis. Resisting cell death
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Describe features of sustaining proliferative signalling (1)
Normal cells rely on positive growth signals from other cells
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Describe features of sustaining proliferative signalling (2)
Cancer cells can reduce their dependence on growth signals by: production of their own extracellular growth factors, over-expression of growth factor receptors, alterations to intracellular components of signalling pathways
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Describe features of evading growth suppressors (1)
Normal cells rely on antigrowth signals to regulate cell growth. Cancer cells can become insensitive to these signals - disruption of retinoblastoma protein (pRb) pathway
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Describe features of evading growth suppressors (2)
pRb prevents inappropriate transition from G1 phase of the cell cycle to synthesis phase. In cancer cells, pRb may be damaged, allowing the cell to divide uncontrollably
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Describe features of activating invasion and metastasis (1)
Eventually, tumours may spawn pioneer cells that can invade adjacent tissues and travel to other sites in the body to form new tumours (metastasis). This allows cancer cells to colonise new areas where oxygen and nutrients are not limiting
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Describe features of activating invasion and metastasis (2)
Metastasis causes 90% of deaths from solid tumours
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Describe features of enabling replicative immortality (1)
Cancer cells need to overcome boundaries on how many times a cell can divide. Limits are usually set by telomeres (ends of chromosomes)
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Describe features of enabling replicative immortality (2)
In normal cells, telomeres get shorted with each cell division until they become two short that the cell can no longer divide. In cancer cells, telomeres are maintained, allowing the cell to divide an unlimited number of times
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Describe features of angiogenesis (1)
Angiogenesis (formation/maintenance of new blood vessels) plays a role in tumour growth. New blood vessels supply cancer cells with oxygen and nutrients, allowing the tumour to grow
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Describe features of angiogenesis (2)
Angiogenesis is mediated by vascular endothelial growth factor (VEGF). Other growth factors also play a role - fibroblast growth factor (FGF), platelet derived growth factor (PDGF). Cancer cells utilise growth factors
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Describe features of resisting cell death (1)
When normal cells become old/damaged, they go through apoptosis (programmed cell death). An important hallmark of many cancers is resistance to apoptosis, which contributes to the ability of the cells to divide uncontrollably
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Describe features of resisting cell death (2)
Cancer cells resist apoptosis and continue dividing
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What are the two emerging hallmarks involved in the pathogenesis of cancer?
Evading immune destruction and deregulating cellular energetics (made possible by two enabling characteristics - tumour promoting inflammation and genome instability and mutation respectively)
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Describe features of evading immune destruction
The immune system is responsible for recognising and eliminating cancer cells, preventing tumour formation. Evasion of this immune surveillance by weakly immunogenic cancer cells is an important hallmark for cancer (weakly immunogenic, overlooked)
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Describe features of deregulating cellular energetics
Uncontrolled growth and division of cancer cells relies not only on the deregulation of cell proliferation but also on reprogramming of cellular metabolism, including increased aerobic glycolysis (Warburg effect)
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Describe features of genome instability and mutation
Cancer cells achieve genome instability by increasing their mutability or rates of mutation, through increased sensitivity to mutagenic agents or breakdown of genomic maintenance machinery
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Describe features of tumour promoting inflammation
Immune cells infiltrate tumours and produce inflammatory responses, which can paradoxically enhance tumourigenesis, helping tumours acquire the hallmarks of cancer
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Describe features of tumour grading (1)
A macroscopic assessment of the degree of differentiation which cells show. Described as well, moderately or poorly differentiated (grade 1, 2, 3 respectively)
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Describe features of tumour grading (2)
Tumours with no differentiation are said to be anaplastic (most dangerous, highly proliferative). Well differentiated tumours are less aggressive (low grade). Grade = how aggressive a cancer is. Better survival rate for grade 1 compared to grade 3
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Describe features of tumour grading for breast cancer (1)
Grade 1 (well differentiated, cancer cells look almost like normal cells, similar size/shape to normal cells, slow growing). Grade 2 (moderately differentiated, cancer cells look less like normal cells, larger, variation in size/shape, grow faster)
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Describe features of tumour grading for breast cancer (2)
Grade 3 (poorly differentiated, cancer cells look most changed, usually fast growing)
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State features of DCIS
Ductal carcinoma in situ. Three grades (low, intermediate, high). Non-invasive breast cancer, doesn't spread, stays in place, not life threatening by increases chance of developing breast cancer later in life
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Describe features of tumour staging
Useful in planning treatments, assessing severity of tumour, prognosis, response to therapy and can help recruitment into clinical trials. Classifies malignant tumours (exception - haematological and brain tumours)
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What is TMN based on? (1)
Size of primary tumour (1-4, 1 being the smallest). Degree of nodal involvement (0-3, 0 being no involvement). Evidence of metastases (0-1, 0 being no metastases)
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What is TMN based on? (2)
Primary tumour (TX - primary tumour cannot be evaluated, T0 - no evidence of primary tumour, Tis - carcinoma in situ/early cancer/not spread, T1/2/3/4 - size/extent of primary tumour)
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What is TMN based on? (3)
Regional lymph nodes (NX - regional lymph nodes cannot be evaluated, N0 - no regional lymph node involvement/no cancer found in lymph nodes, N1/2/3 - involvement of regional lymph nodes/number and extend of spread)
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What is TMN based on? (4)
Distant metastases (MX - distant metastases cannot be evaluated, M0 - no distant metastases/cancer not spread, M1 - distant metastases/cancer has spread)
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Describe features of number staging (1)
Stage 0 (carcinoma in situ, early cancer in cell layers). Stage I/II/III (higher number, more extensive disease, greater tumour size, spread of lymph nodes/organs adjacent to primary tumour)
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Describe features of number staging (2)
Stage IV (cancer has spread to another organ). Best prognosis at stage 0, higher stage gives poorer prognosis. Stage indicates how far the cancer has spread (e.g. breast cancer diagram). Lower stage/higher survival rate
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Describe features of tumour markers
Substance produced by or in response to a tumour. Molecule that can be detected in serum plasma or other body fluids. Limited use in diagnosis (not elevated in all patients, not specific to malignancy). Mainly used to determine response to therapy
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Give examples of tumour markers (1)
CEA (carcinomaembryonic antigen) - colorectal cancer. PSA (prostate specific antigen) - prostate cancer. CA125 - ovarian cancer. CA19-9 - pancreatic cancer
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Give examples of tumour markers (2)
AFP (alpha-fetoprotein)/HCG (beta-human chorionic gonadotropin)/LDH (lactate dehydrogenase) - testicular teratoma/seminoma
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Describe the role of tumour markers in patient management - testicular tumour (1)
Diagnosis (increased AFP/HCG/LDH). Staging (if AFP/HCG/LDH doesn't return to normal after orchidectomy/surgical removal of testicle - residual disease). Prognosis (increased AFP/HCG linked with poor prognosis)
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Describe the role of tumour markers in patient management - testicular tumour (2)
Indicator of response (if AFP/HCG/LDH don't fall after chemotherapy - indicates resistant disease). Detection of relapse (sudden elevation of AFP/HCG/LDH, while in clinical remission, suggests relapse)
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Describe the role of tumour markers in patient management - testicular tumour (3)
Test markers prior to treatment, test markers over treatment course, indication of response to treatment
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Describe features of performance status (1)
Criteria used to assess how a patient's disease is progressing, affects the daily living abilities of the patient and determine appropriate treatment and prognosis. National requirement to determine PS at every patient visit
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Describe features of performance status (2)
Various scales - ECOG, WHO and Karnofsky
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Describe features of the ECOG scale (1)
0 - fully active, able to carry on all pre-disease performance without restriction. 1 - restricted in physically strenuous activity but ambulatory and able to carry out work of a light or sedentary nature e.g. light house work, office work
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Describe features of the ECOG scale (2)
2 - ambulatory and capable of all self-care but unable to carry out any work activities, up and about more than 50% of waking hours. 3- capable of only limited self-care, confined to bed or chair more than 50% of waking hours
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Describe features of the ECOG scale (3)
4 - completely disabled, cannot carry out any self-care, totally confined to bed or chair. 5 - dead
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Describe features of the WHO scale
0 - asymptomatic. 1 - symptomatic but ambulatory (able to carry out light work). 2 - in bed <50% of day (unable to work but able to live at home with some assistance). 3 - in bed >50% of day (unable to care for self). 4 - bedridden
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Describe features of the Karnofsky scale (1)
100 (asymptomatic), 90 (normal activity, minor symptoms), 80 (normal activity, some symptoms), 70 (unable to work, cares to self), 60 (occasional assistance with needs), 50 (considerable assistance), 40 (disabled, full assistance needed)
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Describe features of the Karnofsky scale (2)
30 (needs some active supportive care), 20 (very sick, hospitalisation needed), 10 (moribund), 0 (dead)
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What are metastases?
Local blood tumours which enter circulation, deposited in another area and are reintegrated into tissues
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What are the aims of cancer management? (1)
Prevention (e.g. environmental and lifestyle interventions - diet/exercise/smoking cessation). Cure cancer (induce remission). Control the cancer (if cure not realistic, limit growth/spread of cancer)
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What are the aims of cancer management? (2)
Palliative care (when outlook is poor, this can be used to reduce symptoms/complications without significantly affecting tumour
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What does adjuvant mean?
A course of chemotherapy in patients with no evidence of residual cancer after surgery or radiotherapy, given with the intent of destroying any residual tumour cells
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What does neo-adjuvant mean?
A course, usually shorter than adjuvant chemotherapy, given with the intent of down sizing the primary tumour to make it more amenable to surgery or radiotherapy (given before surgery/radiotherapy)
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What does maintenance mean?
Long term, usually low dose chemotherapy or biological therapy in patients who have achieved a complete remission, with the intention of delaying re-growth or micro-residual disease
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What does palliative mean?
Chemotherapy given to control symptoms or prolong life in patients in whom cure is unlikely
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What does induction mean?
High dose combination chemotherapy given with the intent of inducing a complete remission when initiating curative chemotherapy
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What does consolidation mean?
Repetition of the induction regimen, with the intention of increasing cure rate or prolonging remission
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What does intensification mean?
Chemotherapy after complete remission, often with higher doses/alternative combinations with the intention of increasing cure or remission duration
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What does salvage mean?
Potentially curative combination chemotherapy given to patients who have failed or recurred after curative chemotherapy
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Describe the common principles of combination chemotherapy (1)
Use drugs that are known to be effective as single agents. Use drugs with different toxicity (toxicities don't overlap). Use pulsed intermittent therapy to allow normal cells to recover. Use optimal dose and schedule for each individual agent
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Describe the common principles of combination chemotherapy (2)
If possible, use drugs with synergistic killing effect. There are no clinically important drug interactions between the agents
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Why is combination chemotherapy used?
To try and improve rate and duration of response by combining drugs with different MOA. Also helps to prevent resistance
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Give examples of combination chemotherapy
BEP (testicular cancer). R-CHOP (non-Hodgkin's lymphoma). Trastuzumab and chemotherapy (adjuvant breast cancer)
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State features of pulsed therapy
Therapy given at regular intervals, at time points where there is a high number of tumour cells. Successful therapy (no tumour cells survive). Unsuccessful therapy (high number of tumour cells survive/relapse)
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Describe features of scheduling (1)
Follow protocols used in original clinical trials. Vary from single oral drugs (e.g. capecitabine) to complex multiple drug regimens (e.g. for leukaemia and BMT). Design based on consideration of effects on normal and tumour cells
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Describe features of scheduling (2)
Normal tissues are inevitably damaged by chemotherapy - bone marrow and epithelial lining cells usually recover within 2-3 weeks. On this basis, most chemotherapy is given at 3 weekly intervals
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Describe features of scheduling (3)
Decreases neutrophil count (nadir - risk of infection increases exponentially with depth of neutropenia)
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Describe features of scheduling (4)
Tumour/healthy cell kinetics and chemo-sensitivity with relation to scheduling (graphs - cancer killed (no tumour stem cells, high normal stem cells), patient dead of toxicity (no tumour/normal stem cells)
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Describe features of scheduling (5)
Patient dead of cancer (tumour stem cells > normal stem cells)
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Describe features of scheduling (6)
Precise sequence of drug administration in many regimens is unimportant but there are some situations where drugs must be given in the correct order e.g. Paclitaxel and Carboplatin (ovarian cancer). Paclitaxel administered before Carboplatin
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Describe features of scheduling (7)
If Carboplatin is administered first - more profound myelosuppression (bone marrow toxicity), Paclitaxel clearance decreased by 20% (more toxicity)
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What are the different schedules?
Conventionally 3 weekly (A--A--A--A--A). Dose dense (A-A-A-A-A-A). Dose intense (Ab--Ab--Ab--Ab--Ab). Plain high dose (large A). Alternating (A B A B A B A B [A B A B A B]). Sequential ( A A A A B B B B)
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What are the principles of chemotherapy?
Balance between activity (different MOA, different mechanisms of resistance) and safety (compatible side effects). Increased efficacy
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What is the proportional kill effect? (1)
A given dose of drug skills a constant proportion of tumour cells rather than an absolute number (equal doses will kill equal proportions of cells). Same tolerated doses needed repeatedly, no matter how small the tumour shrinks
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What is the proportional kill effect? (2)
Early treatment when tumours are small - gives better clinical result
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Describe the factors which affect the response to chemotherapy? (1)
Dose intensity - cell death follows 1st order kinetics. Maximal doses must be given. But intended chemotherapy doses may not be given due to toxicity
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Describe the factors which affect the response to chemotherapy? (2)
Tumour burden - large tumours have lower growth fractions, less responsiveness and greater chance to spread to other parts of the body
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Describe the factors which affect the response to chemotherapy? (3)
Drug resistance - inherited or acquired resistance to chemotherapy. Patient-specific factors - other medical conditions, performance status, age, individual variation in kinetics and dynamics
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Describe features of resistance (1)
Due to properties of cancer ells or acquired after exposure to individual drugs. Mechanisms of resistance - altered biochemical pathways, altered cell transported mechanisms to prevent drug concentration in cancer cell, reduced uptake of drug
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Describe features of resistance (2)
Enhanced elimination of drug. Altered drug metabolism, increased clearance, reduced drug activity. Impaired mechanisms of apoptosis (programmed cell death)
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Describe features of cytotoxic drugs with MOA (1)
Disrupt DNA synthesis or its precursors or mitosis
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Describe features of cytotoxic drugs with MOA (2)
Alkylating agents (e.g. cyclophosphamide, cisplatin, nitrosureas) - cause cross linking of DNA strands, break strands, highest kill rate/effective against large tumours)
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Describe features of cytotoxic drugs with MOA (3)
Antimetabolites (e.g. cytarabine, MTX, 5-FU, 6-MP, ralitrexed) - resemble natural metabolites, inhibits enzymes (decrease DNA synthesis) or alter DNA structure
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Describe features of cytotoxic drugs with MOA (4)
Antitumour antibiotics (e.g. doxorubicin, bleomycin) - bind to DNA and RNA, distort its structure
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Describe features of cytotoxic drugs with MOA (5)
Mitotic inhibitors (e.g. vincristine, paclitaxel) - block assembly of microtubules
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What are the sites of action of cytotoxic drugs?
Antibiotics and antimetabolites (G1, S, G2). Vinca alkaloids and mitotic inhibitors (G and M). Taxoids (M and G1). Alkylating agents (whole cell cycle)
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Give the classification of drugs used in breast cancer (1)
Anthracyclines (doxorubicin, epirubicin - cycle non-specific). Taxanes (docetaxel, paclitaxel, M-phase specific). Antimetabolites (5FU, capecitabine, MTX, S-phase specific). Alkylating agents (cyclophosphamide, cycle non-specific)
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Give the classification of drugs used in breast cancer (2)
Vinca alkaloids (vinorelbine, vinblastine, M-phase specific). Monoclonal antibody (trastuzumab, targets HER2 receptor)
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What are the side effects of traditional cancer chemotherapy?
Alopecia, mucositis, pulmonary fibrosis, nausea/vomiting, cardiotoxicity, diarrhoea, cystitis, local reaction, sterility, renal failure, myalgia, myelosuppression, neuropathy, phlebitis
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What are the essential properties of the ideal anticancer agent?
Target is unique to cancer cells. Target is expressed on a high percentage on cancers. Target is present in/on all cells in the tumour. Hitting the target causes death of cancer cell. Agent has low toxicity to normal cells
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What are the current treatment modalities of cancer? (1)
Surgery (removes visible tumour mass). Radiotherapy (destroys fast dividing cancer cells, including cancer cells in adjacent tissue). Chemotherapy (destroys fast proliferating cancer cells)
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What are the current treatment modalities of cancer? (2)
Hormone therapy (inhibits growth and survival of hormone-dependent cancers). Targeted therapy (blocks specific biochemical pathways on which cancer cell growth is dependent)
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What are the current treatment modalities of cancer? (3)
Immunotherapy (treatments that restore or enhance the immune system's natural ability to fight cancer)
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