3 Cancer Flashcards
*Q: Define cancer.
A: a disease caused by an uncontrolled division of abnormal cells in a part of the body
*Q: Define neoplasia. Can be?
A: the presence or formation of new, abnormal growth of tissue = uncoordinated and persists after the cessation of the stimuli that initiated the change
benign or malignant
*Q: Define metastasis.
A: the development of secondary malignant growths at a distance from a primary site of cancer
*Q: Define carcinogen. Name 6 classes.
A: a substance capable of causing cancer in living tissue (causes genetic damage)
chemicals viruses ionising/non ionising radiation hormones bacteria/fungi/parasites miscellaneous
*Q: What is the aim of cancer screening?
A: Detect cancer either at pre-invasive stage/early
*Q: What will make a cancer screening programme successful? (4)
A:Reliable prediction of tumour behaviour
Treatment available
Target population has enough people to justify expense
Cost-effective and reliable screening tool
Q: Most common cancers in men? Women?
A: Prostate W: breast
Lung
Colon/Rectum
*Q: How does cancer link to age? (2)
A: Incidence of cancer worldwide increasing as people are living for longer
in general, higher incidence >55 yrs (to get cancer, need to develop DNA defects which takes time)
*Q: How does cancer link to geography? (2)
A: diff places have diff levels of cancer incidence
stomach cancer is higher in japan than US
colon cancer is lower in japan that US
-both due to diets
melanoma higher in NZ and australia than scandinavia
-people that live there are white and not used to it
*Q: How does cancer link to genetics? (3 mechanisms for hereditary genetics and examples).
A: Autosomal dominant - inherited cancer syndrome where a single mutant gene is responsible eg retinoblastoma, FAP
Autosomal Recessive - inherited defective DNA repair mechanisms eg xeroderma
Unknown/(mixed multiple factors) - Familial Cancer Syndromes eg BRCA, breast
*Q: What can X ray radiation increase the chances of?
A: leukaemia and solid tumours
*Q: What are the 4 classes of regulatory genes? (targets for DNA damage)
A: Oncogenes - growth promoting genes
Tumour Suppressor Genes - growth inhibiting genes
Apoptosis - genes regulating programmed cell death
DNA Repair Genes - prevent mutations in normal cycle
*Q: What are the clinical effects of a tumour? (4)
A: benign and malignant can both affect
- Anxiety about lumps and bumps
- Related to location - pressure, ulceration, infection, bleeding
- Metabolic cancer cachexia (reduced fat and muscle bulk, increased basal metabolic rate) mediated by tumour necrosis factor (TNF)
- Paraneoplastic syndromes which are seen as bizarre but have an underlying cancer cause eg suddenly high calcium levels or increased clotting risk
*Q: What allows Grading of cancer? What does staging give you? (2) What is it based on? (3) Uses? (3) Is staging or grading more useful?
A: Histological - low or high grade- Based on the degree of differentiation -> allows grading
STAGING 1. gives prognosis to patient 2. defines therapy needed
size, spread to regional lymph nodes, metastases presence
combines clinical, radiological and pathological findings
staging
Q: How do you diagnose/test for cancer presence? (2) Confirmation? (2) Metastasise? (3)
A: Tumour markers and blood serology used to test for the presence of cancer
Biopsy or Fine Needle Aspiration (FNA) is used to extract a bit of tissue or fluid to test to confirm the presence of cancer
To see if the cancer has metastasised imagine will be used:
CT
MRI
PET
*Q: What are the 2 basic components of tumours?
A: parenchyma= proliferating neoplastic cells (the functional tissue of an organ)
stroma= the supportive tissue of an epithelial organ, tumour, gonad, etc., consisting of connective tissues and blood vessels (holds it together)
*Q: Describe the name of a benign tumour.
A: suffix: oma
*Q: Describe the name of a malignant tumour. (2)
A: carcinoma for perenchymal tumours
sarcoma for stromal tumours
Q: Describe the name of a tumour from:
glandular tissue.
ovaries.
epidermis.
mucous membrane.
A: adenoma (glandular tissue)
cystadenoma (ovaries)
papilloma (epidermis)
polyp (mucous membrane)
Q: Describe the name of a tumour from stromal tissue:
fat. fibrous/ connective tissue. blood vessels. smooth muscle. bone. cartilage.
A: lipoma (fat tissue)
fibroma (fibrous or connective tissue) angioma (blood vessels) leiomyoma (smooth muscle) osteoma (bone) chondroma (cartilage)
*Q: How do benign and malignant tumours differ in terms of differentiation/anaplasia?
A: - Malignant tumours show anaplasia (very disorganised and doesn’t resemble tissue it came from/ complete lack of differentiation)
- Benign tumour cells are relatively well differentiated (can recognise which tissue it came from)
*Q: How do benign and malignant tumours differ in terms of growth rate?
A: - Benign tumour are slower growing than malignant tumours
-malignant tumours have rapid turnover
*Q: How do benign and malignant tumours differ in terms of local invasion?
A: - Benign tumours don’t tend to infiltrate the basal lamina (can cause pressure effects)-> remain localised
- Malignant tumours infiltrate the basal lamina
*Q: How do benign and malignant tumours differ in terms of metastasises?
A: - Benign tumours don’t metastasise (v rare)
*Q: What are the 4 mechanisms of invasion/metastasis? Which method does breast cancer like? Which is the most common route for sarcoma and carcinomas?
A: lymphatic (spread through lymph channels- breast cancer likes this method)- carcinoma initally
haematogenous (through blood stream)- sarcomas and carcinomas later
body cavities (transcoelomic spread)
contiguous (grows continuously and spreads)
*Q: What are the 4 factors that affect who gets cancer?
A: age
geography
environmental
genetics
Q: Which cancers specifically affect young people? (3) Why?
A: leukaemias
neuroblastoma
wilms tumour
usually associated with very specific genetic abnormalites
*Q: How does cancer link to the environment? (5)
A: UV light
diet and weight
smoking, alcohol
viruses eg HPV, HBV, EBV
Q: What is carcinogenesis? (3)
A: mulistep process from normal cell to cancerours
malignancy is acquired in a step wise fashion
accumulation of successive mutations in DNA (could put up with one but not many)
*Q: What are chemical carcinogens? Structure? Act?
A: =chemicals that damage DNA
no common structural features
act with or without conversion (conversion could be an enzyme or other metabolic conversation to turn non harmful chemical carcinogenic)
Q: Who tends to be affected by oncogenic viruses? Associated with? Examples? (4)
A: young people
immunosuppresion
Human Papilloma Virus (HPV) for cervical cancer
Epstein–Barr virus (EBV) for Burkitt lymphoma
HBV for HCV for hepatic cancers
Q: What’s the mechanism of oncogenic viruses?
A: (oncogenic RNA viral genome transcribed into DNA by E prior to incorp) oncogenic viral DNA directly incorporated int host cell DNA
alters genetics of host (functioning)
Q: What type of radiation can cause cancer? (3)
A: sun, x rays, nuclear bomb fall out
ionsing= damages DNA
Q: What can increased oestrogen exposure cause?
A: increased risk of breast cancer
Q: What is a naturally occurring carcinogen for liver cancer?
A: aspergillus flavus (fungus)
Q: Name 3 miscellaneous agents that cause cancer.
A: asbestos
vinyl chloride
metals eg nickel
*Q: Where are oncogenes derived from? What happens when oncogenes are overactive? Name 3 examples associated with tumours.
A: genes regulating normal cell growth (ON SWITCH)// proto-oncogenes
too much cell growth, cancer
- Myc - burkitt lymphoma
- N-myc - neuroblastoma
- CyclinD1 - mantle cell lymphoma
*Q: What are tumour suppressor genes? When can it cause cancer? 3 examples.
A: OFF SWITCH
doesn’t tell oncogenes to turn off
- Rb gene for genetically inherited retinoblastoma
- P53 (housekeeper of genome)
- BRCA-1 and 2 for breast cancer (are familial)
Q: Which 2 clinical effects of a tumour are often the cause of death?
A: metabolic cancer cachexia
paraneoplastic syndromes
(loss of homeostatic reserve)
Q: How can a benign tumour creating pressure be bad?
A: eg in brain or in any other sensitive place
Q: Name 2 laboratory methods for cancer diagnosis. Other methods? (3)
A: cytology FNA (looking at cells)- freehand or ultrasound guided
histology (take bits of tissue)- biopsy
stains, markers, molecular methods eg microarrays
Q: Why has the cervical screening programme been so successful? How successful? Describe the screening programme itself. What does the disease start as?
A: found a cure associated with HPV
vaccinated against it now
70% reduction in deaths over 30 yrs programme
-detectable with relatively easy low cost process
disease starts as CIN = cervical dysplasia
*Q: Are veins or arteries penetrated more frequently during hemogenous spread of cancer? why? What are the most common sites? (2) why?
A: -veins, thickness of walls
-liver and lungs, lymphatic drainage
*Q: With the lymphatic spread of cancer, what can be evoked? then?
A: immune response -> nodal hyperplasia
*Q: Which gene regulates apoptosis? Overexpression? found?
A: bcl-2 prevents programmed cell death
overexpression= indolent growth of lymphocytes found in many low grade lymphomas
*Q: What are the 5 major classes of chemical carcinogens?
A: -hydrocarbons (polycyclic aromatic ones= E action)
- amines (aromatic ones= other metabolic conversion)
- nitrosamines
- azo dyes (other metabolic conversion)
- alkylating agents (w/o converting)
