Cancer Flashcards
What is Interphase?
Interphase has thee sub phases:
The G1 phase (first gap) centred on growth.
The S phase (synthesis) when the chromosomes are copied.
The G2 phase (Second gap) where the cell completes preparations for cell division.
Then the cell divides. The daughter cells may then repeat the cycle.
Mitosis is broken down into five sub phases, what are they?
Prophase Prometaphase Metaphase Anaphase Telophase
What is a checkpoint in the cell cycle?
Three major ones?
A critical control point where stop and go signals regulate the cycle.
G1, G2, and M phases.
What is the most important checkpoint in the cell cycle and why?
The G1 checkpoint (restriction point). If the cell recieves a go-ahead signal, it usually completes the cell cycle and divides. If it does not receive the signal, the cell exits the cycle and switches to a non dividing state, the G0 phase.
What does the M phase checkpoint in the cell cycle do?
It ensures that all the chromosomes are properly attached to the spindle at the metaphase plate before anaphase.
What external physical factor can influence cell division?
Growth factors.
Proteins released by one group of cells that stimulate other cells to divide.
What is PDGF
Platelet derived growth factor.
Normally in a living organism, platelets release PDGF in the vicinity of an injury. The resulting proliferation of fibroblasts helps heal the wound.
What is density-dependent inhibition of cell division?
Cultured cells normally divide until they form a single layer on the inner surface of the culture container.
If a gap is created, the cells will grow to fill the gap.
At high densities, the amount of growth factors and nutrients is insufficient to allow continued cell growth.
What is anchorage dependence in cell division
Most animal cells exhibit this. To divide they must be anchored to a substratum, typically the extracellular matrix of a tissue.
Control appears to be mediated by connections between the extracellular matrix and plasma membrane proteins and cytoskeletal elements.
How have Cancer cells escaped from cell cycle controls
Cancer cells are free from both density-dependent inhibition and anchorage dependence.
They divide excessively and invade tissues because they are free of the bodes control mechanisms. If and when the cancer cells stop dividing, they do so at random points, not at the normal checkpoints in the cell cycle.
How do cancer cells differ from nearly all mammalian cells during cell division?
Cancer cells may divide indefinitely if they have a continual supply of nutrients. Nearly all mammalian cells divide 20 to 50 times under culture conditions before they stop, age, and die.
Cancer cells may be immortal.
Reactivation of telomerase may play a role
How does the abnormal behaviour of cancer cells begin?
When a single cell in a tissue undergoes nonlethal transformations that convert it from a normal cell to a cancer cell.
If the abnormal cell(s) remain at the originating site, the lump is called a benign tumor.
What is metastasis?
The event where cancer cells lose attachment to nearby cells, are carried by the blood and lymph system to other tissues, and start more tumours.
What does Clonality mean
Originate from a single cell
What does Autonomy & density independent mean?
Growth factors (they either make their own OR the GFR’s are active without GF binding)
What is anaplasia?
Lack of normal coordinated cell differentiation.
Cells are undergoing rapid cell division, so exhibit a high rate of mitosis & have large, dark nuclei.
Develop from mutations that occur along the normal differentiation process.
The earlier the mutation occurs in the differentiation process, the higher the malignancy.
What is a tumour?
Swelling that can be caused by inflammation, infection, trauma, or neoplasia.
What is neoplasm?
A tumour caused by neoplasia.
What is a benign tumour?
Well-differentiated cells clustered together in a single mass; don’t usually cause death unless their size or location interferes with vital functions.
What is a malignant tumour?
Not well-differentiated and has the ability to break loose and enter the circulatory or lymphatic system and form secondary malignant tumours at other sites; usually cause suffering and death if untreated or uncontrolled.
Benign tumours are usually named by adding the suffix ??
oma
What is Carcinoma?
Malignant tumour of epithelial origin. ex. skin, mucous membranes of gland nerves, breasts, lining of respiratory, gastrointestinal, urinary and genital tracts. 80-90% of all cancers.
What is Sarcoma?
Malignant tumours of mesenchymal origin. A solid tissue frothing from connective tissues such as cartilage, bone, muscle, fat: 2% of cancers.
What is Osteosarcoma?
Malignant bone tumour.
What are papillomas?
Benign fingerlike projections that grow on any surface
What are polyps?
Growth that projects from a mucosal surface
What is Leukemia?
Cancer of the organs that form the blood, such as the lymph glands and bone marrow, causing an overproduction of immature white blood cells (leukocytes): about 4% of total. Occurs in two forms. Acute (very severe; most common in childhood) and chronic (less lethal; and adult disease)
What is lymphoma
Abnormal production of immature lymphocytes by the spleen and lymph nodes; 5% (hodgkins)
How does a cell become cancerous?
it usually takes several mutagenic nonlethal “hits” to the same cell before the cell actually becomes cancerous - “multi-hit theory”
What causes mutations?
Carcinogens viruses Ionizing radiation Hereditary physical irritants
What is Oncogenesis?
Normal cells transformed into cancerous cells
Specific genes promote or inhibit cell growth, differentiation, again & cell death (apoptosis) AND some are responsible for DNA repair.
When these genes are damaged or mutated, normal growth patterns are altered.
If this mutation is inherited, offspring will have an increased risk for Ca
Oncogenesis involves: Initiation
Exposure to cells to doses of carcinogenic agent
Multiple divided doses equally as potent as one single dose
Oncogenesis involves: promotion
Induction of unregulated growth in initiated cells by various chemicals and growth factors
Cells that have been irreversibly initiated may be stimulated by promoter after a long latency period
Oncogenesis involves: Progression
Tumour cells develop and become invasive, grow uncontrollably and metastasize.
What are three gene types to worry about?
DNA repair genes (mutators)
Tumour suppressor genes
Proto-oncogenes
What are DNA repair genes (mutators) ?
Code for proteins that are responsible for monitoring and repairing mistakes
What are Tumour suppressor genes?
Code for Proteins that monitor DNA and halt the cell’s cycle until repairs can be made - often will send cell to apoptosis if repair is unsuccessful.
What are Proto-oncogenes genes?
Code for proteins that tell cells to divide.
Normally respond to growth factors and signals that promote cell division.
Effects of Malignancy: Release of biologically active agents
Ectopic hormones
Neuropathies
Dermatological abnormalities
Effects of Malignancy: What are direct effects of tumour growth?
Ablation by crowding
Obstruction of vessels
Rupture of vessels
Effects of Malignancy: What are some hematological disorders
Anemia Bleeding disorders Hypercoagulability disorders Disseminated intravascular coagulation Immunosupression Collagen Vascular disease
Effects of Malignancy: What are some metabolic disorders?
Anorexia Fever Chronic inflammation Inc in FFA utilization rather than glucose Inc anerobic metabolism Dec oxidative phosphorylation Cachexia not well understood
What are methods for clinical evaluation?
History Physical examination Radiological studies Laboratory Pathological examination of tumour tissue
Effects of Malignancy: What are paraneoplatic syndromes?
Tumour produces hormones/factors that cause action at disant site i.e:
Hypercalcemia from squamous cell ca of lung, breast ca, renal Ca & adult t-cell leukaemia/lymphoma from parathyroid hormone secretion
What are Metabolic Constituents Affected By Tumour
Serum calcium Serum phosphorus Glucose in insulinomas Electrolytes in Cushing syndrome Ammonia in hepatoma
Enzymes in cancer and type of cancer
ENZYME CANCER LD acute leukemia, carcinomas LD4,LD5 prostatic cancer, ovarian, testicular Acid phosphatase prostatic cancer Alkaline phosphatase bone and liver
Urinary findings in cancer?
Hematuria
Proteinuria
5-HIAA, VMA
BJ proteins
What are endocrine changes in cancer?
Ectopic hormone production by tumour … ACTH, TSH, ADH
What are markers used for in cancer?
Screen asymptomatic individuals for presence of malignancy To diagnose symptomatic patients For tumour staging To determine tumour prognosis To detect cancer recurrence To monitor response to therapy
Tumour markers in cancer
Proteins, glycoproteins, small polypeptides.
Criteria for markers are:
1. Specific for neoplasm, organ, cell type.
2. Analytical method sensitive for earliest possible detection 1gm or 10^9 tumour cells.
3. Not anabolized or released in non-malignant disease
4. Stoichiometric relationship exists between concentration in serum and total mass of tumour.
5. Concentration in serum reflects tumour catabolism in response to therapy.
6. Rapid simple excretion
7. Simple analytical technique
8. Stable matabolite for transport
9. Predictive for recurrence
10. Diagnosis: sensitivity and specificity
Genetic Screening in cancer
A diagnosis of Cancer at early age
Several Family members with cancer
Relatives with more than one type of cancer
A history of bilateral cancer ( ie both breasts)
A history of multiple cancers in one person where one person was cured and another was diagnosed in later life
Rare and unusual cancers such as male breast cancer
Remember me
MARKERS TISSUE CANCER
- a- Fetoprotein In fetal liver, GIt,liver, and yok sac testicular
- CEA Fetal GIt, liver,
colon, breast,
Pancreas - B -HCG Normal product testicular,
Trophoblasts gestational tumors - PSA Seminal fluid prostrate
- Carbohydrate antigens
CA 19-9 monosialo-carbohydrate AG Pancreatic
CA 125 fetal GIt Ovarian
Ca 15-3 Breast - Neuron specific Small cell lung ca
enolase
