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MSC: Disease of major orgns > Tumour Biology > Flashcards

Tumour Biology Flashcards

1
Q

What is the nature of malignancy?

A

Cancer cells can grow and proliferate independently of normal control mechanisms (neoplastic) and invade other tissues / organs (malignant

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2
Q

Cell Growth Cycle

A

M phase (mitosis): cell division (0.5h-1h)

↓

G1 phase (gap 1): Cell growth variable due to growth factors and integrins. Restriction point control (cyclin dependent protein kinases, cyclins D E A B) which controlled progression to S phase

↓

S phase (synthesis): DNA replication (10h-20h)

↓

G2 phase (gap 2): preparation for mitosis

↓

M Phase to begin all over again

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3
Q

What happens to cells not in the growth cycle?

A

G0 (resting phase)

  • Can procede to Apoptosis (p53 protein, telomerase)
  • Can be stimulated to go back to G1 phase
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4
Q

What are the examples of alterations in the control elements?

A
  • Excess growth factors
  • Abnormal receptors (signal in the absence of growth factors)
  • Excessive signalling proteins
  • Loss of inhibitory proteins.
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5
Q

What are oncogenes in cancer?

A

Oncogenes (>100) ↑

  • Proto-oncogenes code for proteins that regulate cellular growth processes e.g. proliferation, differentiation, apoptosis.
  • 5 groups of proto-oncogenes: (i) growth factors, (ii) growth factor receptors, (iii) signal transducers, (iv) transcription factors, (v) programmed cell death regulators.
  • Mutation, gene amplification, or chromosomal re-arrangement of proto-oncogenes to oncogenes (e.g. Ras)
  • Oncogenes: Autosomal dominant, gain of function mechanism.
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6
Q

What is the purpose tumour supresor genes in cancer?

A

Cell growth regulation pathways (growth advantage)↓

  • e.g. p53 (‘guardian of the genome’)
  • e.g. BRCA1 (familial breast cancer / ovarian cancer) and BRCA2 (breast cancer)
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7
Q

What is the purpose of DNA repair genes in cancer?

A

•DNA repair genes

−Recognise and repair damaged DNA

−DNA repair defects à cancer predisposition

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8
Q

How does cancer develop?

A
  • Derive from a single aberrant cell with an initial mutation.
  • Accumulation of mutations and epigenetic changes (e.g. DNA methylation) cause defects in normal control of cell division, apoptosis, and differentiation contributing to the development and progression of cancer.
  • Tumour progression usually takes several years (following Darwinian-like evolution and natural selection of mutations).•
  • In normal cells, progressive shortening of telomeres results in replicative cell senescence. Genetic/epigenetic changes (e.g. inactivation of p53 pathway) and maintenance of telomerase activity (and thus telomeres) avoid replicative cell senescence in cancer.
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9
Q

What is the classification for cancer?

A

Types of cells

  • Carcinomas (Epidermal) −Most common
  • Sarcomas (Mesenchymal)
  • Leukaemias (Haematopoietic cells of the bone marrow)
  • Lymphomas (Lymphoid tissue e.g. lymph nodes / spleen)

Differentiation

  • Well-differentiated
  • Poorly-differentiated
  • Anaplastic (aggressive)

Extent

  • Benign (non-invasive)
  • Malignant (invasive)
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10
Q

What are factors for metastasis?

A
  • Tumour growth and vascularisation.
  • Separation from other cells (through changes in adhesion proteins).
  • Cleavage of basement membrane and extracellular matrix.
  • Entry into blood or lymphatic vessels (increased enzyme activity e.g. metalloproteinases, serine proteases and cysteine proteases).
  • Spread through the bloodstream.
  • Trapping in the capillaries of a distant organ (e.g. lungs, liver).
  • Penetration and growth in the distant organ.
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11
Q

Why do biochemical changes occur in cancer?

A
  • Physical effects of the tumour (primary or secondary)
  • Metabolic activity of the tumour
  • Substances produced by the tumour
  • Systemic response to tissue damage (non-specific)
  • Chemotherapy
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12
Q

What are contributing factors for renal dysfunction?

A
  • Fluid losses (vomiting, diarrhoea, diuretics)
  • Hypercalcaemia (humoral or local mechanisms)
  • Hyperuricaemia (tumour destruction)
  • Protein deposition (Bence Jones protein)
  • Glomerular or tubular damage (chemotherapy is nephrotoxic)
  • Urinary tract obstruction (tumour growth)
  • Tumour lysis syndrome
  • Immuno-mediated renal disease: Nephrotic syndrome, glomerulonephritis, minimal
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13
Q

What are contributory factors for Hyponatraemia?

A

Sodium Losses

  • Fluid losses
  • Adrenal destruction
  • Tumour ADH secretion (uncontrolled)

Water retention

  • Tumour ADH secretion (uncontrolled). SIADH commonly in small lung cellc nacer
  • Chemotherapy

Pseudohyponatreamia

  • Hyperproteinaemia (myeloma)
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14
Q

What is SIADH?

A

Syndrome of Inappropriate Antidiuresis. Can be caused by carcinomas (e.g. lung, oropharynx, GI tract, genitourinary tract), lymphomas and sarcomas)

Diagnosis of exclusion

  • Hypo-osmolar Hyponatreamia
  • Clinical euvolaemia (No clinical signs of hypovolaemia (e.g. postural hypotension, tachycardia, dry mucous membranes, etc, No clinical signs of hypervolaemia (e.g. oedema / ascites)
  • Urine osmolality >100 mOsm/kg (inappropriately high for serum osmolality)
  • Urine sodium > 30 mmol/L (i.e. increased urinary sodium excretion)
  • Exclude other causes of euvolaemic hypo-osmolality: Renal dysfunction, Adrenal insufficiency, Thyroid dysfunction, Recent diuretic use
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15
Q

How is hyponatraemia related SIADH treated?

A

Treat for Hyponatraemia

  • Fluid restriction
  • Demeclocycline (blocks ADH action in renal tubules thereby allowing water excretion). Caution: May cause renal impairment.
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16
Q

What are physical effects of cancers?

A

Obstruction

  • Bile duct (obstructive jaundice): ↑ Bilirubin, ↑ ALP, ↑ GGT e.g. carcinoma of the head of the pancreas
  • Bowel: Intestinal obstruction and fluid/electrolyte disturbance
  • Urethra / ureters / bladder neck: Renal failure

Tissue damage

  • Normal tissue destruction releases enzymes: ↑ LDH, ↑ AST (minimal)
  • Hypopituitarism (primary pituitary or secondary deposit from breast/lung)
  • Diabetes insipidus
  • Hypoadrenalism (bilateral, secondary from breast or lung cancer)

Bleeding or exudation

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17
Q

What are clinical features of liver involvement in cancers?

A

Frequent site of secondary tumours (GI tract via portal system)

Clinical features:

  • Pain and liver enlargement.
  • Jaundice (extensive liver involvement).
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18
Q

What are Biochemical features of Liver related cancers?

A

•Biochemical features:

  • None
  • Mild to moderate increase in transaminases (ALT / AST)
  • Cholestasis: ↑ ALP, ↑ GGT, normal or slightly ↑ bilirubin * . Caused mostly by secondary tumour (infiltration or focal lesions causing local obstruction to bile flow)

Note: Chemotherapy causes liver damage and/or cholestasis.

Note: Placental-like ALP secreted by certain tumours e.g. lung, seminoma of testis and gynaecological malignancy. Other ALP variants in cancer e.g. Ragan isoenzyme.

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19
Q

What is the calcium/bone involvement in cancer?

A
  • Common site of metastasis (spine, ribs, pelvis). Can also be Breast, prostate, lung, kidney, thyroid, GI tract cancers and bone destruction (pain, pathological fractures)
  • Osteoclast activation by tumour or cytokines (IL-6, IL-1, TNFα)
  • Local production of PTHrP (parathyroid hormone-related protein) - Breast cancer secondaries
  • ALP: ↑ ALP (bone loss promotes osteoblastic response) e.g. breast and prostate cancer. Normal (in the absence of fractures): Lytic lesions e.g. myeloma. Bone-specific ALP may be increased when total ALP is normal
  • Hypercalcaemia: Osteolytic lesions
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20
Q

What is the action of osteoclast inhibitors?

A
  • Osteoclast inhibitors (e.g. bisphosphonates) decrease bone destruction, relieve pain and reduce fracture risk.
  • Treatment of symptomatic bone secondaries with radiotherapy may relieve pain.
21
Q

What is Hypercalcaemia of malignancy?

A

Increased calcium resorption from bone and increased renal reabsorption

Increased osteoclastic bone resorption

  • Humoral hypercalcaemia of malignancy e.g. squamous carcinomas (respiratory tract), breast, renal, ovarian and bladder cancer.
  • Local osteolytic hypercalcaemia: Tumour metastasis in bone promote local bone resorption via increased osteoclast activity e.g. myeloma (TNFβ, IL-1, IL-6)

•Symptoms: Bones, moans, stones, and abdominal groans. Polyuria and polydipsia. Dehydration / renal dysfunction.

22
Q

What is the biochemistry of Hypercalcaemia related malignancy?

A
  • ↑ Ca
  • ↓ Phosphate (may be masked by renal failure)
  • ↑ ALP (bone lesions)
  • ↓ K (common)
  • ↓ PTH
23
Q

What is the treatment for hypercalcaemia of malignancy?

A

Treatment:

  • Rehydration
  • Tumour removal
  • Reducing bone resorption (e.g. bisphosphonates)
  • Steroids (myeloma and haematological
24
Q

What is the causes of exudation and the biochemistry of the exudate?

A
  • Malignancy important cause of exudation (leaky capillaries).
  • Ascites occur in peritoneal carcinomatosis, HCC, hepatic metastasis, pseudomyxoma peritonei, mesothelioma, breast / large bowel / bronchial / stomach / pancreatic / ovarian / endometrial cancers.
25
Q

What is the cause of anaemia of malignancy?

A
  • Iron deficiency anaemia (chronic blood loss)
  • Anaemia of chronic disease - defective utilisation or transfer of iron
  • Malignant infiltration of bone marrow
  • Auto-immune haemolytic anaemia (e.g. B cell lymphoroliferative disorders). Often unresponsive to corticosteroids.
  • Microangiopathic haemolytic anaemias (e.g. carcinomas)
  • Red cell aplasia (thymomas, adrenocarcinomas, squamous cell carconomas, etc). ? T-cell mediated.
  • Fatigue (inflammatory and cytokine contribution also)
26
Q

What are features of bleeding in malignancy?

A

Early manifestation of GI or urinary tract cancer

  • May present with iron deficiency anaemia
  • Detection of blood in urine or faeces. Normally lose 1.5 mL of blood in GI tract each day (2 mg Hb / g faeces)
  • Heamoglobin progressively degraded.
  • Destruction of globin and modification of haem to haem-derived porphyrins.
  • Cancers bleed intermittently (multiple samples)
  • Sample from surface of stool (more likely to find blood)
27
Q

What are the tests used in the national bowel screening test?

A

Screening every two years men and women aged 60 to 74. One-off test (bowel scope screening) at 55 in some areas

Guiac-based faecal occult blood test (gFOBT):

  • Relies on a chemical reaction to produce the colour change.
  • Medication restrictions (e.g. NSAIDs such as aspirin, naproxen, and ibuprofen).
  • Dietary restrictions.

Immunochemical FOB test (iFOBT, FIT):

  • Uses antibodies to detect only human blood from the lower digestive tract (colon).
  • +No dietary, drug, or dental procedure restrictions.
  • -Avoid collecting samples during a menstrual period.
28
Q

What are biochemical markers for increase cellular activity and growth?

A

↑ Urate (nucleic acid breakdown)

  • Clinical gout rare. Renal failure from renal tubular precipitation.
  • Nausea, vomiting, lethargy, loin pain, haematuria, and dysuria.

↑ LDH

  • Tissue destruction (mild – moderate increases)
  • Lymphoma , leukaemia, ovarian and testicular cancer (5-10 x ULR)
  • Commonly non-specific isoenzyme profile
  • LDH is also a tumour product e.g. lung, cancer and stomach cancer

Lactic acidosis (high rate of glycolysis, pyruvate to lactate)

  • More frequent in metastatic disease

Pseudohyperkalaemia

  • Leukaemia with high white blood cell count (>100 000 x 109/L)
  • WBC destruction during venepuncture and centrifugation releases K
  • Lithium heparin sample for slow spin analysis or blood gases

Most common in leukaemias, lymphomas and small cell cancer of lung

29
Q

What are the areas of carbohydrate metabolism that cause metabolic changes?

A

Carbohydrate metabolism:

  • Hyperglycaemia
  • Hypoglycaemia (e.g. insulinoma)
  • Lactic acidosis (metastatic disease, decreased utilisation of lactate in liver)
  • Increased glucose turnover (TNFα, IL-1)
  • Abnormal glucose tolerance (insulin resistance)
  • Increased glucose transport into tumour cells (membrane-bound glucose transporter)
30
Q

What are tissue responses to injury?

A
  • Some tumours utilise lipids (rather than glucose) as energy source which is fatty acid mobilisation
  • ↓ Cholesterol (most common lipid abnormality)
  • Hypercholesterolaemia that normalises after therapy (e.g. HCC)
  • Hypertriglyceridaemia in some cancers e.g. myeloma, carcinoma of colon, hepatocellular carcinoma (HCC)
  • Abnormal lipid composition in malignant cells (e.g. cholesterol /phospholipids in cell membrane) and unusual lipid synthesis (e.g. 2-methyloleate in hepatomas)
  • ? Cytokine mediated (e.g. TNFα, INFγ, IL-1, IL-6)
  • Moderate ↑ in cholesterol (cis-platin therapy for germ cell tumours)
    *
31
Q

What are tissues responses to injury in regards to acute phase proteins?

A
  • Cancer-induced tissue damage invokes acute-phase response - Cytokines (IL-6, TNFα, IL-1)

Acute phase proteins

  • Positive: Alpha-1-antitrypsin, Haptoglobin, Caeruloplasmin, Fibrinogen, C3, CRP, Ferritin (very high in some lung and kidney cancers)
  • Negative: Albumin, Transferrin
32
Q

What are tissue responses to injury in regards to trace metals?

A

Increased

  • Copper (↑ caeroloplasmin)

Decreased

  • Zinc (↓albumin, ↑ excretion, metalloproteinases)
  • Iron (↓ transferrin and ↑ ferritin in APR). Iron deposited in reticuloendothelial organs.
  • Selenium
33
Q

What are features of Cachexia?

A
  • Weight loss - Some contribution from cancer treatments
  • Anorexia: loss of appetite, premature satiety, pain/difficulty feeding
  • Anaemia
  • Pyrexia (infection or tumour products)
  • Increased: Glycolysis (Lactate production by tumours. Converted to glucose in liver / kidneys. Consumes energy.), Lipolysis (fat breakdown, fatty acid oxidation), Protein catabolism
  • Insulin resistance
  • Hypoalbuminaemia
  • Oedema
34
Q

What are causes Paraneoplastic Syndrome?

A
  • Hypercalcaemia (see previous notes) **
  • SAIDH (see previous notes) **
  • Cushing’s Syndrome
35
Q

Why does hypoglycaemia occur in malignancy?

A
  • Large mesodermal tumours and carcinomas of liver / adrenal coretex. Mesenchymal tumours.
  • Unregulated overproduction of insulin-like growth factor II (IGF-II) - Much higher concentration than insulin so hypoglycaemic potential
  • IGF-II bound to binding-proteins (IGFBP), predominantly IGFBP-3
  • Binding to IGFBP-3 and an acid-labile sub-unit (ALS) forms a large complex that cannot cross the capillary endothelial barrier
  • Tumour-induced hypoglycaemia: ↓ IGF-1 concentration, N or ↑ IGF-II concentration, ↓ IGF-1/IGF-II ratio, ↓ IGFBP-3 concentrations, Attenuated GH response to stimuli (GH controls IGFs, IGFBP-3 and ALS synthesis in the liver)
  • Antibodies to the insulin receptor may also have a role (bind and activate the receptor)
  • Biochemical features: ↓ Insulin and C-peptide in presence of hypoglycaemia
  • ?? IGF-I, IGF-II and IGFBP-3 measurement

Treatment: Growth hormone (symptom relief), prednisolone (supress tumour IGF-II production).

36
Q

What are syndromes of malignancy?

A

Gynaecomastia

  • Tumour production of hCG (e.g. hydatidiform mole, chriocarcinoma, germ cell tumours)
  • hCG has structural homology with LH and TSH → cross-receptor stimulation
  • LH stimulated oestrogen production → gynaecomastia
  • TSH receptor stimulation → thyrotoxicosis

Tumour-induced osteomalacia (rare, mesenchymal tumours)

  • Muscle weakness and bone pain
  • Biochemical: ↓ ↓ Phosphate, N Calcium, ↓ 1,25 dihydroxyvitamin D. PTH may be raised.

Extra-pituitary acromegaly

Polycythaemia (EPO secretion in renal and hepatocellular carcinomas)

Hypertension (rare, renin secretion by tumours of the renal juxtamerular apparatus or neuroendocrine system). Resembles secondary hyperaldosteronism.

Neuroendocrine tumours of the GI tract

Hyperparaprotineaemia (hyperviscosity with IgM, Bence Jones protein induced renal dysfunction, immune paresis, pseudohyponatraemia, hypercalcaemia)

Thymoma (minimal input from Biochemistry)

Neuromyopathic syndromes (minimal input from Biochemistry)

Dermatological syndromes (minimal input from Biochemistry)

37
Q

What causes Gonadal dysfunction (failure) in patients?

A
  • Radiotherapy or chemotherapy: Target rapid cellular proliferation
  • Spermatogenesis and ovarian follicle formation affected ―? Direct effect on germ cells or indirect suppression of hypothalamic GnRH or pituitary gonadotrophin secretion
  • Sperm production may not recover after cessation of treatment
  • Temporary or permanent cessation of menstruation (↑LH, ↑ FSH, ↓ E2) - Radiation therapy, Risk increases with age
  • To protect ovarian function, ? GnRH analogues to suppress oocyte maturation via the hypothalamic pituitary axis and make germinal epithelium quiescent
  • Sperm banking / embryo storage.
  • Radiotherapy can decrease size and change musculature and vasculature of uterus.
38
Q

What are causes of Electrolyte disturbances?

A

Drug-induced nausea and vomiting (e.g. cis-platin and mechlorethamine).

  • Compounded by hypercalcaemia and hyponatraemia
  • Reduced by anti-emetics and steroids

Chemotheropeutic agents commonly toxic to kidneys (especially tubular epithelium)

  • Cis-platin causes tubular dysfunction and nephrotoxicity at high doses

Acute oliguric renal failure (cisplatin, carboplatin, ifosfamide, methotrexate, mithramycin)

Glomerular damage (renal failure or proteinuria) e.g. streptozotocin or gallium nitrate

Renal magnesium wasting (cis-platin, nephrotoxic, proximal tubular damage).

  • May cause hypocalceamia.

Hypokalaemia (cis-platin, nephrotoxic).

  • Amphotericin for fungal infections (infections are more common, immunosuppressive effects of tumours & cytotoxic drugs)

Hypocalcaemia

  • Mild, asymptomatic hypocalcaemia in breast and prostate carcinomas with osteoblastic bone metastases.
  • Complication of bisphosphonates and Denosumab (particularly in the context of vitamin D deficiency or renal insufficiency)

Hyponatraemia (cyclophosphamide).

  • Impaired water excretion in distal tubles and collecting ducts; resembles SAIDH

Vascular damage with hypertension and haemolytic uraemic syndrome (mitomycin C).

  • Anaemia and raised LDH.

Folate deficiency (methotrexate, inhibits THF dihydroreductase).

39
Q

What causes hepatic dysfunction in malignancy?

A
  • Hepatic metabolism of many drugs. Susceptible to damage by chemotherapeutic agents and metabolites
  • Cellular damage usually mild and asymptomatic
  • Mild to moderate elevation in transaminases (ALT / AST)
  • Fatty changes and intra-hepatic cholestasis common (↑ ALP / GGT)
  • Drugs with greater hepatic involvement include: nitrosoureas, antimetabolites e.g. methotrexate, L-asparaginase, combination chemotherapy, high-dose chemotherapy preceding bone marrow transplant
40
Q

What is Tumour Lysis Syndrome?

A

Massive necrosis of tumour cells during treatment with cytotoxic drugs

  • Particularly in large, chemosensitive tumours (lymphomas / leukaemias)
  • Potentially life-threatening
  • Often during initial chemotherapy cycle
41
Q

What are symptoms of Hypercalcaemia of malignancy?

A

Symptoms:

  • Bones,
  • Moans
  • Stones
  • Abdominal groans
  • Polyuria and polydipsia
  • Dehydration / renal dysfunction.
42
Q

What is the fluid biochemistry of exudates?

A

High Total protein: > 30 – 35 g/L

Light’s criteria (if any present; high sensitivity, low specificity):

  • Fluid:serum protein > 0.5
  • Fluid:serum LDH > 0.6
  • Pleural fluid LDH > 2/3 URL for plasma LDH

Higher cholesterol than transudates (variable criteria, > 1.2 to 1.6 mmol/L)

43
Q

What are factors for metastasis?

A
  • Tumour growth and vascularisation.
  • Separation from other cells (through changes in adhesion proteins).
  • Cleavage of basement membrane and extracellular matrix.
  • Entry into blood or lymphatic vessels (increased enzyme activity e.g. metalloproteinases, serine proteases and cysteine proteases).
  • Spread through the bloodstream.
  • Trapping in the capillaries of a distant organ (e.g. lungs, liver).
  • Penetration and growth in the distant organ.
44
Q

What is the mechanism for Humoral hypercalcaemia of malignancy?

A

PTHrP is main mediator (larger peptide with N-terminal homology with PTH). Binds to PTH receptors in bone and renal tubule to mimic PTH and increase calcium.

  • PTHrP has an important role in embryo growth and development.
  • It also causes Bone resorption > bone formation.
  • The biochemical features show ↑Calcium, ↓Phosphate, suppressed PTH, ↓1,25-Vitamin D

Increased hydroxylation of 25-OH Vitamin D by lymphoma cells (increased intestinal calcium absorption)

PTH secretion by tumour (rare)

45
Q

What are tests for faecal blood?

A

Tests for faecal blood:

  • Immunochemical tests (intact human haemoglobin, colon or rectal bleeding).
  • Guaiac test (detect peroxidase activity of intact haem, upper and lower GI tract bleeding).
  • Detection of haem-derived porphyrins (upper and lower GI tract bleeding). Limitations: Not specific for human haemoglobin
46
Q

What causes false postives and negative in the Guiac-based faecal occult blood test (gFOBT)?

A

False positives:

  • Substances or conditions that cause bleeding e.g. dental procedure causing bleeding gums or drugs that cause GI bleeding (anticoagulants, aspirin, steroids, and large doses of iron preparations, etc.)
  • Other sources of haemoglobin (e.g. red meat within three days before testing)
  • Other substances that will react with the FOB test (eating fish, turnips, horseradish, or drugs e.g. colchicines and oxidising drugs).
  • Menstrual bleeding.

False negatives:

  • Large doses of vitamin C (prevents colour formation in reaction)
  • Failure to collect multiple samples (many conditions only produce blood sporadically/infrequently).
47
Q

What are biochemical fetures of Tumour Lysis Syndrome?

A
  • Hyperkalaemia
  • Hyperuricaemia
  • Hyperphosphateamia
  • Hypocalcaemia (precipitated by phosphate released from cells)
  • Tachyarrhythmias or sudden cardiac death
  • Increased LDH (cytoplasmic release)
  • Causes acute renal failure: anuria, acute tubular necrosis
48
Q

How can tumour lysis syndrome be prevented?

A
  • Maintenance of adequate hydration
  • Allopurinol (xanthine oxidase inhibitor; to inhibit uric acid synthesis)
  • Monitoring of fluids and electrolytes (with appropriate correction)
  • Urinary alkalinisation
  • Renal dialysis

MSC: Disease of major orgns (23 decks)

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