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Neoplasia Flashcards

1
Q

differentiate between the definitions tumour, neoplasm and oncology.

A
  • tumour : any clinically detectable lump or swelling.
  • neoplasm : abnormal growth of cells that persists after initial stimulus removed.
  • oncology : study of tumours and neoplasms.
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2
Q

what is the difference between a benign neoplasm and malignant neoplasm?

A
  • benign : gross and microscopic appearances that will remain localised, not spreading to other sites.
  • pushes outer margins, closely resembles parent tissue.
  • malignant : abnormal growth that persists after initial stimulus removed and invades surrounding tissue with potential to spread distally.
  • may have ulcerations and necrosis, poorly differentiated mostly.
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3
Q

define metastasis.

A
  • malignant neoplasm that has spread from its original site to new non-contagious site.
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4
Q

what is dysplasia?

what is anaplastic?

A
  • pre-neoplastic alteration in which cells show disordered tissue organisation, reversible, pleomorphism seen, large hyper-chromatic nuclei and high nuclear:cytoplasmic ratio.
  • cells with no resemblance to any tissue.
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5
Q

how is neoplasia graded? what is taken into account?

A
  • DIFFERENTIATION : higher grades indicate poor differentiation.
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6
Q

why do we get neoplasia?

A
  • carcinogenesis.
  • genetic damage.
  • accumulation of mutations.
  • mutations caused by initiators and proliferation caused by promoters.
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7
Q

give some examples of initiators.

A
  • chemicals : smoking, alcohol, diet and obesity.
  • infectious agents : HPV.
  • radiation.
  • inherited mutations.
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8
Q

which genes being affected increases risk of neoplasia?

A
  • growth promoting proto-oncogenes.
  • growth inhibiting tumour suppressor genes.
  • genes that regulate apoptosis.
  • genes involved in DNA repair.
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9
Q

what is the significance with proto-oncogene mutations?

A
  • participates in signalling pathways that drive proliferation.
  • ‘gain of function’ mutations and mutations in encode proteins called oncoproteins promote cell growth.
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10
Q

what are tumour suppressor genes?

A
  • stops cell proliferation, usually subject to ‘loss of function’ mutations.
  • both alleles damaged for transformation to occur.
    eg: TP53.
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11
Q

what about apoptosis regulating genes and DNA repair genes?

A
  • apoptosis ; less cell death and enhanced survival.
  • DNA repair : ‘loss of function’ mutation, impairs ability to recognise and repair non-lethal genetic damage, accumulation of mutations.
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12
Q

how would you generally name neoplasms?

A
  • benign -oma.
  • malignant : carcinoma if epithelial, sarcoma in stromal.
    CHECK SLIDEZ.
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13
Q

define invasion in terms of metastatic neoplasia.

A
  • breach of basement membrane with progressive infiltration and destruction of surrounding tissue.
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14
Q

describe the journey of metastases.

A
  • grow, invade at primary site.
  • enter transport system and lodge at secondary site.
  • grow at secondary site to from new tumour.
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15
Q

what are the 3 key events of carcinoma invasion?

A
  • adhesion : reduction in E-cadherin expression to more motile, changes in integrin expression.
  • stromal proteolysis : altered expression of enzymes, degrades basement membrane and stroma to allow invasion. surrounding tissue provide growth factors and proteases.
  • motility : changes to actin cytoskeleton.
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16
Q

how does it spread to distant sites?

A
  • blood vessels, lymphatics, body cavity fluids.
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17
Q

what is the significance of micrometaastases?

A
  • failed colonisation deposits wait for optimum conditions such as immunosuppression to proliferate and invade.
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18
Q

what determines site of secondary tumour?

A
  • regional damage of blood, lymph etc.
  • lymphatic metastases drain to lymph nodes.
  • breast cancer ipsilateral axillary lymph nodes.
  • blood-borne : next capillary bed.
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19
Q

common neoplasms that spread to bone can be detected on plain films. what are some examples.

A
  • breast, bronchus, kidney, thryroid, prostate.

- osteolytic lesions due to destruction of bone.

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20
Q

what is meant by personalities of neoplasms.

A
  • malignant more aggressive metastasises very early on.
  • small cell carcinoma of bronchus v.aggressive.
  • basal cell carcinoma on the other hand, almost never metastasises.
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21
Q

how does the hosts defence respond to neoplasia?

A
  • tumour antigens recognised by CD8+ cytotoxic cells.
  • immunocompromised increased risk.
  • however might be missed by CD8+ as loss of or reduced antigen presentation, expression of immuno-suppressions.
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22
Q

what are the local effects of neoplasms?

A
  • direct invasion and destruction of normal tissue.
  • ulceration leading to bleeds.
  • compression of structures.
  • blocking of tubes and orifices.
  • raised pressure due to tumour growth ( brain).
23
Q

what are some systemic effects of neoplasms?

A
  • increased tumour burden.
  • together with secretions like cytokines reduced apetite and weight loss (cachexia), malaise, immunosuppression, thrombosis.
  • hormone production.
24
Q

what is a paraneoplastic syndrome?

A
  • symptoms in cancer nearing individuals that cannot be explained by anatomic distribution of tumour or hormones from the tissue at tumour origin.
  • important because early sign of occult neoplasm, cause complications, mimic metastatic disease and confound treatment.
25
Q

what is the most common paraneoplastic syndrome?

A
  • hypercalcaemia.
  • osteolysis : induced by cancer due to primary bone lesions like myeloma or secondary metastases calcaemia humoral substances produced.

(miscellaneous : neuropathies, skin problems, fever, clubbing, myositis).

26
Q

Name some carcinogenic factors but differentiate between intrinsic and extrinsic factors.

A
  • intrinsic : hereditary, age, sex.

- extrinsic : chemicals, radiations, infection, behaviour like smoking, obesity.

27
Q

4/10 cancers can be prevented. what factors could be controlled to do this?

A
  • smoking.
  • maintain healthy weight.
  • balanced diet.
  • sun safety.
  • cut back on alcohol.
  • being active.
  • OBESITY.
28
Q

what cancers could smoking cuase?

A
  • mouth, pharynx, nose, larynx, oesophagus, liver, pancreas, stomach, bowel, cervix etc.
29
Q

what is the significance of chemical carcinogens and carcinogenesis?

A
  • 2-napthylamine found in industrial dyes and cigarettes affects risks depending on dose nd there is a delay between exposure and malignancy onset.
  • chemical carcinogenesis involved initiation and promotion, and 2-napthylamine is a complete carcinogen doing both.
30
Q

how might radiation act as a risk factor for neoplasia?

A
  • can damage DNA directly or indirectly by crashing into water molecules causing free radicals.
  • eg : UV responsible for 1/4 of skin neoplasms, radon gas, medical test radiation.
31
Q

how might infections play a role in neoplasia?

A
  • indirectly due to chronic inflammation inducing constant fibrosis and regeneration.
  • directly via HPV.
  • indirectly via Hep B & C.
  • reduced immunity via HIV.
32
Q

why is HPV so significant in neoplasia?

A
  • associated with cervical carcinoma.
  • it creates 2 proteins, E6 and E7. E6 inhibits P53 which prevents cell from apoptosis.
  • interferes with retinoblastoma protein which is an important cell cycle checkpoint!
  • combined they increase uncontrolled proliferation.
33
Q

how are proto-oncogenes, tumour suppressor genes, DNA repair genes, RAS gene and the retinoblastoma gene different?

A
  • tumour suppressor : ‘loss of function’ mutation.
  • proto-oncogenes : ‘gain of function’ leading to formation of oncogenes which make onco-proteins which increases cell proliferation.
  • retinoblastoma : G1/S cell cycle checkpoint differentiation controller.
  • RAS : human oncogene that the most commonly mutated. mutated in 15-20% of all malignant neoplasms.
  • DNA repair genes : caretaker genes that prevent accumulation of DNA damage. liked with inherited cancers.
34
Q

what can proto-oncogenes code for?

A
  • growth factors, growth factor receptors, transcription factors (controls rate of transcription), intracellular kinases.
35
Q

what is xeroderma pigmentosa?

A
  • autosomal recessive.
  • mutation in 7 genes that affect DNA nucleotide excision repair.
  • very sensitive to UV damage and develops skin cancer at young age.
36
Q

what is hereditary non-polyposis colon cancer (HNPCC) syndrome?

A
  • autosomal dominant associated with colon cancer.

- germ-line mutation that affects one of several DNA mismatch repair genes.

37
Q

what is the genetic link in familial breast carcinoma?

A
  • BRCA1/BRCA2 genes involved in repairing double strand DNA breaks.
  • found in sporadic malignant neoplasms.
38
Q

is chromosome aggregation normal?

A
  • this happening in mitosis is abnormal in malignant cells, this accounts for accelerated mutation rate known as genetic instability.
  • caretaker genes maintain the genetic stability.
39
Q

name some hallmarks of cancer.

A
  • self sufficient growth signals.
  • resistance to stop signals.
  • cell immortalisation, no limit to times of division.
  • sustained ability to induce angiogenesis.
  • resistance to apoptosis.
  • ability to invade and metastasise.
40
Q

what are the commonest types of cancer in adults and children?

A
  • in adult males prostate shows high incidence and in women breast cancer, then lung cancers and bowel cancers common in both.
  • children younger than 14, Leukaemia, CNS tumour and lymphomas are common.
41
Q

what are the leading causes of cancer related death?

A
  • pancreatic, lung, brain cancers have the lowest survival rates.
42
Q

what factors are important in predicting the outcome?

A
  • age, general health, tumour site, tumour type, differentiation, tumour stage.
43
Q

what staging system is used for solid tumours?

A
  • TNM staging system used worldwide for solid tumours.
  • T : size of primary tumour.
  • N: extent of regional lymph node involvement.
  • M : metastatic spread via blood.
  • Ann Arbor staging for lymphoma.
  • Dukes staging system for bowel cancer.
44
Q

what is the significance of the tumour stage?

A
  • a measure of overall burden of malignant neoplasm.
  • converted to a stage 1-4.
  • 1 : early localised disease.
  • 2 : advanced local disease.
  • 3 : regional metastasis.
  • 4 : advanced disease with distant metastasis.
    (contains levels within the stages too depending on tumour size, metastases state etc).
45
Q

what is the significance of grading in neoplasia?

A
  • grades describe the degree of differentiation of neoplasm.
  • G1 : well-differentiated.
  • G2 : moderately differentiated.
  • G3 : poorly differentiated.
  • G4 : undifferentiated or aplastic.
  • depending on grading at diagnosis prognosis varies.
46
Q

what are the principles of treatment for cancer?

A
  • surgery.
  • radiotherapy.
  • chemotherapy.
  • hormone therapy.
  • treatments that target specific molecular alterations.
  • immunotherapy.
47
Q

differentiate between adjuvant vs neoadjuvant treatment.

A
  • adjuvant treatment is given after surgical removal of primary tumour to eliminate subclinical disease, post curative treatment.
  • neoadjuvant is given prior to surgical excision to to reduce size of primary tumour, prior to curative.
48
Q

describe how radiation therapy works in battling cancer.

A
  • kills proliferating cells by triggering apoptosis via interfering with mitosis.
  • small doses given to kill rapidly dividing cells in G2, causing direct or free-radical induced DNA damage detected at checkpoints triggering apoptosis.
49
Q

describe how chemotherapy works in battling cancer.

A
  • antimetabolites mimic normal substrates involved in DNA replication.
  • alkylating and platinum based drugs (cisplatin) that cross link 2 DNA strands.
  • antibiotics to inhibit enzymes needed for DNA synthesis.
  • plant derived drugs that block spindle formation.

*hair loss, trouble breathing, nausea, weakened immunity, bruising, rashes, neuropathy side effects.

50
Q

describe how hormone therapy works in battling cancer.

A
  • selective oestrogen receptor modulators that bind to oestrogen receptors preventing binding at cancer cells.
  • used to treat hormone receptor positive breast cancer.
51
Q

how would targeting oncogenes help treat cancer?

A
  • helps create drugs that specifically target cancer cells.

eg : imatinib.

52
Q

describe how immunotherapy works in battling cancer.

A
  • target immune system to help fight cancer by recognising and attacking.
  • is burden overwhelming this won’t fully help.
53
Q

what is the significance of tumour markers?

A
  • various substances released by cancer cells into circulation can be measured.
  • sometimes used for diagnosis, to monitor tumour burden, as treatment assessments, recurrence assess.
    eg : prostate specific antigen in prostate carcinoma.
54
Q

what is the importance of cancer screening?

Give some examples of screening programmes available in UK.

A
  • meant for healthy people with no symptoms, as an attempt to detect cancers as early as possible.
  • as early diagnosis means high chance of cure.

Breast screening : 47-73 ages women, Cervical : 25-64 women, bowel screening : 60-74 men and women.

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