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302: Scientific Bases of Medicine > Oncology and Pathology > Flashcards

Oncology and Pathology Flashcards

1
Q

Which Tumours like to travel to the bone?

A

lung
breast
prostate
ovary

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2
Q

Which tumors metastasis to everywhere in the body?

A

melanoma
kidney
thyroid

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3
Q

Which bones do tumour mainly metastasis to?

A

Spine!!!,
Pelvis,
Femur,
Humerus,
Ribs,
Skull

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4
Q

What are the names of cancers based on their tissue origin?

Epithelial cells →

Mesoderm cells →

Glandular cells →

A

Epithelial cells → Carcinomas

Mesoderm cells → Sarcomas

Glandular cells → Adenocarcinomas

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5
Q

What are the exposures/ factors that led to cancer

A
  • Radiation
  • Ageing
  • Pollution
  • Environment
  • Diseases (COPD)
  • Genetics
  • Occupation
  • Asbestos
  • Tobacco
    • second hand smoke
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6
Q

What are Hallmarks of Cancer?

A
  • Avoid immune destruction
  • Unlimited replicative potential
  • Tumour promoting inflammation
  • Invasion and metastasis
  • Angiogenesis
  • Genome instability and mutation enabling
  • Evasion of cell death - limited response to apoptotic signals
  • Reprogramming energy metabolism
  • Growth signal autonomy - do not need GF signaling to divide
  • Evasion of growth inhibitory signals
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7
Q

Explain the normal activation of transmembrane Tyrosine Kinases receptors?

A
  • they are involved in mediating cell-to-cell communication and controlling various biological functions
  • they ae activated by receptor-specific ligands - dimerization’s results in down stream transmembrane conformational changes placing the tyrosine kinase in an ‘active’ confirmation
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8
Q

What are the two ways Tyrosine Kinase Receptors can be dysregulated?

A
  • ligand-_dependent_ firing mutating to ligand-_independent_ firing
  • receptor remains the same however has autocrine signaling/ activation
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9
Q

What Tyrosine Kinase Growth Factor receptors are altered in human tumours?

A
  • EGF-R/ErbB1
    • overexpression → non-small cell lung cancer, breast, head and neck, stomach, colorectal, esophageal, prostate, bladder, renal, pancreatic and ovarian carcinomas, glioblastomas
    • truncation of ectodomain → glioblastoma, lung and breast carcinoma
  • ErbB2/HER2/Neu
    • overexpression → 30% of breast adenocarcinomas
  • FGF-R3
    • overexpression; amino acid substitutions→ multiple myeloma, bladder and cervical carcinomas
  • Flt-3
    • tandem duplication → acute myelogenous leukemia
  • Kit
    • amino acid substitution → gastrointestinal stromal tumour
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10
Q

Give examples of receptors making autocrine growth factors and what Human tumours they present in?

A
  • Met: HGF ligand → miscellaneous endocrinal tumours, invasive breast and lung cancers, osteosarcoma
  • IGF-1R: IGF-2 ligand → colorectal
  • EGF-R: TGF-∝ ligand → squamous cell lung, breast and prostate adenocarcinoma, pancreatic, mesothelioma
  • VEGF-R (Flt-1): VEGF-A ligand → neuroblastoma, prostate cancer, Kaposi’s sarcoma
  • ErbB2 (HER2 or NEU)/ErbB3: NRG ligand → Ovarian carcinoma
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11
Q

What are the therapeutic options for the following hallmarks of cancer?

A
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12
Q

what is the treatment strategies in cancers that have an EGFR mutation?

A
  • EGFR- Tyrosine kinase inhibitors - Afatinib
  • Anti-EGFR antibody inhibitors
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13
Q

What is a common mechanism of resistance to Tyrosine Kinase Inhibitors?

A

T790M mutations in the gene that codes for EGFR (epidermal growth factor receptor). This increases the affinity for ATP

  • 60% of progressive disease is due to the T790M mutation
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14
Q

How do cancers occur?

A
  • Oncogenesis is a multistage process, cells accumulate damage in several important genes related to mitosis/ cell differentiation
  • most mutations acquired in our somatic cells
  • some cancers inherited due to mutations in the germline
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15
Q

Give an example of an inherited mutation in an Oncogene

  • what does it cause?
A

RET oncogene (MEN2A - Multiple endocrine neoplasia type 2)

  • Parathyroid cancer
  • Pheochromocytoma
  • Medullary thyroid cancer
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16
Q

Give an overview and epidemiological background of Multiple Endocrine Neoplasia type 2 (MEN2)

A
  • inherited autosomal dominant
  • occurs in 1:40,000
  • RET proto-oncogene codes for tyrosine kinase receptor
  • should be suspected when ≥ 2 endocrine tumour occur together
  • 95% of people with genetic variant will present with medullary thyroid cancer
    • Pheochromocytoma occurs in 50%
    • Hyperparathyroidism in 20-30% of those with the variant
17
Q

How would a person with MEN2A present clinically?

A
  • Medullary thyroid cancer
    • mass or lump in in neck, may be painful
    • Cushing syndrome
    • facial flushing​
  • Excess hormone production from
    • pheochromocytomas (adrenals)
      • High blood pressure
      • glucose intolerance
      • pallor and vasoconstriction ​
    • and/or adenomas in parathyroid glands
  • with symptoms of these diseases
    • bone pain due to metastasis
    • weight loss
    • severe diarrhea (due to calcitonin and hormones released)
18
Q

What is the management for Medullary thyroid cancer?

A
  • Total thyroidectomy and neck dissection
  • Thyroid hormone replacement
  • Tyrosine Kinase inhibitors in metastatic or unresectable cases
19
Q

What is the management in Phaeochromocytoma?

A
  • Medical treatment of blood pressure
  • unilateral adrenalectomy (must be removed before nay other surgery)
20
Q

What is the management of hyperparathyoidsm

A
  • resect affected gland
  • annual screening
21
Q

What screening tests are available for MEN2A?

A
  • MTC : annual calcitonin, check TFTs, annual neck/thorax imaging​
  • Phaeo: annual plasma metanephrines, BP, annual abdominal scan​
  • Primary hyperparathyroidism: annual calcium​
  • Genetic testing: can detect >95%s of variants in RET gene​
  • Children of affected individual have 50% chance of inheriting the gene variant​
  • 95% of MEN2A patients will have an affected parent
22
Q

Give an example of a Tumour suppressor genes cancer?

A
  • Retinoblastoma - inherited cases more likely to have bilateral disease at younger age compared to sporadic case of RB
23
Q

What is the aetology and epidemiology of retinoblastoma?

A
  • Majority of cases are related to variants in teh RB1 retinoblastoma gene
    • <1% may be due to N-myc amplification
  • 10% of children with Rb have a family history

Unilateral Rb cases: genetic variants in both copies of RB1 gene in retina (somatic variants)​ Variants present in the retinoblastoma tumour tissue & not usually in DNA in blood​

Of the 40% tumours that are bilateral: germline mutation in >95% cases

24
Q

What is the management of retinoblastoma?

A
  • Care led by tertiary service (Birmingham and London)​
  • Clinical genetic services​
  • Up to 50% new cases: enucleation (removal of the eye)​
    • less often if identify families who are gene carriers/at risk & have follow up surveillance​
  • Local treatment: laser therapy/cryotherapy​
  • Chemotherapy (systemic or locally)
25
Q

What is the aetiology and epidemiology of breast cancer?

A
  • Most common cancer in UK – affects 1 in 8 women (affects 1 in 870 men)​
  • Majority NOT due to inherited gene but..​5-10% of cases due in inherited altered gene​
    • BRCA1 and BRCA 2​
    • Autosomal dominant inheritance (one copy of gene with a variant, one without a variant)

​

  • Women with a variant in BRCA 1 or BRCA 2 genes – increased risk of breast and ovarian cancer​
  • Men with a variant (usually BRCA 2) increased risk of prostate and male breast cancer​
    • These women and men may be offered screening
26
Q

How does a inherited genetics effect ones predisposition to breast cancer?

A
  • Main genes BRCA 1 and BRCA 2​
  • Tumour suppressor genes – these regulate cell division, apoptosis and DNA repair​
  • If inherit a BRCA variant the individual will not definitely get cancer, but the chances will be increased significantly​
  • Woman BRCA 1 or BRCA 2: 80% chance of breast cancer before 80yo and lifetime risk of ovarian cancer 10 to 60%​
  • Men BRCA 1 variant: breast cancer risk not increased, ​
  • but with BRCA 2 variant: slightly higher than general population and 20-25% lifetime risk of prostate cancer
27
Q

What points are pertinent in a family history when screening for risk of breast cancer?

A
  • Several women who have breast and or ovarian cancer​
  • Breast cancer diagnosed at a younger age​
  • Young age and G3 triple negative (ER,PR,HER2) histology​
  • Woman with primary breast cancer more than once/ had early breast and ovarian cancer​
  • Male with breast cancer in a family with female relatives with breast cancer
28
Q

What is the chance of passing on a breast cancer gene variant to offspring

A

1 in 2 chance

50%

29
Q

What are the NICE guidelines on genetic testing?

A

offer genetic testing where >10% chance of carrying a gene variant

Ideally, test an affected family member first: predictive genetic testing​

Still possible if no affected family members alive but strong family history

302: Scientific Bases of Medicine (9 decks)

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