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HLTH3200 > Disorders of Cell Growth > Flashcards

Disorders of Cell Growth Flashcards

1
Q

What is a tumour

A
  • Swelling or mass
  • Two general types of tumours
  • Benign (non-cancerous)
  • Malignant (cancerous)
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2
Q

What is a neoplasm

A
  • An abnormal mass of tissue
  • Growth of which exceeds and is uncoordinated with that of normal tissues
  • Persists in same excessive manner after cessation of stimuli which evoked change
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3
Q

What is neoplasia and dysplasia

A

Neoplasia:
- Cancer, new growths of cells in the body
- Mutated proto-oncogenes / tumour suppressor genes
Dysplasia:
- Irreversible
- Replacement of one mature cell type with a less mature cell type
- Mutations in genome, epigenetic changes, principally in epithelia

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4
Q

What are the features of a benign tumour

A
  • Nomenclature (-oma)
  • Localised
  • Non-invasive, slow growth
  • Resemble tissue of origin
  • Encapsulated / circumscribed edge, intact surface
  • Exophytic growth
  • Homogenous cut surface
  • No metastases
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5
Q

What are the features of a malignant tumour

A
  • Nomenclature (-carcinoma or -sarcoma)
  • Non-localised
  • Invasive, rapid growth
  • Poor resemble of tissue of origin
  • Poorly defined and irregular border, ulcerated, vascular permeation
  • Endophytic growth
  • Heterogenous cut surface / necrosis
  • Metastases common
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6
Q

What are the common causes of cancer

A
  • Sporadic (non-familial) cancers caused by DNA damage and genomic instability
  • Oncogenic viruses carry genes that can lead to cancer (HPV / EBV)
  • Inheritance of one defective copy of a tumour suppressor gene / cancer susceptibility gene
  • Li-Fraumeni Syndrome - Mutant TP53
  • Hereditary Breast / Ovarian Cancer (HBOC) - Mutant BCRA1 / BRCA2
  • Lynch Syndrome - Abnormal DNA mismatch repair
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7
Q

What are some genetic mutations found in cancer

A
  • Gene Deletion / Inactivation: Loss-of-function, tumour suppressor genes (TP53)
  • Gene Amplification: Copy number changes, hyper-activity of proto-oncogenes, oncogenes (MYC, EGFR)
  • Protein Activating Mutation: Gain-of-function, BRAF V600E, IDH1 R132
  • Translocations: BCR-ABL
  • Epigenetic Alterations: Histone H3
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8
Q

What are proto-oncogenes

A
  • Encode proteins that normally control cell growth / proliferation
  • When mutated become oncogenes that cause self-sufficiency
  • Extracellular signalling, hormones, GFs, signal transduction and nuclear proteins
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9
Q

What are oncogenes

A
  • Jammed accelerator
  • Genes / proteins that activate normal cell proliferation
  • These genes are mutated in cancer resulting in uncontrolled proliferation
  • Gain-of-function mutation (dominant)
  • MYC, RAS, EGFR/ERBB1, HER2/ERBB2
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10
Q

What are tumour suppressor genes

A
  • Defective brakes
  • Genes / proteins that normally prevent cell proliferation are mutated in cancer resulting in uncontrolled proliferation
  • Loss of function mutation (recessive) or loss of heterozygosity
  • TP53, RB, CDKN2A (Ink4a / Arf), CDKN2B (Ink4b)
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11
Q

What is the p53 tumour suppressor gene (loss of function mutation)

A 
p53
- Tetramer DNA complex containing TFs (can bind DNA), - When mutated multiple cellular processes are disrupted
Activated By:
- Lack of nucleotides
- UV / ionising radiation
- Oncogene signalling
- Hypoxia
- Blockage of transcription
Effect:
- Cell cycle arrest and senescence or return to proliferation
- DNA repair
- Block of angiogenesis 
- Apoptosis
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12
Q

What are gain of function mutations

A
  • Results in constitutive kinase activity, increased stimulation
  • Cause of melanoma (BRAF V600E), lung cancer, colorectal cancer, thyroid carcinoma, paediatric low grade glioma and craniopharyngioma
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13
Q

List the 6 hallmarks of cancer

A
  • Sustained proliferative signalling
  • Resistance to anti-growth signals
  • Immortality
  • Resistance to apoptosis
  • Sustained angiogenesis
  • Invasion / metastasis
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14
Q

What is sustained proliferative signalling (1)

A
  • Constitutively activated growth signalling

- Often driven by oncogenes

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15
Q

What is resistance to anti-growth signals (2)

A
  • Unregulated cell cycle progression (mutated CDKs, kinases and cyclins)
  • Inactivated cell cycle checkpoints (inactivation of tumour suppressors)
  • Leads to cells with aneuploidy, DNA damage and incomplete DNA replication
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16
Q

What is immortality (3)

A
  • No limit to cell divisions
  • Telomere length extension by telomerase, infinite replicative ability
  • Inactivated cell death pathways
  • Hayflick Limit: Number of times cell can divide before telomeres shorten and inhibit duplication
17
Q

What is resistance to apoptosis (4)

A
  • Resistance to programmed cell death
  • Activation of survival signalling pathways (AKT)
  • BCL2 over-expression in cancer prevents induction of apoptosis
18
Q

What is sustained angiogenesis (5)

A
  • Formation of blood vessels
  • Activated vascular endothelial GF signalling
  • Tumour: Transformed or neoplastic cells, proliferating
  • Stroma: Normal cells (normal DNA), connective tissue, BV and host immune/inflammatory cells, provides support to enable tumour growth
19
Q

What is invasion / metastasis (6)

A
  • Loss of cell-to-cell interactions
  • Loss of contact inhibition
  • Loss of anchorage dependence
  • Cells in culture and in vivo exhibit contact-inhibition
  • Cancer cells lack contact inhibition feedback mechanisms, clumps or foci develop
20
Q

Describe how molecular understanding of cancer can be used in research

A

Discovery:
- Elucidation of oncogenic mechanisms
- Identification of therapeutic targets
- Identification of cancer biomarkers
Validation:
- Validation of candidate therapeutic targets and biomarker signatures
Clinical Utility:
- Classification of patients based on disease prognosis
- Stratification of patients based on predicted therapeutic response

21
Q

What is multistep carcinogenesis

A
  • Carcinogenesis is a multistep process resulting from accumulation of multiple genetic alterations
  • Collectively give rise to transformed phenotype and associated hallmarks
  • Most cancers have at least 6-9 different mutations
22
Q

What are common translocations / genetic changes in cancer

A

Translocations:

  • Burkitt’s Lymphoma: Affects antibody rearrangement (T cells)
  • Acute Promyelocytic Leukaemia (APL): Stalls myeloid differentiation
  • Acute Lymphoblastic Leukaemia (ALL): Constitutive ABL kinase activity
  • Ewing’s Sarcoma: Inhibits differentiation, solid tumour
  • Deletions: Loss of tumour suppressor genes
  • microRNAs (miRNA): Increase expression of oncogenes, decrease expression of tumour suppressor genes
  • Epigenetic Changes: Post-translational modification of histones, abnormal DNA methylation
23
Q

What is grading and staging of cancers

A
  • Staging: Progression or spread through the body

- Grading: Cell differentiation and rate of cell growth

24
Q

What are common characteristics of cancer

A
  • Genetic origin – DNA damage / change and epigenetic changes (histone modifications)
  • Accumulation of specific mutations promoting cancer
  • Cell division without growth control
  • Parasitic in nature
  • Require endocrine support of host
  • Dependent on host blood supply and nutrition
  • Heritable changes which get passed on to daughter cells
  • Usually clonal, derived from one single cell
25
Q

What are the 4 fundamental features to distinguish and characterise benign vs malignant neoplasms

A
  • Differentiation and anaplasia
  • Rate of growth
  • Local invasion
  • Metastasis
26
Q

Describe differentiation and anaplasia in benign vs malignant

A
  • Benign: In parenchyma fairly normal, well differentiated cells, still fulfil tissue function, mitosis rare but normal
  • Malignant: In parenchyma differentiated to completely undifferentiated cells with loss of tissue function, nuclei hyper chromatic and large, several nuclei possible, anaplasia
27
Q

Describe rate of growth in benign vs malignant

A
  • Benign: Slow growth (months to years) and mitosis is rare but normal
  • Malignant: Fast growth, atypical, numerous mitosis, growth rate usually inversely proportional to level of differentiation
28
Q

Describe local invasion in benign vs malignant

A
  • Benign: Remains localised at site of origin, most are encapsulated but not all
  • Malignant: Progressive growth, infiltration, invasion, destruction and penetration of surrounding tissue, no development of well defined capsules
29
Q

What is metastasis

A
  • Metastasis: Spreading of malignant neoplasms
  • Metastases: Secondary implants, originating from a primary lesion, of a different cellular origin (different morphology, colour, cell to cell signalling)
30
Q

Describe metastasis in benign vs malignant

A
  • Benign: Never
  • Malignant: Pathways of dissemination, seeding within body cavities, lymphatic / hematogenious to liver, lungs, veins and arteries (less)
31
Q

Describe the process of metastasis

A
  • Detachment at tumour site invasion of surrounding connective tissues
  • Intravasation into blood / lymph / body cavities, evasion of host defence (immune escape)
  • Extravasation from blood vessel into secondary sites
  • Proliferation and angioneogenesis (VEGF)

HLTH3200 (14 decks)

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