Tumour Progression, Invasion and Metastasis Flashcards

1
Q

Characteristics of Malignant Tumours:
What occurs during Progression?
→ How does this differ from Benign tumours?

What occurs during Invasion?

What occurs during Metastasis?

A
  • Unlimited growth as long as an adequate blood supply is available
    → Benign tumours have limited growth
  • Migration of tumour cells into surrounding tissues, where they’re free to disseminate via the blood or lymph
  • Spread of tumour cells from primary site to form a Secondary tumour
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2
Q

TUMOUR PROGRESSION:
What are the Molecular changes occurring here?

What is this process associated with?
→ What properties can vary between cells in a tumour?

A
  • • Acquisition of specific mutations - by Carcinogens
    • Clonal expansion - by Tumour promotors
    • Genomic Instability
    • Epigenetic changes
  • Cellular Heterogeneity - Selective pressures will determine the cell types in a tumour
    → Antigenicity, Growth rate, Response to hormones and cytotoxic drugs, Capacity for invasion and metastasis
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3
Q

TUMOUR INVASION:
What changes occur in the tumour during this stage?
——————

Neovascularisation:
What promotes Angiogenesis?

What are the main factors involved here?
→ How are they stored?
→ What are they released by?

Epithelial to Mesenchymal Transition (EMC):
What is this?

What is LOST during this?

Regulation of Proteolytic Activity:
What do most tissues have to regulate Proteinases?
→ How does this relate to Tumours?

A
  • • Increased mechanical pressure due to rapid proliferation
    • Hypoxia, leading to neovascularisation
    • Epithelial to Mesenchymal Transition (EMC)
    • Increased production of degrading enzymes by tumour and stromal cells
    ——————
  • HYPOXIA
  • VEGF, FGF2, TGF-β, HGF/SF
    → Bound to components of the ECM
    → Matrix Metalloproteinases (MMPs)
  • Angiogenesis Inhibitors e.g. Anti-VEGF like Bevacizumab, VEGF Receptor Inhibitors like Sorafenib
  • Remodelling of cell-cell and cell-ECM interactions, leading to the detachment of Epithelial cells from each other and its basement membrane
  • Epithelial shape, Cell polarity, Cytokeratin intermediate filament, and Epithelial junction protein (E-CADHERIN)
  • Fibroblast-like shape, N-CADHERIN, Invasiveness, Vimentin intermediate filament, Mesenchymal gene expression, and Protease secretion
  • TIMP (Tissue Inhibitor of Metalloproteinases), which inhibit Proteinases
    → Some tumours have ↓TIMP
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4
Q

METASTASIS:
Why is it a very inefficient process?

What is the Seed and Soil Hypothesis?

Compared to Tumour Invasion, what does Colonisation require to become a Secondary tumour?

A
  • Tumour cells can easily extravasate most of the time, but find it difficult to become a Secondary tumour (Micro/Macrometastasis)
  • There are Specific Adhesions between Tumour and Endothelial cells in the target organ, creating a favourable environment for colonisation
  • Mesenchymal-Epithelial Transition (MET)
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5
Q

Liquid Biopsies:
What are they?

If a blood biopsy is taken, what can be detected?

What are CTCs? What does their presence in blood indicate?

A
  • Sampling and analysis of Non-solid biological tissue (e.g. blood) for detection of molecular biomarkers
  • Circulating Tumour Cells (CTCs), Cell free DNA etc.
  • Tumour cells travelling in the blood - Indicates tumour growth and spread
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