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Introduction to Cell Proliferation and Cell Death (1.18.2.11) - Coggle…
Introduction to Cell Proliferation
and Cell Death (1.18.2.11)
What is different about cancer cells?
Cancer cells divide continuously and uncontrollably
They behave differently to normal cells
They have an altered metabolism
They will spread if the environmental and nutritional conditions of the tumour deteriorate
Definitions:
Neoplasia = new, uncontrolled growth of cells
Tumour = a swelling of part of the body, without inflammation, caused by abnormal growth of cells
Mutagenesis = the production of genetic mutations
Oncogenesis = The development of a tumour
Angiogenesis = the development of new blood vessels
Apoptosis = Programmed cell death
Necrosis = Lethal cell injury or accidental death
What are the two types of tumours?
Benign
Low mitotic rate
No metastasis
Good demarcation from surrounding tissue
Well differentiated mass
Minimal nuclear or cell pleomorphism (variation in size and shape)
Malignant
High mitotic rate
Frequent metastasis
Invading surrounding tissues blood and lymphatic vessels
Disorganisation of tissue
Increased nuclear or cell pleomorphism and multiple nuclei
Leukemia blood smear labelling:
Monocyte
Lymphocyte
Erythrocyte
Cell death: Necrosis and Apoptosis
Necrosis = Lethal cell injury or accidental death in a living organism.
The necrotic cells die in an organism with failure of membrane integrity
This is a pathological process
The cell membrane becomes permeable following cell injury
The dead cells induce an inflammatory reaction
Causes:
Injury
Cells may be injured
due to mechanical damage, Lack of nutrients or oxygen, or exposure to chemicals
Infection
Cancer
Infarction
Toxins
Inflammation
Necrosis is accompanied by the release of lysosomal enzymes which digest cell components. Nectrotic cells release harmful chemicals that damage other cells
Necrotic cells undergo changes such as: Swelling as plasma membrane passage control is disrupted, their internal organelles swell, and cell contents leak out, leading to inflammation of surrounding tissues
Hepatic necrosis due to bacterial infection = hepatits.
Necrotic hepatocytes can exhibit nuclear pyknosis (condensation and reduction in the size of a cell nucleus) and karyorrhexis (nuclear fragmentation with pieces scattering in the cytoplasm)
Apoptosis
This is a physiological process that results in the deletion of individual cells in physiological growth control
Tightly regulated
Selective process for deletion of superfluous cells, infected cells, transformed cells
Involved in: embryo development, tissue turnover, pathological stages as reduced apoptosis= neoplasia, and increased apoptosis= atrophy
Stages of apoptosis
Early: Decreased cell size, altered cell membrane function, Large DNA strand breaks, Increase in cellular calcium levels
Intermediate: DNA cleavage into 180-200bp fragments, further decrease in cell size, decreased pH
Late: Loss of membrane function, formation of apoptotic bodies, phagocytosis (without inflammation)
Example of apoptosis = development
Essential in development as tissues must be removed during growth.
Limb development - interdigital mesoderm between fingers must be removed, if it isn't = webbed phalanges
Ossification e.g death of chondrocytes
Nervous system e.g death of neurones
Intrinsic vs Extrinsic signals for apoptosis
Intrinsic: Act inside the cell, requires p53 to recognise damaged cell. Mitochondria is needed.
This can be stress induced.
Extrinsic: acts inside the cell initially (death surface receptor mediated) but leads to irreversible chain of events inside cell.
Differences between apoptosis and necrosis
Necrosis
Always pathalogical
Groups of cells
Cell swelling
Membrane integrity lost
No role for mitochondria
Leakage of lysosomal enzymes
Loss of nuclei
Dead cells ingested by neutrophils and macrophages
No caspase protease activation
Apoptosis
Physiological or pathological
Single cell
Cell shrinkage
Membrane integrity maintained
Role for mitochondria and cytochrome C
No leakage of lysosomal enzymes
Characteristic nuclear changes
Dead cells ingested by neighboring cells
Activation of specific caspase proteases
Formation of apoptotic bodies
