overview Flashcards
what is cancer
- uncontrolled growth
- in most solid tumours between 25-65% of the tumour is made up of non cancer cells - not all changes are mutations
why do we study cancer science
- its a global killer - 9.6 million deaths worldwide
- 1 in 2 UK adults will develop some form of cancer in their life times
- 489,700 people will be diagnosed with cancer, and around 162,000 people will die from the disease in the UK each year
cancer definition
it is complex and with over 200 types of cancer no rule is true for all but generally:
- cancer cells have escaped the normal limitations of external due driven cell division
- have modified their local environment to exceed the natural defined tissue borders
- forms a multicellular mass driven by a transformed cancer cell
- have mechanisms to survive immune surveillance and cell death
cancer cells have escaped the normal limitations of external due driven cell division
in your body cells do not normally grow, they are not in active cell cycle and are controlled by growth factors
- cancer cells have escaped this
stimulants of cell growth - growth factors
stimulants of cell growth:
- Growth factors: molecules that bind to specific receptors, triggering a cascade of signals that promote cell growth and division Such as epidermal growth factor and fibroblast growth factors
stimulants of cell growth - hormones
- hormones: certain hormones, such as oestrogen and testosterone, can stimulate cell growth and division
stimulants of cell growth - ECM
- the ECM is the network of proteins and other molecules that surrounds cells and helps to maintain tissue structure.
- some ECM components such as collagen and laminin, can regulate cell growth and division by providing mechanical and chemical signals
limiters of cell growth - chemical microenvironment
chemical microenvironment is the cellular niche where a cell resides. factors such as oxygen levels, pH, temperature, nutrient availability
situational regulators of cell growth - cytokines
these are small proteins that are released primarily by immune cells and act as signalling molecules.
- some cytokine, such as interleukins and interferons, can sometimes promote cell growth and division and other times suppress
how do cancer cells modify their local environment to exceed the natural defined tissue borders
Ecm degradation - matrix metalloproteinases
Ecm remodelling: production and secretion of ECM proteins
Ecm crosslinking: modifying the ECM proteins by crosslinking, that makes the ECM stiffer and stronger
ECM receptors - cancer cells can also express receptors on their surface that Bind to specific ECM such as integrins
Angiogenesis: cancer cells can also promote the formation of new blood vessels
AUTOPHAGY
- membrane blebbing
- autophagic vacuoles
- increased lysosomal activity
apoptosis
- chromatin condensation
- nuclear fragmentation
- apoptotic body
- membrane blebbing
-cell shrinkage
anoikis
is apoptosis by induced by loss of ECM attachments
non programmed cell death (necrosis)
- mitochondrial swelling
- cell swelling
- membrane rupture
mechanisms to survive immune surveillance and death
- Mutations in genes that regulate apoptosis: P53
- Upregulation of anti apoptotic proteins such as BCL-2 and MCL-1, which inhibit the initiation of apoptosis
- Down regulation of pro apoptotic proteins such as BAX or BAK
-Activation of survival signalling pathways - altering the balance of death receptors and ligands: such as FAS and TNFR1
where does cancer come from - epithelial cells
these cells line the surface of internal organs and glands, forming a barriers.
epithelial cells can give rise to a wide variety of carcinomas, including lung, breast and colon
where does cancer come from - mesenchymal cells
- these cells form the connective tissue multiple cell types, including bone cells, muscle cells, and fat cells.
- give rise to sarcomas, such as osteosarcoma
where does cancer come from - hematopoietic cells
- these cells give rise to blood cells
- they are found in the bone marrow
- can give rise to leukemias
where does cancer come from - lymphoid cells
- these cells are a type of white blood cell that are important for the immune system
- can give rise to lymphomas
where does cancer come from - germ cells
- these cells are responsible for producing eggs and sperm.
- can give rise to germ cell tumours, such as testicular seminoma and ovarian teratoma
where does cancer come from - gilomas
- arise from the glial cells, which are supportive cells of the brain
- gliomas are most common type of brain tumour
where does cancer come from - meningiomas
- these tumours arise from the meninges
- usually benign
where does cancer come from - pituitary tumours
- arise from the pituitary gland
- can be benign or malignant and can affect hormone production
where does cancer come from - neuroblastoma
these tumours arise from the nerve cells in the brain or spinal cord.
where does cancer come from - shwannomas
- arise from the Schwann cells, which are the supportive cells that surround nerve fibres
histological subtyping
microscopic appearance of the cancer cells and the structure of the tumour
molecular sub typing
this method looks at the genetic and molecular characteristics of the cancer cells.
immunohistochemical sub typing
this method looks at the proteins expressed in cancer cells EGFR/ ER/ PR
imaging and subtype
this method looks at the imaging features of the tumour, such as size, location and shape, and how it appreas on X-ray, CT scan, MRI or PET scans
TNM system
T (tumour) - how far the tumour has grown through the bowel wall
T1- tumour is in inner layer of bowel
T2 - tumour has grown into the muscle layer of the bowel wall
T3 - tumour has grown into outer lining of the bowel wall
T4 - has grown through the outer lining of the bowel wall
TNM system
N (nodes) - whether the cancer has spread to nearby lymph nodes
N0 - no lymph nodes contain cancer cells
N1 - cancer cells in up to 3 nearby lymph nodes
N2 - cancer cells in 4 or more nearby lymph nodes
TNM system
M (metastases) - whether the cancer has spread to other parts of the body
M0 - hasnt spread
M1 - Has spread
cancer hallmarks
- self sufficiency in growth signals
- evading apoptosis
- insensitivity to anti growth signals
- tissue invasion and metastasis
- sustained angiogenesis
- limitless replicate potential
