Cancer Flashcards
Hallmark: Sustained
Proliferative Signaling
- Uncontrolled cellular proliferation (replication)
- receptors activate intracellular activation of regulatory factors -> affecting DNA synthesis, entrance into the cell cycle, and changes in expression of other genes related to cell metabolism for optimal growth
- Basically receptors activate regulatory factors for optimal cell growth
Hallmark: Evading Growth Suppressors
- secrete and increase growth factor
- Inactivation of Retinoblastoma Protein (Rb) Tumor Suppressor
- Activation of Protein Kinases That Drive The Cell Cycle
- Mutation In The TP53 Gene (Tumor suppressor Gene)
Hallmark: Genomic Instability
3 causes:
- Activate Proto-oncogenes makes too much Oncogenes
- Mutation of genes that causes deactivation or suppression of tumor suppressors
- Mutation of genes that cause cell death thus allowing uncontrolled growth
Oncogenes & Tumour- suppressor genes
Proto-oncogenes:
- normal genes for cell growth
Oncogenes:
* mutant genes
Tumour-suppressor genes
* proteins regulate proliferation (uncontrolled growth)
* anti oncogenes
Hallmark: Replication Immortality
- cells can divide a limited number of times (Hayflick limit)
Telomeres: - protective caps on each chromosome
Hallmark: Inducing Angiogenesis
- Angiogenesis = growth of new vessels. Also called neovascularization
Hallmark: Avoiding cell death
- Programmed cell death (apoptosis) = cells can self-destruct
- TP53 gene incharge of apoptosis
Hallmark: Avoiding Immune destruction
Immune surveillance hypothesis:
- most cancers are suppressed by an immune response against tumour-associated antigens
* cancer development = evasion of immune response
Immunotherapy hypothesis:
- predicts that the immune
system could be used to target tumour-associated antigens and destroy tumours clinically
Hallmark: Tumour promoting inflammation
Chronic inflammation: Is an important factor in the development of cancer.
- wound-healing response that includes proliferation and new blood vessel growth
What is Metastasis
Is the spread of cancer cells
from the site of the original tumour to distant tissues and organs through the body
How Do Cancer cells Develop the ability To Invade (Locally) And
Metastasize?
- Most endothelial characteristics are lost, unable to adhere to basement membrane
- increases migratory capability
- Resistance to apoptosis (cell death) increases
- turns into stem cell = better growth in foreign microenvironments
Cancer cells secrete protease, what does protease do?
Proteases digest the extracellular matrix and basement membranes.
= Create pathways through which cells can move
Characteristics Of Cancer Cells
Anaplastic:
- very little resemblance to the cells they originated from
Pleomorphic:
- variable size, shape and structure
Substantial amount of stroma (microenvironment), but is disorganized with loss of normal tissue structure
Lacks a capsule
Capable of invading nearby structures
Benign Vs. Malignant Tumors
- Benign
- Slow growth
- Well-defined
- capsule
- Not invasive
- Well differentiated
- Low mitotic index
- Does not metastasize
- Malignant
- Rapid growth
- Not encapsulated
- Invasive
- Poorly differentiated: Anaplasia
- High mitotic index
- Can spread distantly (metastasis)
What is a stroma?
early and enlargement of the tumor = synthesis of proinflammatory mediators
* surrounds and infiltrates the tumor
* Stroma promotes cancer progression and metastatic potential