IC3

• Cancer is a disease in which some cells in the body grow uncontrollably and spread to other parts of the body.
• Abnormal or damaged cells grow and multiply, forming lumps of tissue.
• Tumors can be cancerous (malignant) or not (benign).
• Tumors are clonal and tumor evolution involves strong environmental selection pressures such as low pH and hypoxia, scarce nutrients, immune attack, cytotoxic drugs and radiotherapy.
• Immune evasion in the tumor microenvironment involves fibroblasts, immune cells, surrounding blood vessels, signaling molecules, and cancer-specific antigens.
• Cancer cells evade the host immune system through manipulation of their own immunogenicity, production of immunosuppressive mediators, and promotion of immunomodulatory cell types.
• Cancers show genetic instability with a high rate of random mutation, leading to genetic and phenotypic variation, which provides a survival advantage.
• Tumor phylogeny allows the detection of clonal and subclonal alterations.
• Cancer cells express cell surface proteins that interact with “checkpoint” proteins on immune cells to “deactivate” the immune signals.
• Cancer cells can downregulate the expression of specific receptors on immune cells and express specific proteins to interact with the immune cells to cease the inflammatory response.
• Cells have an arsenal of DNA repair pathways/proteins to deal with DNA damage.
• Some chemotherapeutics work by causing DNA damage to cells.
• DNA damage can be induced by a variety of stresses including ionizing radiation, UV or other environmental chemicals.
• Crosslinks are chemical linkages of DNA strands.
• Endogenous sources of DNA damage include hydrolysis, oxidation, alkylation, and mismatch of DNA bases, that can arise from endogenous metabolic or DNA replication processes.
• When DNA repair fails, and mutations accumulate, they might lead to the interference of important cell defense mechanisms, ultimately promoting cancer development.
• Cancer spreads through a process called metastasis.
• Some clones compete better than others.
• Some subclones may progress, others remain stable or regress.
• The T5 clone has some growth advantage.
• The T5 clone’s advantage might be: ability to grow well in hypoxic conditions and low pH, ability to migrate into new areas, resistance to immune surveillance, resistance to anti-cancer drugs and radiotherapy, and sub-populations may differ in invasiveness, growth rate, drug resistance, ability to metastasize, and many other characteristics.
• A single cell becomes transformed to a tumour cell.
• Subclonal cells contain different driver genes that emerge over time.
• Clonal sweeps give rise to driver gene mutation homogeneity.
• Molecular features of cancer include "hallmarks of cancer", cell cycle deregulation, DNA damage and genomic instability, immune evasion, and tumor heterogeneity.
• Antibodies are used in the treatment of HER2+ve breast cancer.
• Genetic and environmental factors are risk factors of cancer.
• Radiation therapy and drugs are used in the treatment of cancer.
• Genetic mutations that cause cancer include oncogenes and tumor suppressors.
• Metastasis is the spread of cancer cells from the place/organ of origin to distant places to form new tumors.
• Cancerous tumors that spread to other sites are malignant tumors, while benign tumors do not spread or invade.
• Cancerous tumors stimulate angiogenesis, a process where new blood vessels are formed to feed the tumor.
• A tumor is a swelling of a part of the body, generally without inflammation, caused by an abnormal growth of tissue, whether benign or malignant.
• The growth of a tumor exceeds the growth of normal tissues.
• The growth of a tumor is uncoordinated with the growth of normal tissues.
• Inhibition of cell cycle progression or promotion of apoptosis is important to prevent damaged DNA from being propagated.
• Mutations in cancer can cause cell cycle deregulation.
• Cell cycle regulation involves G1 checkpoint, G2/M checkpoint, and mitotic checkpoint.
• CDK/Cyclins are drivers of the cell cycle.
• G1 Checkpoint determines appropriate growth conditions, G2 Checkpoint determines state of pre-mitotic cell, and Metaphase Checkpoint ensures proper spindle assembly and correct attachment to centromeres.