10- drug targets Flashcards
Tumour Suppressor Genes as Targets:
Tumour suppressor genes contribute to cancer when absent, but developing low-molecular-weight compounds to replace their functions is challenging.
Minor successes involve restoring some p53 function by modifying the protein’s structure.
Caretaker Proteins (DNA Repair Proteins) as Targets:
Caretaker proteins, responsible for DNA repair, are crucial for maintaining genomic integrity.
Loss of caretaker proteins leads to uncontrolled replication of damaged DNA, but their functions cannot be easily restored by small molecules
Oncogenes as Targets:
Oncoproteins, hyperactive forms of normal cellular proteins, are attractive targets for anticancer therapies.
Inhibiting hyperactive oncoproteins can reduce accelerated growth and return cells to a more normal state.
Targeting Multi-Step Tumour Progression:
Understanding whether changes responsible for early-stage tumour progression continue to play critical roles in later stages is essential.
Targeting early mutations may cause collapse, but persistence or relapse can occur.
Proteins as Attractive Targets:
Proteins are attractive targets for drug intervention due to the ease of synthesizing low-molecular-weight drugs and their better penetration into tumors.
New Drug Approaches to Cancer Treatment:
Existing treatments are effective but toxic, acting as crude poisons.
New compounds, based on a better understanding of genetic alterations in cancer cells, offer more targeted and less toxic alternatives
Biological Therapies and Targets:
Biological therapies target key tumor suppressor genes, oncogenes, signaling pathways, apoptosis, tumor microenvironment, and telomeres.
Monoclonal antibodies, small molecule inhibitors, RNA interference, gene therapy, and immunotherapy are strategies for turning biology into a cure.
Personalized Medicine and Targeted Therapies:
Targeted therapies based on a patient’s mutation profile involve personalized medicine.
Examples include targeting HER2 in breast cancer and specific mutations like BRAF in melanoma.
Synthetic Lethality:
Synthetic lethality involves the combination of mutations or losses in two genes, resulting in cell death.
Examples include the use of PARP inhibitors in BRCA1/2-mutated cancers, causing synthetic lethality and cell death.