38 Questions
What is the primary goal of prevention in cancer?
Avoidance of risk factors
What is the role of molecular oncology in diagnosis?
Classification and monitoring of cancer
What is the effect of mutations in oncogenes on cell growth?
Allows for excessive cell growth in absence of growth factors
What is an example of a growth factor receptor oncogene?
PDGFBR
What is the term for the protein encoded by an oncogene?
Oncoprotein
What was the focus of the TCGA study on head and neck squamous cell carcinomas?
Sequencing of head and neck squamous cell carcinomas
What is the normal function of the gene product that is inactivated by mutations?
Stopping excessive cell growth
How many mutations are usually required to inactivate a tumor suppressor gene?
Two mutations
What is the function of the tumor suppressor gene TP53?
Stopping cell division in response to DNA damage
What is the result of DNA damage that is not repaired properly?
Genomic instability
What is the normal response of normal cells to internal or external signals?
Programmed cell death
How do tumor cells resist cellular death?
Through mutations in the programmed cell death signaling pathway
What is the function of tumor suppressor genes such as BRCA1 and MLH1?
DNA repair
What is the result of the loss of tumor suppressor gene RB?
Retinoblastoma
What is the primary difference in energy metabolism between normal cells and cancer cells?
Normal cells use oxidative phosphorylation, while cancer cells use aerobic glycolysis.
What is the purpose of using radiolabeled glucose in PET scans?
To visualize tumor metastases
What is the name of the phenomenon where cancer cells exhibit high glucose uptake and aerobic glycolysis?
Warburg effect
What is the energy yield of aerobic glycolysis in cancer cells?
2 ATP
What is the purpose of the Krebs cycle in normal cells?
To generate ATP for cellular processes
What is the difference in glucose metabolism between normal cells and stem cells?
Stem cells and normal cells have similar glucose metabolism pathways.
What is the role of oncogenes in cancer cell proliferation?
They drive increased cancer cell proliferation
What is the significance of the Warburg effect in cancer metabolism?
It is a hallmark of cancer cell metabolism
What is the primary target of standard cytotoxic chemotherapy?
All rapidly growing cells
What is the advantage of molecularly targeted therapy compared to standard cytotoxic chemotherapy?
Fewer side effects
What is the primary mechanism of action of cetuximab?
Inhibiting EGFR
Which patient group may benefit more from EGFR-targeted therapy?
HPV-negative patients
What is the limitation of using EGFR-targeted therapy in HPV-positive HNSCC?
Inferior to cisplatin
What is the primary reason why we don't all develop tumors?
Cells have robust mechanisms to repair genetic lesions
What is the role of molecular knowledge in molecularly targeted therapy?
Identifying molecular changes in tumor cells
What is the primary advantage of consulting the NCCN guidelines?
They are updated regularly
What is the term used to describe the process by which a growing tumor induces its own blood supply?
Angiogenesis
What is the consequence of mutations in tumor suppressor genes?
Promoting cancer
What type of genes are responsible for regulating programmed cell death?
Genes regulating programmed cell death
What is the term used to describe genetic mutations that affect cell cycle regulation and lead to neoplasia?
Driver mutations
What is the primary difference between proto-oncogenes and oncogenes?
Oncogenes are mutated, while proto-oncogenes are not
What is the term used to describe the process by which the immune system recognizes and clears abnormal cells?
Immune surveillance
What type of genetic lesions can lead to cancer?
Both DNA mutations and epigenetic changes
What is the term used to describe the 10 key characteristics of cancer cells?
Hallmarks of cancer
Study Notes
Molecular Basis of Cancer
- Cancer arises from genetic lesions that affect cell cycle regulation, leading to increased cell proliferation and survival.
- The immune system clears most abnormal cells, but mutations can create "neo-epitopes" recognized by the immune system.
- Growing tumors must induce blood supply (angiogenesis) to exceed 1-2mm in size.
Risk Factors
- Exposure to radiation, chemicals/toxins/alcohol, and viruses
- Reproductive history, inflammation, immunodeficiency, hereditary, and age
- Geographic factors, including local differences, culture, and health disparities
Genetic Lesions
- Genetic damage can occur in DNA or epigenetic (DNA methylation or chromatin changes)
- Targets of genetic damage include growth regulatory genes, tumor suppressor genes, genes regulating programmed cell death, and DNA repair genes
Oncogenes and Proto-Oncogenes
- Oncogenes are genes that promote cell growth and proliferation when mutated
- Proto-oncogenes are normal genes that can become oncogenes when mutated
- Examples of oncogenes include PDGFB, PDGFBR, KRAS, MYC, and CDK4
Oncoproteins
- Oncoproteins are proteins encoded by oncogenes
- Mutations in oncogenes create constitutionally active versions of gene products that promote excessive cell growth
Tumor Suppressor Genes
- Mutations in tumor suppressor genes inactivate gene products that normally stop excessive cell growth
- Examples of tumor suppressor genes include p16, RB, TP53, CDH1, BRCA1, and MLH1
- Loss of tumor suppressor RB can lead to retinoblastoma
Cellular Alterations
- 10 hallmarks of cancer include:
- Self-sufficiency in growth signals
- Insensitivity to anti-growth signals
- Tissue invasion and metastasis
- Limitless replicative potential
- Evading apoptosis
- Sustained angiogenesis
- Tissue inflammation
- Evading immune surveillance
- Deregulating cellular energetics
- Genomic instability and mutation
Cancer Treatment
- Molecularly targeted therapy can be more effective than standard cytotoxic chemotherapy
- Examples of targeted therapy include EGFR inhibitors like cetuximab
- NCCN guidelines provide guidance on therapy for head and neck cancers
Head and Neck Cancer
- TCGA study sequencing of head and neck squamous cell carcinomas identified potential oncogenes
- EGFR is often overexpressed in head and neck cancer
- HPV-negative patients may benefit from EGFR-targeted therapy
Cellular Death
- Tumor cells resist cellular death by mutations in the programmed cell death signaling pathway
- Normal cells respond to internal or external signals for programmed cell death
Cellular Energetics
- Cancer cells use aerobic glycolysis (Warburg effect) to generate energy for rapid growth
- PET scans use radiolabeled glucose to track tumor metastases
Learn about the differences between proto-oncogenes and oncogenes, oncoproteins, and the 10 hallmarks of cancer. Understand the risk factors and epidemiology of cancer.
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