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48 Cards in this Set

  • Front
  • Back
Name the five causes of DNA damage
Cellular metabolism
UV light exposure
ionizing radiation
chemical exposure
replication errors
Name four cellular responses to DNA damage
- cell cycle checkpoint activation
- transcriptional program activation
- DNA repair (BER, NER, mismatch repair, etc.)
- apoptosis
Name 6 common features of cancer cells
- self-sufficient growth
- insensitivity to growth inhibition
- escaping apoptosis
- limitless replicative potential
- tissue invasion and metastasis
- angiogenesis
What is the Knudson hypothesis?
In the children with inherited retinoblastoma, the first insult was inherited in the DNA, and any second insult would rapidly lead to cancer. In non-inherited retinoblastoma, two "hits" had to take place before a tumor could develop, explaining the age difference in incidence.
What are two challenges to the Knudson hypothesis?
- tumorigenesis is a multi-step process, involving activation of oncogenes and inactivation of tumor suppressor genes
- haploinsufficiency: in some cases (PTEN), the inactivation of ONE allele of a gene is sufficient to knockout that gene's activity
What are the 5 steps in carcinogenesis?
- initiation
- promotion
- progression
- invasion
- metastasis
What molecules make up the proto-oncogene group?
- growth factors
- growth factor receptors
- signal transduction molecules
- transcription factors
These are regular genes in our body that get messed up and become an oncogene.
List examples of the ways in which oncogenes can be activated.
- activating mutations
- gene amplification
- chromosomal translocation
Define translocation or transposition as it is related to the activation of proto-oncogenes, and give an example of it.
- where the gene is jumped from one area of DNA to another, resulting in a new promoter that transcribes the gene more frequently
- Bcr-Abl
- Myc
Define gene amplification as it relates to proto-oncogene activation and give an example.
- where the gene is duplicated several times along the DNA strand, thereby causing a higher rate of transcription
- ErbB-2/HER2
Define point mutation as it is related to the activation of proto-oncogenes, and give an example of it.
- A single point mutation occurs in the proto-oncogene that activates its out-of-control activity, resulting in a hyperactive or degradation-resistant protein
- Ras
Name the growth factor receptor that is an oncoprotein and its type.
erbB-2/HER2/Neu
receptor tyrosine kinase
structurally similar to epidermal growth factor
Name the signaling molecules that are oncoproteins.
- Src: Tyrosine kinase (non-receptor)
- Abl: Tyrosine kinase (non-receptor)
- Bcr-Abl: t(9;22) in CML
- Ras: GTP-binding protein
- Bol-2: t(14;18) in B-follicular lymphoma
Name the transcription factors that are oncoproteins.
fos
jun
Myc
How is ErbB-2/HER2/Neu activated?
- Activated via HETERODIMERIZATION with other ErbB proteins
- Dimerization causes AUTO-PHOSPHORYLATION of the TYROSINE KINASE domain, which then activates the cascade of signaling events that MEDIATES GENE TRANSCRIPTION
Where is ErbB-2/HER2/Neu found, and what is its oncogenic alteration?
Breast cancer; gene amplification
How does HER2 differ from other members of the EGFR family?
It doesn't appear to have a ligand that activates its activity; rather, it must dimerize with another HER molecule to be activated.
How does ErbB-2/HER2/Neu mediate gene transcription and cell proliferation?
Through the Ras signaling pathway
How does ErbB-2/HER2/Neu promote cell survival and inhibit cell death?
Through the PI3 kinase-Akt signaling pathway
The deregulation of what signalling network is needed for the development and progression of proliferative diseases such as cancer and cardiac hypertrophy?
Receptor tyrosine kinase signalling network
What developments have been made to interfere with receptor tyrosine kinase signalling network transduction?
- Neutralizing antibodies, which block the bioactivity of RTK ligands
- RTK-targeted antibodies, which either target overexpressed receptors or receptor heterodimerization
- small-molecule inhibitors of RTK kinase activity
How is Bcl-Abl activated to an oncogene, where is it found, and what is its special power?
- Encoded on the Philadelphia Chromosome t(9;22)
- Found in chronic myeloid leukemia (CML)
- Potent tyrosine kinase activity
What are Ras proteins, what do they do, and how do they lead down the road to cancer?
- small GTP-bound proteins (active when GTP is bound)
- mediate various cellular responses through activation of the protein kinase pathways (e.g. PI3-K, MAPK pathways)
- a SINGLE MUTATION on codons 12, 13, or 61 can result in an CONSTITUTIVELY-ACTIVATED PROTEIN, leading to aberrant cell proliferation
- 30% of all human cancers have activated mutations of Ras genes
What do Bcl-2 proteins do and what in kind of neoplasia are they found?
- Govern MITOCHONDRIA OUTER MEMBRANE PERMEABILIZATION (APOPTOSIS)
- Is PRO-CELL SURVIVAL
- Other members of the Bcl-2 family are PRO-CELL DEATH (Bax)
- only active as a dimer (homo or hetero)
- found in B-cell lymphoma
- cancer happens when pro-death are inactivated or pro-survival are activated
Name the five causes of DNA damage
Cellular metabolism
UV light exposure
ionizing radiation
chemical exposure
replication errors
Name four cellular responses to DNA damage
- cell cycle checkpoint activation
- transcriptional program activation
- DNA repair (BER, NER, mismatch repair, etc.)
- apoptosis
Name 6 common features of cancer cells
- self-sufficient growth
- insensitivity to growth inhibition
- escaping apoptosis
- limitless replicative potential
- tissue invasion and metastasis
- angiogenesis
What is the Knudson hypothesis?
In the children with inherited retinoblastoma, the first insult was inherited in the DNA, and any second insult would rapidly lead to cancer. In non-inherited retinoblastoma, two "hits" had to take place before a tumor could develop, explaining the age difference in incidence.
What are two challenges to the Knudson hypothesis?
- tumorigenesis is a multi-step process, involving activation of oncogenes and inactivation of tumor suppressor genes
- haploinsufficiency: in some cases (PTEN), the inactivation of ONE allele of a gene is sufficient to knockout that gene's activity
What are the 5 steps in carcinogenesis?
- initiation
- promotion
- progression
- invasion
- metastasis
What molecules make up the proto-oncogene group?
- growth factors
- growth factor receptors
- signal transduction molecules
- transcription factors
These are regular genes in our body that get messed up and become an oncogene.
List examples of the ways in which oncogenes can be activated.
- activating mutations
- gene amplification
- chromosomal translocation
Define translocation or transposition as it is related to the activation of proto-oncogenes, and give an example of it.
- where the gene is jumped from one area of DNA to another, resulting in a new promoter that transcribes the gene more frequently
- Bcr-Abl
- Myc
Define gene amplification as it relates to proto-oncogene activation and give an example.
- where the gene is duplicated several times along the DNA strand, thereby causing a higher rate of transcription
- ErbB-2/HER2
Define point mutation as it is related to the activation of proto-oncogenes, and give an example of it.
- A single point mutation occurs in the proto-oncogene that activates its out-of-control activity, resulting in a hyperactive or degradation-resistant protein
- Ras
Name the growth factor receptor that is an oncoprotein and its type.
erbB-2/HER2/Neu
receptor tyrosine kinase
structurally similar to epidermal growth factor
Name the signaling molecules that are oncoproteins.
- Src: Tyrosine kinase (non-receptor)
- Abl: Tyrosine kinase (non-receptor)
- Bcr-Abl: t(9;22) in CML
- Ras: GTP-binding protein
- Bol-2: t(14;18) in B-follicular lymphoma
Name the transcription factors that are oncoproteins.
fos
jun
Myc
How is ErbB-2/HER2/Neu activated?
- Activated via HETERODIMERIZATION with other ErbB proteins
- Dimerization causes AUTO-PHOSPHORYLATION of the TYROSINE KINASE domain, which then activates the cascade of signaling events that MEDIATES GENE TRANSCRIPTION
Where is ErbB-2/HER2/Neu found, and what is its oncogenic alteration?
Breast cancer; gene amplification
How does HER2 differ from other members of the EGFR family?
It doesn't appear to have a ligand that activates its activity; rather, it must dimerize with another HER molecule to be activated.
How does ErbB-2/HER2/Neu mediate gene transcription and cell proliferation?
Through the Ras signaling pathway
How does ErbB-2/HER2/Neu promote cell survival and inhibit cell death?
Through the PI3 kinase-Akt signaling pathway
The deregulation of what signalling network is needed for the development and progression of proliferative diseases such as cancer and cardiac hypertrophy?
Receptor tyrosine kinase signalling network
What developments have been made to interfere with receptor tyrosine kinase signalling network transduction?
- Neutralizing antibodies, which block the bioactivity of RTK ligands
- RTK-targeted antibodies, which either target overexpressed receptors or receptor heterodimerization
- small-molecule inhibitors of RTK kinase activity
How is Bcl-Abl activated to an oncogene, where is it found, and what is its special power?
- Encoded on the Philadelphia Chromosome t(9;22)
- Found in chronic myeloid leukemia (CML)
- Potent tyrosine kinase activity
What are Ras proteins, what do they do, and how do they lead down the road to cancer?
- small GTP-bound proteins (active when GTP is bound)
- mediate various cellular responses through activation of the protein kinase pathways (e.g. PI3-K, MAPK pathways)
- a SINGLE MUTATION on codons 12, 13, or 61 can result in an CONSTITUTIVELY-ACTIVATED PROTEIN, leading to aberrant cell proliferation
- 30% of all human cancers have activated mutations of Ras genes
What do Bcl-2 proteins do and what in kind of neoplasia are they found?
- Govern MITOCHONDRIA OUTER MEMBRANE PERMEABILIZATION (APOPTOSIS)
- Is PRO-CELL SURVIVAL
- Other members of the Bcl-2 family are PRO-CELL DEATH (Bax)
- only active as a dimer (homo or hetero)
- found in B-cell lymphoma
- cancer happens when pro-death are inactivated or pro-survival are activated