CDS 4000-STUDY GUIDE FOR FINAL EXAM UPDATED ACTUAL
Questions and CORRECT Answers
Understand the hallmarks of cancer and how they - Sustaining proliferative signalling: increasing cell numbers
promote tumorigenesis - Evading growth suppressors: removing cell cycle control
- Registering cell death: allowing mutated cells to survive
- Enabling replicative immortality: allowing unlimited divisions
- Inducing angiogenesis: feeding tumor growth
- Activating invasion and metastasis: expanding disease throughout body
Clonal evolution Cancer cells acquire genetic mutations over time, leading to development of
new mutations.
Clonal heterogeneity Different cells make up a tumor, arising from ongoing mutation and evolution.
Daughter cell acquires a mutation then passes on, then eventually another
daughter cell acquires another one. It passes on..
How does this promote tumorigenesis clonal Clonal evolution drives tumorigenesis by accumulating mutations that give
evolution and clonal heterogeneity growth advantages, while clonal heterogeneity allows tumors to adapt,
progress, metastasize, and resist treatment.
Driver mutations Confer a growth advantage to a cell through the alteration of fundamental
cellular processes; Essential for tumor transformation/growth; smallest number
of total mutations in any tumor. Few in number
Passenger mutations Not essential for tumor growth/ survival; have accumulated over the course of
a lifetime of exposure to mutagens or during the deregulated mitoses of
malignant transformation; largest number of total mutations in any tumor
the difference between driver mutations and passenger Based on current data, the total number of genes estimated to be mutated in
mutations, and their roles in tumorigenesis. any single cancer type is 50-100 as opposed to 500-1000.
Types of cancer genes 1. oncogene
2. tumor suppressor
3. Apoptosis gene
4. DNA repair
https://quizlet.com/1167529813/cds-4000-study-guide-for-final-exam-flash-cards/ 1/13
, What are the four steps for the process of a normal cell 1) Initiating mutation- normal cell acquires mutation from exposure to
to frank malignancy? carcinogen
2) Acquisition of genomic instability- baby of mutated cell now unstable and
will have more mutated babies (clones)
3) acquisition of Cancer hallmarks- clones begin to pick up driver mutations,
which id giving those babies more attributes that'll lead to cancer
4) Further genetic evolution- we've picked up enough driver mutations and
cancer hallmarks to produce a full-blown cancer cell that will just keep
replicating more cancer cells, while also still acquiring more mutations that'll
lead to a big clump of heterogeneous cancer cells leading to a difficult to all-
in-one cure (due to heterogeneity) cancer diagnosis.
Oncogenes and how they promote to tumorigenesis Gain of function
mutations promote growth and proliferation of tumors by over activating signal
transduction molecules and growth factors.
Tumorigenesis → constinating cell division, no need for growth factors,
continuous proliferation. Results in uncontrolled cell growth
ex. myc,myb molecules and growth factors bcr/abl.
Mutations in Tumor suppressor Gene Loss of function:
In cancer, mutation of the tumor suppressor gene impairs the body's ability to
control the cell cycle (loss of function), leading to uncontrollable cell growth.
Ex. Rb, p53, BRAC1,2
Mutations in Apoptosis Genes: In cancer, mutations of the apoptosis gene disrupts programmed cell death -->
cells refuse to die
Example of apoptosis gene is bcl-2
Location: Mitochondria/cytoplasm
Mutations in DNA Repair Gene In cancer, mutations in the DNA repair gene disrupts normal DNA repair -->
mutations accumulate because there is no repair team
Examples of DNA repair genes: msh-2, mlh-1
Understand the cellular functions and locations of the ....
four types of cancer genes (slides 21 and 23).
Where are oncogenes located? Oncogenes are located:
- Cytoplasm or membrane (GFR, GF, signal transduction molecules)
- nucleus --> transcription factors (MYC)
Where are tumor suppressor genes located? What is Tumor suppressor genes are located in the nucleus, (p53, RB, CDK) where they
their function? regulate the cell cycle.
Where are DNA Repair genes located? What is their DNA repair genes are located in the nucleus (MSH2) where they repair DNA
function? errors and maintain genomic stability.
https://quizlet.com/1167529813/cds-4000-study-guide-for-final-exam-flash-cards/ 2/13
Questions and CORRECT Answers
Understand the hallmarks of cancer and how they - Sustaining proliferative signalling: increasing cell numbers
promote tumorigenesis - Evading growth suppressors: removing cell cycle control
- Registering cell death: allowing mutated cells to survive
- Enabling replicative immortality: allowing unlimited divisions
- Inducing angiogenesis: feeding tumor growth
- Activating invasion and metastasis: expanding disease throughout body
Clonal evolution Cancer cells acquire genetic mutations over time, leading to development of
new mutations.
Clonal heterogeneity Different cells make up a tumor, arising from ongoing mutation and evolution.
Daughter cell acquires a mutation then passes on, then eventually another
daughter cell acquires another one. It passes on..
How does this promote tumorigenesis clonal Clonal evolution drives tumorigenesis by accumulating mutations that give
evolution and clonal heterogeneity growth advantages, while clonal heterogeneity allows tumors to adapt,
progress, metastasize, and resist treatment.
Driver mutations Confer a growth advantage to a cell through the alteration of fundamental
cellular processes; Essential for tumor transformation/growth; smallest number
of total mutations in any tumor. Few in number
Passenger mutations Not essential for tumor growth/ survival; have accumulated over the course of
a lifetime of exposure to mutagens or during the deregulated mitoses of
malignant transformation; largest number of total mutations in any tumor
the difference between driver mutations and passenger Based on current data, the total number of genes estimated to be mutated in
mutations, and their roles in tumorigenesis. any single cancer type is 50-100 as opposed to 500-1000.
Types of cancer genes 1. oncogene
2. tumor suppressor
3. Apoptosis gene
4. DNA repair
https://quizlet.com/1167529813/cds-4000-study-guide-for-final-exam-flash-cards/ 1/13
, What are the four steps for the process of a normal cell 1) Initiating mutation- normal cell acquires mutation from exposure to
to frank malignancy? carcinogen
2) Acquisition of genomic instability- baby of mutated cell now unstable and
will have more mutated babies (clones)
3) acquisition of Cancer hallmarks- clones begin to pick up driver mutations,
which id giving those babies more attributes that'll lead to cancer
4) Further genetic evolution- we've picked up enough driver mutations and
cancer hallmarks to produce a full-blown cancer cell that will just keep
replicating more cancer cells, while also still acquiring more mutations that'll
lead to a big clump of heterogeneous cancer cells leading to a difficult to all-
in-one cure (due to heterogeneity) cancer diagnosis.
Oncogenes and how they promote to tumorigenesis Gain of function
mutations promote growth and proliferation of tumors by over activating signal
transduction molecules and growth factors.
Tumorigenesis → constinating cell division, no need for growth factors,
continuous proliferation. Results in uncontrolled cell growth
ex. myc,myb molecules and growth factors bcr/abl.
Mutations in Tumor suppressor Gene Loss of function:
In cancer, mutation of the tumor suppressor gene impairs the body's ability to
control the cell cycle (loss of function), leading to uncontrollable cell growth.
Ex. Rb, p53, BRAC1,2
Mutations in Apoptosis Genes: In cancer, mutations of the apoptosis gene disrupts programmed cell death -->
cells refuse to die
Example of apoptosis gene is bcl-2
Location: Mitochondria/cytoplasm
Mutations in DNA Repair Gene In cancer, mutations in the DNA repair gene disrupts normal DNA repair -->
mutations accumulate because there is no repair team
Examples of DNA repair genes: msh-2, mlh-1
Understand the cellular functions and locations of the ....
four types of cancer genes (slides 21 and 23).
Where are oncogenes located? Oncogenes are located:
- Cytoplasm or membrane (GFR, GF, signal transduction molecules)
- nucleus --> transcription factors (MYC)
Where are tumor suppressor genes located? What is Tumor suppressor genes are located in the nucleus, (p53, RB, CDK) where they
their function? regulate the cell cycle.
Where are DNA Repair genes located? What is their DNA repair genes are located in the nucleus (MSH2) where they repair DNA
function? errors and maintain genomic stability.
https://quizlet.com/1167529813/cds-4000-study-guide-for-final-exam-flash-cards/ 2/13
