HISTOTECHNOLOGY SOLUTION MANUAL
EXAM PREP 2026 COMPLETE QUESTIONS AND
SOLUTIONS
◉2. How is cancer different from most other types of genetic diseases?
Answer: Solution:
Most cancers arise from genetic changes in somatic cells that arise
during an individual's lifetime, whereas other types of genetic diseases
are inherited through the germ line.
◉3. Outline Knudson's two-hit hypothesis of retinoblastoma and
describe how it helps to explain unilateral and bilateral cases of
retinoblastoma. Answer: Solution:
The multistage theory of cancer states that more than one mutation is
required for most cancers to develop. Most retinoblastomas are
unilateral because the likelihood of any cell acquiring two rare mutations
is very low, and thus retinoblastomas develop in only one eye. Bilateral
cases of retinoblastoma occur in people born with a predisposing
mutation, so that as few as one additional mutational event can result in
cancer. Thus, the probability of retinoblastoma is higher in these
individuals and likely to occur in both eyes. Because the predisposing
mutation is inherited, people with bilateral retinoblastoma have relatives
with retinoblastoma.
, ◉4. Briefly explain how cancer arises through clonal evolution.
Answer: Solution:
A mutation that relaxes growth control in a cell will cause it to divide
and form a clone of cells that are growing or dividing more rapidly than
their neighbors. Successive mutations that cause even more rapid
growth, or the ability to invade and spread, each produce progeny cells
with more aggressive, malignant properties that outgrow their
predecessors and take over the original clone.
◉5. What is the difference between an oncogene and a tumor-suppressor
gene? Give some examples of the functions of proto-oncogenes and
tumor suppressors in normal cells. Answer: Solution:
An oncogene stimulates cell division, whereas a tumor-suppressor gene
inhibits cell growth. Proto-oncogenes are normal cellular genes that
function in cell growth and regulation of the cell cycle: from growth
factors such as sis to receptors like ErbA and ErbB, protein kinases such
as src, and transcription factors like myc. Tumor suppressors inhibit cell
cycle progression: RB and p53 are transcription factors and NF1 is a
GTPase activator.
◉12. Why do mutations in genes that encode DNA-repair enzymes often
produce a predisposition to cancer? Answer: Solution:
Mutations that affect DNA repair result in high rates of mutation.
Mutations may convert proto-oncogenes into oncogenes or inactivate
tumor-suppressor genes.
◉15. How is DNA methylation related to cancer? Answer: Solution:
EXAM PREP 2026 COMPLETE QUESTIONS AND
SOLUTIONS
◉2. How is cancer different from most other types of genetic diseases?
Answer: Solution:
Most cancers arise from genetic changes in somatic cells that arise
during an individual's lifetime, whereas other types of genetic diseases
are inherited through the germ line.
◉3. Outline Knudson's two-hit hypothesis of retinoblastoma and
describe how it helps to explain unilateral and bilateral cases of
retinoblastoma. Answer: Solution:
The multistage theory of cancer states that more than one mutation is
required for most cancers to develop. Most retinoblastomas are
unilateral because the likelihood of any cell acquiring two rare mutations
is very low, and thus retinoblastomas develop in only one eye. Bilateral
cases of retinoblastoma occur in people born with a predisposing
mutation, so that as few as one additional mutational event can result in
cancer. Thus, the probability of retinoblastoma is higher in these
individuals and likely to occur in both eyes. Because the predisposing
mutation is inherited, people with bilateral retinoblastoma have relatives
with retinoblastoma.
, ◉4. Briefly explain how cancer arises through clonal evolution.
Answer: Solution:
A mutation that relaxes growth control in a cell will cause it to divide
and form a clone of cells that are growing or dividing more rapidly than
their neighbors. Successive mutations that cause even more rapid
growth, or the ability to invade and spread, each produce progeny cells
with more aggressive, malignant properties that outgrow their
predecessors and take over the original clone.
◉5. What is the difference between an oncogene and a tumor-suppressor
gene? Give some examples of the functions of proto-oncogenes and
tumor suppressors in normal cells. Answer: Solution:
An oncogene stimulates cell division, whereas a tumor-suppressor gene
inhibits cell growth. Proto-oncogenes are normal cellular genes that
function in cell growth and regulation of the cell cycle: from growth
factors such as sis to receptors like ErbA and ErbB, protein kinases such
as src, and transcription factors like myc. Tumor suppressors inhibit cell
cycle progression: RB and p53 are transcription factors and NF1 is a
GTPase activator.
◉12. Why do mutations in genes that encode DNA-repair enzymes often
produce a predisposition to cancer? Answer: Solution:
Mutations that affect DNA repair result in high rates of mutation.
Mutations may convert proto-oncogenes into oncogenes or inactivate
tumor-suppressor genes.
◉15. How is DNA methylation related to cancer? Answer: Solution:
