Biology 10
Final Exam Review Questions
1.) A) What type of inheritance pattern does albinism represent, according to the pedigree
shown above?
Recessive
B) If a person with albinism has a baby with someone who is a carrier for the disorder, what
are the probabilities that their offspring will have albinism? What are the chances that they
will be a carrier? Use a Punnett Square to explain/ support your answer.
Aa crossed with Aa  Genotypes: 50% aa and 50% Aa
Phenotypes: 50% albinism and 50% carrier
2.) A) What kind of inheritance pattern does the following represent? Explain your answer.
Incomplete/ semi dominance. The 2 traits are blended to show an inbetween trait in the
offspring.
B) If two of the pink flowers are crossed and give rise to offspring, what will be the phenotype
and genotype ratios of their offspring? Use a Punnett square to support your explanation.
Rr + Rr Genotype Ratios:
Phenotype Ratios:
25% RR
50% Rr
25% rr
25% Red
50% Pink
25% White
3.) a) If a woman is the carrier of a mutation in a gene on her X-chromosome for a recessive
disorder, will her phenotype reflect the disorder?
No. Since a woman has 2 X chromosomes, the recessive disorder/ mutation will not appear
in her phenotype, as the healthy/ normal X chromosome will dominate.
b) If this woman mates with a male who is completely healthy for this mutation, what are
the chances that their children will be affected by the mutation? What are the chances that
their children will be carriers of the mutation? Explain with a Punnett Square.
X*X + XY  Genotypes: X*X
XX
X*Y
XY
There is a 25% chance of their offspring showing the disorder. If they have a boy, it is a 50%
chance the boy will be affected.
There is a 25% chance of having a carrier child. If the child is a girl, it is a 50% chance the girl will
be a carrier.
The boys cannot be carriers and the girls will not show the disorder.
c) The above scenario is an example of what type of inheritance pattern?
Sex-linked/ x-linked inheritance
4.) A student wants to perform an investigation on the enzyme pepsin. Pepsin is responsible for
breaking down peptide bonds in proteins, which aids in their digestion in the stomach. The
student decides to test the activity of pepsin under varying conditions of pH.
The student sets up a set of axes upon which to plot her data as follows:
Enzyme Activity
0
7
14
pH
a) Based on what you know about the nature of the stomach and the nature of enzymes,
make a sketch on the axes above based on what you predict the results of the student’s
investigation will show.
b) Explain the shape and details of your sketched-graph.
Shape should have highest/ peak activity below pH 7, as the stomach is acidic in nature.
Therefore, it is logical that pepsin has an optimum pH in the acidic pH range.
Activity should drop off quickly from optimum, especially as pH rises. Enzyme is
denatured at pH conditions away from its optimum pH, and therefore activity decreases
because active site’s shape is changed, can’t bind with substrate and the rate of rxn is
significantly decreased.
c) After completing her investigation, the student decides to carry out a second
investigation to test how pepsin is affected by temperature. She formulates a hypothesis
that the enzyme activity will increase proportionally as the temperature is increased.
Comment on her hypothesis.
The hypothesis is incomplete. Yes, increasing T will likely increase activity at first, as
increased T means increased kinetic energy, will increase collisions between enzyme and
substrate/ increase energy of collisions/ make rxn happen faster. Eventually, when the
temperature gets too high, the enzyme will denature and therefore activity decreases
because active site’s shape is changed, can’t bind with substrate and the rate of rxn is
significantly decreased. So after increasing for a while, the activity should show a sharp
decrease after an “optimum temp.”
5.) The following article was adapted from:
http://www.telegraph.co.uk/news/science/science-news/11631626/v.html
The trial was funded by the manufacturer of T-VEC, Amgen, and is published in the Journal of Clinical Oncology.
A genetically engineered virus has ‘cured’ patients of cancer for the first time in a breakthrough which raises hopes
of an end to chemotherapy. In a worldwide study which was led by the Institute of Cancer Research in the UK,
scientists showed that the new treatment allowed some patients with skin cancer to live for more than three years –
the benchmark many oncologists use to define a cure.The therapy – called T-VEC - works by infecting and killing
cancer cells while also sparking the immune system into action against tumours.
Currently most cancers are treated with using invasive chemotherapy, radiotherapy and surgery, all of which carry
the risk of further harm. The new therapy has far fewer side effects and does not damage healthy tissue or cells.
While the breakthrough came in skin cancer patients, scientists said it raises hopes that the same process could be
used for other cancers.
Malignant melanoma is the fifth most common cancer in the UK, with more than 13,000 diagnosed each year. It
kills more than 2,000 people each year. Professor Paul Workman, Chief Executive of The Institute of Cancer
Research, London, said: “We may normally think of viruses as the enemies of mankind, but it’s their very ability to
specifically infect and kill human cells that can make them such promising cancer treatments. “In this case we are
harnessing the ability of an engineered virus to kill cancer cells and stimulate an immune response.”
The clinical trials, which have been ongoing for more than three years, have been conducted in 64 centres across
the UK, US, Canada and South Africa. The results show that 163 patients with stage three and early stage four
melanoma who were treated with T-VEC lived for an average of 41 months. That was compared with an average
survival of 21.5 months for 66 patients who were given the current best immunotherapy drugs. And the response
was most pronounced in patients with less advanced cancers, underlining the potential benefit as a first-line
treatment for metastatic cancers which cannot be surgically removed. T-VEC is a modified form of herpes virus
which multiplies inside cancer cells and bursts them from within. It has been genetically engineered to produce a
molecule called GM-CSF, which stimulates the immune system to attack and destroy the tumour. It has also been
modified to remove two key genes so that it can’t replicate within healthy cells. Normal cells detect and destroy TVEC before it can cause damage – but it replicates easily in cancer cells because their infection defences are
compromised by genetic errors.
It is one of a new wave of virus-based drugs to show benefits in cancer trials, and is now the first to do so in a
major randomised, controlled phase III trial. “There is increasing excitement over the use of viral treatments like TVEC for cancer, because they can launch a two-pronged attack on tumours – both killing cancer cells directly and
marshalling the immune system against them,” said Prof Kevin Harrington, Professor of Biological Cancer
Therapies at The Institute of Cancer Research.
“Because viral treatment can target cancer cells specifically, it tends to have fewer side-effects than traditional
chemotherapy or some of the other new immunotherapies.
Dr Hayley Frend, science information manager at Cancer Research UK, said: “Using a virus to both kill cancer cells
and nudge the immune system into attacking them is exciting.“Previous studies have shown T-VEC could benefit
some people with advanced skin cancer but this is the first study to prove an increase in survival. The next step will
be to understand why only some patients respond to T-VEC, in order to help better identify which patients might
benefit from it.” The research was also welcomed by British academics who said the results were ‘very promising.’
Prof Leonard Seymour, Professor of Gene Therapies, University of Oxford, said: “This T-Vec study shows powerful
stimulus of an anticancer immune response in patients with melanoma skin cancer. “Increasingly we understand
that cancer is characterised by suppression of the immune system within tumour deposits, meaning that cancer
vaccines have struggled to create useful responses. “However T-VEC appears to be able to overcome this
suppression. At this stage it’s very promising that this appears to have positive results for melanoma skin cancer.”
After reading the article, evaluate this new treatment.
a) What positive evidence is there that this treatment will likely be successful at treating
cancer patients?
-Initial Clinical trials have shown that many patients live longer with this treatment than
with other treatments.
-Results were achieved/ repeated in 64 centers.
b) Is there anything negative about the evidence or the current state of the study that should
make us skeptical of its chances for working effectively?
-Still in initial clinical trials. Results may not be repeated or as reliable or as groundbreaking as
they are tested over time.
c) What would you want doctors to do before making this procedure more widespread? Is
there anything to be concerned about with this type of treatment?
-More trials to test for potential side effects. More long term monitoring of patients.
Potential for immune response due to introduction of a virus/ Unknown long term response
of the body to these genetically modified viruses.
d) Overall, what is your overall opinion about whether or not this treatment will eventually
become widespread? Explain your answer.
Any suitable response weighing pros & cons of new treatment and coming to a logical
conclusion.