Geneticist: _Amit Singh__________ Teacher: _Stanley C Hughes_________________________
Cell Proliferation and Cancer
Misconceptions:
1. Cancer does not come from outside but it is a transition of our own cells into cancerous cells.
2. Cancer is caused only by smoking or other carcinogens.
3. I can prevent cancer by not smoking or using other carcinogens. 4. There is only one type of cancer.
State Standards:
1. Summarize the general processes of cell division and differentiation, and explain why specialized cells are useful to organisms and explain that complex multicellular organisms are formed as highly organized arrangements of differentiated cells.
2. Illustrate the relationship of the structure and function of DNA to protein synthesis and the characteristics of an organism.
3. Explain that a unit of hereditary information is called a gene, and genes may occur in different forms called alleles (e.g., gene for pea plant height has two alleles, tall and short).
4. Describe that spontaneous changes in DNA are mutations, which are a source of genetic variation. When mutations occur in sex cells, they may be passed on to future
generations; mutations that occur in body cells may affect the functioning of that cell or the organism in which that cell is found.
5. Describe advances in life sciences that have important long-lasting effects on science and society (e.g., biological evolution, germ theory, biotechnology and discovering germs). 6. Analyze and investigate emerging scientific issues (e.g., genetically modified food, stem
cell research, genetic research and cloning). Major science concepts:
1. Genetic basis of cancer
2. Scienttific Research is ongoing and advancing constantly 3. DNA replication and gene mutations
4. Genetics of cell cycle and cell division
Learning outcomes:
Students will be able to:
1. Explain what factors lead to cancer.
2. To integrate their knowledge of cell structure, division, and function and relate them to understand how cancer develops.
3. Explain the difference between benign, malignant, and metastatic tumors 4. List and determine the differences between at least 5 different types of cancers
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Student Skills:
1. Research internet
2. Analysis of information from videos and powerpoints 3. Writing
4. Production of multimedia 5. Discussion
Resources:
Video From HHMI
Biology: The Dynamics of Life by Glencoe
Since the information may require a lot of referencing we will use:
Reference Material: Cell and Molecular Biology of Cell “Gerald M Karpe” Cancer Biology
National Cancer Institute (NCI) American Cancer Society (ACS)
Suggested sites for students to find information for their Power Point/Webquest
• www.cancer.org • www.nytimes.com/learning/students/scienceqa/archive/010529.html • www.sciencedigest.org/0996T.htm • www.ncpa.org/studies/s214.html • www.nytimes.com/learning/students/scienceqa/archive/950922b.html • www.world.std.com/~krahe/html1.html • www.ul.is/~childsp/CinA/Issue62/TOC10_Medicine.htm • www.nancyrakela.com/cancer.html • www.cnn.com/HEALTH/cancer/9905/16/alternative.cancer
Flow Chart of Concepts
Cell Types and Organelles ÆCell Cycle Æ Mitosis/Meiosis Æ Mendelian and Human Genetics
ÆDNA replication, mutations Æ Development of Cancer Cells ÆApplied Genetics ÆProtein Synthesis
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Outline of Teaching Plan
EXPLANATION
Power point produced by Dr. Singh to further explain the genetic aspects of cancer and cancer development. (2, 52 minute periods)
ELABORATION
The students will then produce a 10 slide power point presentation on the cancer of their choice. The students must have general characteristics, history, genes involved, symptoms, conventional care, unconventional care and cancer statistics. (outside class time involved)
ENGAGEMENT:
Cancer Statistics and Introduction, pre-test (1, 52 minute period), Movie on Cancer HHMI (2, 52 minute periods),
EXPLORATION
Webquest visit list of websites provided by us. The students will then produce a 10 slide power point on the cancer of their choice. (1, 52 minute period + outside class time)
EVALUATION
Pre Test (15 minutes) Post Test (15 minutes)
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Assessment Strategy:
Formative assessment
The students will then produce a 10 slide power point presentation on the cancer of their choice. The students must have general characteristics, history, genes involved,
symptoms, conventional care, unconventional care and cancer statistics as at least one slide in their power points. The students may work in pairs. Each type of cancer will only be researched by one group.
Summative assessment (Be sure to match these to your objectives/learning outcomes.)
This is a copy of the pre and post test questions.
1. What is the word that describes uncontrolled cell growth forming malignant tumors that can result in the invasion of surrounding healthy tissues?
A. Mitosis B. Cancer C. Diabetes D. Clumping E. Meiosis 2. How does cancer develop in the human body?
A. Cancer is an infectious disease which results from contact with a patient suffering from cancer.
B. New sets of cells get introduced from the outside which starts dividing without any control and cause tumors
C. Our own cells change their nature and start dividing in an uncontrolled fashion and form tumors.
D. All of the above E. None of the above
5. What is the most important property of a cancer cell? A. its chromosome complement
B. its loss of growth control C. its size
D. its secretions
E. its inability to divide
6. What generally happens if cancer cells are introduced into a host animal? A. nothing happens; they do not survive in a host
B. they are converted to normal cells in the host C. they generally cause tumors in the host animal
D. the host animal’s immune system destroys the transformed cancer cells. E. Both A and D
7. Which statement below is a correct statement about the abilities of normal cells and cancer cells to grow and divide when cultured under conditions favorable for cell growth?
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A. Malignant cells grow and divide at a somewhat faster rate
B. Normal cells grow and divide at a faster rate than malignant cells C. Malignant and normal cells grow and divide at similar rates D. Neither type of cell grows well in culture
E. Normal cells do not grow at all, while malignant cells grow rapidly
8. What enzyme possessed by cancer cells is not found in normal cells that results in cancer cells ability to divide indefinitely and not die off?
A. Telomerase B. RNA polymerase
C. DNA-directed DNA polymerase D. Reverse transcriptase
E. RNA-directed DNA polymerase
9. Who made the first known correlation between environmental agents and cancer development? A. Harry Potter B. Percival Pott C. Percival Lowell D. Charles Darwin E. Archibald Garrod
10.What do all of the environmental agents that can cause cancer have in common? A. They can all alter genes
B. They are all soluble in water C. They are all made of nucleotides D. They are all made of amino acids
E. They can alter proteins present in the cell cytoplasm that are responsible for the onset of cancer
11.Why do some viruses transform normal cells into cancer cells?
A. They take over the normal cells and cause them to make progeny viruses B. They carry genes whose products interfere with the cell’s normal-growth
regulating activities
C. They carry genes whose products interfere with the cell’s normal bioenergetics pathways
D. They carry genes whose products interfere with the cell’s normal secretory activities.
E. Both B and D
12.What types of genetic alterations might make it possible for humans to develop cancer? A. those that are inherited from their parents
B. viral line mutations
C. those that occur during a human’s lifetime D. automatic mutations
6 E. Both A and C
13.What types of genetic alterations might make it possible for humans to develop cancer? A. those that a parent obtains from his child
B. mutations that occur in sex cells
C. those that occur in eggs after menopause D. somatic mutations
E. Both B and D
14.Studies of identical twins suggest that ___________.
A. the genes we inherit have a significant influence on our risks of developing cancer B. the greatest impact on cancer development comes from genes altered during our
lifetime
C. genes play a very small role in cancer development D. genes play no role in cancer development
E. Both A and B
15.Cancer results from the uncontrolled growth of a single cell and is therefore considered to be ___________.
A. Polyclonal B. Biclonal C. Monoclonal D. variant E. Obstreperous 16.Another work for a malignant transformation is _____________.
A. Oncorariness B. Ontogenesis C. Cancerogenesis D. Tumorigenesis E. Oncogenation
17.Which cells below possess unlimited growth potential and are able to give rise to all other types of cells?
A. stem cells B. progenitor cells
C. differentiated end products of a tissue D. anatomical cells
E. Both B and C
18.Which cells generally lack the ability to divide? A. stem cells
B. progenitor cells
C. cells that are differentiated and are the end products of tissue D. anatomical cells
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19.You are studying two cell lines, one malignant and one normal. You carry out an experiment in which you fuse malignant and normal cells. What is likely to happen?
A. all of the hybrid (fused) cells behave like malignant cancer cells B. some of the hybrid cells lose malignant traits
C. some of the hybrid cells gained more extreme malignant traits D. most of the hybrids dies shortly after fusion
E. the hybrids began to fuse together spontaneously making giant multinucleate cells 20.The fusion of malignant and normal cells results in some cases in the loss of malignant
traits. What do these results suggest?
A. Normal cells possess factors that can suppress uncontrolled cancer cell growth B. They suggest the existence of oncogenes
C. Malignant cancer cells posses something that suppresses uncontrolled cancer cell growth
D. They suggested the existence of cancer-causing genes E. Both B and D
21.Mutant forms of tumor suppressor genes act in a dominant fashion, both copies of the gene must be _____________ before their function is lost.
A. mutated or deleted B. preserved
C. reserved D. conserved E. both A and D
22.How can one identify oncogenes?
A. By identifying the DNA suspected of containing the oncogene into cultured cells and looking for altered growth properties
B. By fusing two normal cells together C. By fusing two malignant cells together
D. By introducing the DNA suspected of containing the oncogene into cultured cells looking for altered nuclear membrances
E. B,C, and D only
23.What was the initial explanation for the sensitivity of cancer cells to radiation therapy and chemotherapy as compared to normal cells?
A. Cancer cells are sensitive to radiation and chemotherapy because they divide more rapidly
B. Cancer cells are less resistant to drugs or radiation because once they sustain genetic damage, they either progress through the cell cycle while repair is incomplete and they may undergo apoptosis
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C. Cancer cells are sensitive to radiation and chemotherapy because they divide more slowly
D. Cancer cells are less resistant to drugs or radiation because once they sustain genetic damage, they either arrest the cell cycle until repair is complete or undergo apoptosis
E. Cancer cells are sensitive to radiation and chemotherapy because they will not undergo apoptosis
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Amit Singh,
Center for Tissue Regeneration & Engineering at Dayton (TREND)
Department of Biology, University of Dayton, Dayton, OH, 45469
amit.singh@notes.udayton.edu amitsingh60@gmail.com
Cancer: Where friends turn foe
Normal body cells grow, divide and die in an orderly fashion.
. Cancer cells are different because they continue to divide and grow.
. Cancer cells form as a result of damaged DNA.
Cancer (L. Crab) Statistics . Second most common cause of death in US . One in 3 Americans may die of cancer
US Mortality, 2001
Source: US Mortality Public Use Data Tape 2001, National Center for Health Statistics, Centers for Disease Control and Prevention, 2003.
1. Heart Diseases 700,142 29.0
2. Cancer 553,768 22.9
3. Cerebrovascular diseases 163,538 6.8 4. Chronic lower respiratory diseases 123,013 5.1 5. Accidents (Unintentional injuries) 101,537 4.2 6. Diabetes mellitus 71,372 3.0 7. Influenza and Pneumonia 62,034 2.6 8. Alzheimer’s disease 53,852 2.2 9. Nephritis 39,480 1.6 10. Septicemia 32,238 1.3
Rank Cause of Death No. of deaths % of all deaths
Incidence of new cancer cases & deaths in US
Sarcoma‐rise from
connective tissue such
as muscle or bone and
are more common in
younger people. Carcinomas‐which
occur in epithelial tissue
and are more common
in older people. It
includes lung, breast,
prostate, and colon. Leukemia Lymphoma
What is Cancer? .
Types of Cancer (nature)
1 2 Metastasis ‐ cancer cells penetrate into lymphatic system and blood vessels
Benign tumorsdo not penetrate (invade) adjacent tissues, nor do they spread to distant sites.
They remain localized and surgical excision can be curative in many cases.
In contrast, malignant tumorshave a propensity to invade contiguous tissues.
Moreover, owing to their ability to gain entrance into blood and lymph vessels, cells from a
malignant neoplasm can be transported to distant sites, where subpopulations of malignant
cells take up residence, grow, and again invade as satellite tumors (called metastases).
• Benign tumors generally do not spread by invasion or metastasis
• Malignant tumors are capable of spreading by invasion and metastasis
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2
Growth
pattern
Benign Malignant
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TABLE I Characteristics of Benign and Malignant Tumors
Characteristics Benign Malignant
Growth pattern expansive infiltrative
Rate of growth slow fast
differentiation good atypical, poor
metastasis absent typical
Normal squamous epithelial cells
of the cervix. Uniform shape
with central nucleus.
Abnormal cells (carcinoma in situ)
preinvasive cancer in cervix. Heterogenous
shape & large nuclei
Early detection
can help save
lives or prolong
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Human Genome Project Chromosome X Bioinformatics ~30.000 genes ~300.000 protein ~3.000.000 interaction 1 human cell ~3.000.000.000 bp DNA
Molecular Biology & Informatics
Cancer cell do not grow faster than normal cells
•In normal tissues, the rates of new cell growth
and old cell death are kept in balance
•In cancer, due to loss of normal growth control
this balance is disrupted due to 1) uncontrolled cell growth or
2) loss of apoptosis
Rather, their growth is just uncontrolled
Serum deprivations affect growth of normal and
transformed cells
Cancer cells grow regardless of presence or absence
of exogenous growth factors.
1 fertilized egg 50x1012
Proliferation Differentiation Death
1016cell divisions/lifetime Normal Growth Scenario
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Proliferation Differentiation Death
Transit
Proliferating
Exiting Renewing
Cellular Equilibrium
Proliferation Differentiation Death
Disruption of cellular equilibrium leads to Cancer: Post mitotic Stem cell Differentiated Normal senescent differentiated cell Benign tumor Grade 2 malignancy Grade 3 or 4 malignancy
Stem cells as the target of carcinogens
Malignant cells Normal cell Fourth or later mutation Third mutation Second mutation First mutation
In cancer, both genotype and phenotype keep changing over
time
What causes Cancer?
• Cancer is caused by alterations or mutations in the genetic code • Can be induced in
somatic cells by:
– Carcinogenic chemicals – Radiation – Some viruses
• Heredity - 5%
Hanahan and Weinberg, Cell 100: 57, 2000 Apoptosis
Oncogenes
Tumor Suppressor
Inv. and Mets Angiogenesis
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5 • Cancer is a genetic disease.
–Mutations in genes result in altered proteins –Most cancers result from mutations in somatic cells –Some cancers are caused by mutations in germline cells
What is the molecular basis of cancer?
Standard Dogma
•Proto‐oncogenes (Ras – melanoma)
•Tumor suppressor genes (p53 – various cancers)
Modified Dogma
•Mutation in a DNA repair gene leads to the accumulation
of unrepaired mutations (xeroderma pigmentosum) Theories of cancer genesis
Cancer: genome disease
Cancer: Genome Dısease
•Loss of DNA
•Gain of DNA
•Changes in nucleotides
•Epigenetic effects
Signs for genomic changes in cancer
Changes in chromosome numbers
‐Aneuploidy
Chromosomal changes
‐ Increase in DNA copy number ‐15 different region
‐ Loss in chromosomal ‐200.000 regions
Micro changes ‐ Microsatellite changes ‐ Nucleotide changes
Chromosomal changes in the genome of cancer cells: tip of the iceberg
Terminal Deletion http://www.tokyo-med.ac.jp/genet/cai-e.htm Ring Chromosome Robertsonian Translocation Deletion Reciprocal translocation Isochromosomes Insertion Inversion Duplication
Large deletions or insertions
Chromosomes in breast cancer appear multicolored because they have exchanged genetic material.
SKY chromosome painting: breast cancer Normal SKY chromosomes
are not multicolored.
Abnormal chromosome complement from a breast cancer cell line
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DNA Loss in cancer cells: beyond coincidence.
p53 locus Chromosom al loss: Mostly, it is a sign for the loss of a tumor suppress or gene PTEN locus CDKN2 locus RB1 locus ??? locus Glio blastoma multiformi
Cancer: Genome Dısease
•Loss of DNA
•Gain of DNA
•Changes in nucleotides
•Epigenetic effects
Nucleotide changes in the genome of cancer cells: unseen site of the iceberg
Nucleotide Deletions Nucleotide Insertions Nucleotide Substitutions
http://www.tokyo‐med.ac.jp/genet/cai‐e.htm
Genes Disease Function Inheretance Cancer Risk FA Genes F-A DNA Damage respose ? OR Lösemi
XP Genes
X-P NER Type
DNA Repair OR Skin Ca.
BLM Bloom DNA Helicase ? OR Various cancers
WRN Werner DNA Helicase ? OR Sarcoma
RECQ4 Rothmund-Thomson DNA Helicase OR Sarcoma
MLH1, MSH2, PMS1, PMS2 MMR DNA Repair OD Colon, Endometrium Ca. OR Lösemi, NF1
BRCA1, BRCA2 DNA Repair
OD Breast, Ovary, Prostate, Pancreas
Ca
ATM A-T DNA Damage sense ?
OR Lymphoma, Leukemia OD Breast Ca. ?
p53 Li-Fraumeni DNA Damage sense OD Various cancers
The causes of genomıc changes ın cancer:Hereditary predisposition
Cancer: Genome Dısease
•Loss of DNA
•Gain of DNA
•Changes in nucleotides
•Epigenetic effects
Genetic and Epigenetic Silencing of Tumor Suppressor Genes
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7 Carcinogenic Chemicals
Viruses
Rearrangements (deletion, translocation..) Point mutations
Alters DNA of genes controlling cell proliferation. (Proliferation becomes abnormal)
Cancer Cell
Normal Cell
Damaged DNA
Causes of genomıc changes ın cancer UV Radiation
Replication errors
Approximately 90‐95% of all cancers are sporadic. 5‐10% are inherited.
Tumor Suppressor genes (brakes: both copy loss)
Proto‐oncogenes
(accelerators, one copy loss)
• Oncogenes: mutated forms of proto‐oncogenes.
Proto‐oncogenes code for cellular proteins which regulate
normal cell growth and differentiation.
• Tumor suppressor genes • DNA repair genes
Genes Playing Role in Cancer
Normal
Proto-oncogenes Cell growth and proliferation Tumor suppressor genes
+ -Cancer Mutated or “activated” oncogenes Malignant transformation Loss or mutation of
Tumor suppressor genes ++
Cancer-Associated Mutations Oncogenes
Tumor suppressor genes DNA repair genes Carcinogen – activating genes – deactivating genes Cell cycle genes Cell cycle checkpoint genes Cell death genes Cell signaling genes Cellular differentiation genes Cellular senescence genes Metastasis/invasion genes
The result:
• Overproduction of growth factors
• Flooding of the cell with replication & division signals • Uncontrolled stimulation in the intermediary
pathways
• Cell growth by elevated levels of transcription factors
Revolution in cancer treatment: ‘Smart Bullets Period’
1. Immunotherapy: antibodies or immune cells to attack
tumor cells
2. Inhibit the activity of cancer promoting proteins 3. Prevent the growth of blood vessels that nourish tumor
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8 Spontaneous remission:
Passive Immunotherapy: Treat patients by administering
antibodies
“Humanized antibodies”. Example Herceptin against Her2
for Breast cancer
Rituxan for non‐hodgkins B‐cell lymphoma
Active immunotherapy: involve person’s own immune
system to fight cancer
Genetically modify host immune cell, grow in culture and
then reintroduce into host to kill the cancer cells
HERCEPTIN
STI-571
Multiple mutations lead to colon cancer Genetic changes ‐‐> tumor changes Cellular
Tumor Progression
Stage
0
Colorectal
Cancer
• Known as “cancer in
situ,” meaning the
cancer is located in
the mucosa (moist
tissue lining the colon
or rectum)
• Removal of the polyp
(polypectomy) is the
usual treatment
Stage
I
Colorectal
Cancer
• The cancer has grown
through the mucosa
and invaded the
muscularis (muscular
coat)
• Treatment is surgery
to remove the tumor
and some surrounding
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Stage
II
Colorectal
Cancer
• The cancer has grown beyond
the muscularis of the colon or
rectum but has not spread to
the lymph nodes
• Stage II colon cancer is treated
with surgery and, in some
cases, chemotherapy after
surgery
• Stage II rectal cancer is treated
with surgery, radiation therapy,
and chemotherapy
Stage
III
Colorectal
Cancer
• The cancer has spread to
the regional lymph nodes
(lymph nodes near the
colon and rectum) • Stage III colon cancer is
treated with surgery and
chemotherapy • Stage III rectal cancer is
treated with surgery,
radiation therapy, and
chemotherapy
Stage
IV
Colorectal
Cancer
• The cancer has spread
outside of the colon or
rectum to other areas of
the body
• Stage IV cancer is treated
with chemotherapy.
Surgery to remove the
colon or rectal tumor
may or may not be done • Additional surgery to
remove metastases may
also be done in carefully
selected patients
Activation mechanisms of proto-oncogenes
proto‐oncogene ‐‐> oncogene
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Metaplasia
an adaptive substitution of one type of adult tissue to
another type of adult tissue
under stress a more vulnerable type of tissue will be
replaced by another more capable of withstanding
stress
Dysplasia
An abnormality in cell size, appearance, with or
without a disorganized growth pattern
Neoplasia
A disease of cells characterized by alteration of normal growth regulatory mechanisms
Desmoplasia
The formation and proliferation of connective
tissue in response to neoplastic growth
Definitions
Neoplasm ‐(new growth) abnormal mass of
tissue, the growth of which exceeds and is
uncoordinated with the normal tissues Tumor ‐a non‐specific term meaning lump or
swelling. Often syn. for neoplasm Cancer ‐any malignant neoplasm or tumor Metastasis ‐discontinuous spread of a malignant
neoplasm to distant sites
Neoplastic
progression
• Benign or malignant neoplasms can acquire
increasingly aggressive features
• Most malignant neoplasms arise de novo
• Some malignant neoplasms are thought to be
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Gene expression profiling
of 2 different leukemias
Microarray can be used to determine chopice of treatment.
A good signature based on 70 selected genes can be used a
marker
Patients with poor signature are treated aggressively
Activation of a proto‐oncogene to an oncogene
Role of pRB in regulating cell cycle p53: the guardian of the genome
53K Dalton 1990: tumor suppressor gene, mutation: Li‐Fraumeni syndrome p53 P21 Inhibit
cyclin dependent kinase G1 to S
Bax Initiate apotosis
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Model for p53 function
Cancer cell do not grow faster than normal cells
•In normal tissues, the rates of new cell growth
and old cell death are kept in balance
•In cancer, due to loss of normal growth control
this balance is disrupted due to 1) uncontrolled cell growth or
2) loss of apoptosis
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Oncogenes
proto‐oncogene = ras Oncogene = mutated ras Always activated Always stimulating proliferation
amino acid position
Ras gene 12 59 61 Tumor c-ras (H, K, N) Gly Ala Gln normal cells H-ras Gly Ala Leu lung carcinoma
Val Ala Gln bladder carcinoma K-ras Cys Ala Gln lung carcinoma
Arg Ala Gln lung carcinoma
Val Ala Gln colon carcinoma N-ras Gly Ala Lys neuroblastoma
Gly Ala Arg lung carcinoma Murine sarcoma virus H-ras Arg Thr Gln Harvey strain K-ras Ser Thr Gln Kirsten strain
Amino acid substitutions in Ras family proteins (inactivates GTPase)
p53
• Phosphyorylated p53 activates
transcription of p21gene
• p21 Cdk inhibitor (binds Cdk‐cyclin
complex ‐‐> inhibits kinase
activity)
• Cell cycle arrested to allow DNA to be repaired
Summary of Experience and Reflections
The lesson planning stage worked well. We came up with strong ideas on content that is not covered well in the curriculum in the state of Ohio. Our strategy was to incorporate content that would be personal and useful, therefore interesting to each student. We choose Cancer and cell proliferation for our topic. We used the conference time for brain-storming and initial planning purposes. We consulted the Ohio State standards to make sure that our topic was within the state and local curriculum. Although there is no mention of cancer in the state
standards or local curricular goals, mutations, cell proliferation, and the cell cycle are topics that are required to be covered in the state standards.
We followed the 5 E lesson planning strategy set forth by the conference. For the “engagement” we used statistics from the American Cancer Society to bring to light the affect that cancer has on the world. We used a pre-test to gauge what students knew about cancer. Then we watched a lecture by Burt Vogelstein of HHMI. For the exploration part of the lesson we gave students a small research project where they would look at different types of cancers and produce a power point to inform other students of their findings. The third portion of the lesson was the “explanation” where Dr. Singh brought in a power point and lectured the students on the basics of cancer development. The fourth portion “elaboration” is complete with the students finishing their research on the cancer type that they choose. The evaluation process started with a pre-test and ended with a post-test. The students scored significantly higher on the post test than the pretest. The third part of the evaluation was the power point.
Reflection
I like our lesson plan very well but there are a few things that I would like to improve about it. First I would like to incorporate a lab portion to the lesson plan. This would give students a practical example of how scientist would study the content. Second I would like to change the pre-test and post-test. Adjusting the questions to fit the knowledge base of the students and to fit the standards set forth in the curriculum would be my next revision to our lesson plan. The questions need to be reworded to fit the ability of 9th and 10th grade students. The information given in the lecture needs to better match the questions given in the test. Third I would like to take a field trip to the genetics labs at the University of Dayton. This is a difficult maneuver to pull off. It is difficult to get field trips approved through the high school. The genetics labs are not built to have 90 students trek through them in short amounts of time.
I would like to enhance the power point presentation by uploading them to the schools moodle website. This would allow students to see each others work without taking the time to present them during the week. Having Dr. Singh come in and speak with the students was very rewarding. The students enjoyed having a speaker talk to them about research subjects.
The conference, meetings, food, hotel, travel and work done in Seattle, was interesting and fun. I enjoyed the conference very much. The location was great. I appreciated the atmosphere, weather, the ease of moving around the city, and the interesting things to do in Seattle. The conference itself was pleasing. It had a good mix of speakers, time to get know each other, and working on the ideas for our lesson plan. Content was appropriate and
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understandable and useful. My only suggestion is the speakers from the previous GENA
workshop need to keep in mind that most biology teachers have average students, and we do not teach a genetics course. If we include the cell cycle, Mendelian genetics, human genetics, DNA, applied genetics, and evolution we spend less than one quarter of our school year on genetics. Biology teachers at my high school feel that genetics is very important to the curriculum of biology. However we are required to cover many other topics during the school year. Increasing the amount of time standard biology courses spend on genetics will be a difficult sell with the curriculum directors. Trying to expand the courses available to include a genetics course would allow genetics to be explored in more detail, and keep students and teachers more up to date in the genetics world.
