Sunday, May 4, 2008
Monday, April 28, 2008
Question Set #2 continued...
2. What effect might inbreeding have on this disorder?
A number of extrinsic and intrinsic factors contribute to the development of cancer, a disease still far from satisfactorily controlled in most communities worldwide. Studies have shown that cancer are possibly caused by both recessive and or dominant genes. Furthermore, inbreeding leads to an increase in homozygosity of a population. It also may result in a significantly higher phenotypic expression of deleterious recessive genes. One would think that inbreeding would decrease genetic variance and positive heritability. With this, inbreeding would cause an increase of the likelihood of cancer due to the reduction of genetic diversity. It would also cause a variance of susceptibility of diseases and a weaker immune system to fight the cancer cells.
A number of extrinsic and intrinsic factors contribute to the development of cancer, a disease still far from satisfactorily controlled in most communities worldwide. Studies have shown that cancer are possibly caused by both recessive and or dominant genes. Furthermore, inbreeding leads to an increase in homozygosity of a population. It also may result in a significantly higher phenotypic expression of deleterious recessive genes. One would think that inbreeding would decrease genetic variance and positive heritability. With this, inbreeding would cause an increase of the likelihood of cancer due to the reduction of genetic diversity. It would also cause a variance of susceptibility of diseases and a weaker immune system to fight the cancer cells.
Sunday, April 27, 2008
Question Set 2 Answer # 1 Ayok Monydit
1. What is the estimate of H2 for Cancer? How much influence does selection have on this?
H2 is defined as the proportion of total phenotypic variance at the populatioin level that is contributed by genetic variation. According Nature Reviews Cancer 4, 769-780 (October 2004) the h2 for this prevalent types of cancer are as follows.
Lung h2=0.26
Breast h2=0.27
Prostate=0.42
Colorectal=0.35
According to Carlo Maley, ans assistant professor at Wistar Univeristy, "the dynamics of evolution are fully in play within the environment of a tumor. A tumor cell population is constantly evolving through natural selection. Mutations that aid in the survival and reproduction of cells in a tumor are the things that drive it towards malignancy. When applying chemotrophy (cell chemistry) to a cluster of cancer cells, we are likely to find resistant mutant allele. 3 of Darwin's postulates are important when analyzing the evolution of cancer cells. These factors are genetic variation, heritabilty, and natural selection. Cancer cells are highly variable on a genetic level, no two cells will be completely identicle. Most Varation found in cancer cells is hertibale, that is, it is passed from parent to offspring. This excludes variation that is result of mutation. Last but not least, variation is acted upon by natural selection (some alleles possibly mutants become fixed or lossed). These 3 factors are the guidline for determining wheather a cancer cell will evolve or not.
References
http://www.sciencemuseum.org.uk/on-line/lifecycle/79.asp
http://www.hhmi.org/biointeractive/cancer/cancer_evolution.html
Genetic predisposition to colorectal cancer
Nature Reviews Cancer 4, 769-780 (October 2004)
doi:10.1038/nrc1453
H2 is defined as the proportion of total phenotypic variance at the populatioin level that is contributed by genetic variation. According Nature Reviews Cancer 4, 769-780 (October 2004) the h2 for this prevalent types of cancer are as follows.
Lung h2=0.26
Breast h2=0.27
Prostate=0.42
Colorectal=0.35
According to Carlo Maley, ans assistant professor at Wistar Univeristy, "the dynamics of evolution are fully in play within the environment of a tumor. A tumor cell population is constantly evolving through natural selection. Mutations that aid in the survival and reproduction of cells in a tumor are the things that drive it towards malignancy. When applying chemotrophy (cell chemistry) to a cluster of cancer cells, we are likely to find resistant mutant allele. 3 of Darwin's postulates are important when analyzing the evolution of cancer cells. These factors are genetic variation, heritabilty, and natural selection. Cancer cells are highly variable on a genetic level, no two cells will be completely identicle. Most Varation found in cancer cells is hertibale, that is, it is passed from parent to offspring. This excludes variation that is result of mutation. Last but not least, variation is acted upon by natural selection (some alleles possibly mutants become fixed or lossed). These 3 factors are the guidline for determining wheather a cancer cell will evolve or not.
References
http://www.sciencemuseum.org.uk/on-line/lifecycle/79.asp
http://www.hhmi.org/biointeractive/cancer/cancer_evolution.html
Genetic predisposition to colorectal cancer
Nature Reviews Cancer 4, 769-780 (October 2004)
doi:10.1038/nrc1453
Wednesday, April 16, 2008
Update on Patrick Swayze: On a side note
An update on Patrick Swayze and response against rumors.
By Joal Ryan
Wed, 5 Mar 2008 02:34:20 PM PST
Patrick Swayze is undergoing treatment for pancreatic cancer but does not have just weeks to live, the actor's reps and doctor said Wednesday.
"Patrick has a very limited amount of disease and he appears to be responding well to treatment so far," Dr. George Fisher, Swayze's personal physician, said in a statement. "All of the reports stating the timeframe of his prognosis and his physical side effects are absolutely untrue."
Fisher's remarks were in rebuttal to the National Enquirer, which broke the news of Swayze's illness on its website and said the Dirty Dancing star had recently dropped 20 pounds and been given only five weeks to live.
"Patrick is continuing his normal schedule during this time," the actor's reps said, "which includes working on upcoming projects."
Speaking to E! News, Swayze's mother, dancer and choreographer Patsy Swayze, echoed the optimism of the star's doctor.
"I don't really want to talk about it, but I know he's sick," Patsy Swayze said. "But he has great doctors and a great prognosis, and that's all I can say."
According to the Pancreatic Cancer Action Network, pancreatic cancer is the deadliest of the leading cancers. Fewer than 5 percent of patients live more than five years after diagnosis.
Swayze, 55, filmed an A&E pilot in December called The Beast, in which he stars as an unconventional, undercover FBI agent. The network said Wednesday it was still considering the show for pickup next season.
As recently as Monday, Swayze was spotted running an errand at a Simi Valley, California, dance studio. An employee there told E! News the actor "looked good" and not at all as if he'd lost a lot of weight.
Producer Bobby Schwartz, who worked with Swayze last summer on the as yet unreleased indie drama Powder Blue, likewise vouched for the star's fitness on that set.
"When we were shooting, the guy looked very young, very healthy, very energetic," Schwartz told E! News.
Swayze is best known for a string of hits in the 1980s and 1990s that included Ghost, Point Break, Road House and the career-changer, Dirty Dancing, in which he played Catskills bad boy Johnny Castle.
—Additional reporting by Whitney English
(Originally published Mar. 5, 2008 at 2:04 p.m. PT.)
Monday, April 14, 2008
Kim's Reflection: p53 genes, vital in development
The articles were interesting as well as thought provoking. I thought they were good choices for our service learning project and helped in thinking beyond just cancer, and more towards the different facets of it. Some parts of the paper were a bit difficult to read, but was doable. P53 genes function at conserving stability by preventing genome mutation. Nevertheless, it is hypothesized that the p53 play an important role in neoplastic development. Its interesting to find that a person inherits only one functional copy of this important gene from their parents and through the mutation of this gene, it may lead to life-threatening diseases. From the Lee and Bernstein article, it states that it is unclear how the p53 mutations lead to neoplastic development, however; I found it a bit trivial to study the p53 gene in mice. Would continuing to study mice help in being able to control these genes? Are the p53 gene in mice similar to humans, if so to what degree? The paper, written by Lee and Bernstein was written in 1993, are there any new studies that show any different data or promising data that is able to control this gene?
P53 Article Relection ~ Brice Austin
I found the articles interesting; although, confusing at times. The main "take-home" point, I belive, is that the transgenic p53 mutations can cause cancerous tumors. P53 is responsible for neoplastic deveopment. This means that they create many other regulatory genes. In mice the wild type p53 protein keeps the p53 gene from mutating, lessening results tumors. Is there anything similar to this protein in humans? Commonly tumors still develop because the p53 tarnsgenic form still suppreses the activity of the wild type protein. Can the protein be added to or made stronger?
Thursday, April 10, 2008
Ayok: What I have learned so far
The article I found most intresting to read was Lee and Bernstein's "P53 mutations increaces resistance to ionizing radiation."
The P53 gene is thought to play an important role in neoplastic development. It is thought to function as a cell cycle marker after irradiation, suggesting that mutant forms of p53 gene significantly increaces cellular resistance to a variety of hemtapoietic cell lineages(p53-2,p53-3,pL53-2). Researchers believe that p53 acts in a dominant negative manner to suppress the activity of the wild type p53 protein. Wild type p53 has been postulated to play a role in DNA repair. In this particular article, transgenic mice expressing mutant alleles of p53 were used to measure the resistance of hematopoietic cells to radition. to assess the effects of the mutant allele, the ability of radiatioon to prevent colony formation of cancer cells in a variety of tissues were observed(spleen, liver, lung, thymus). Results showed that mice that were hemizygous or either transgene showed no abnormatlities but infactt ad high incidence of lymphiod tumors. This research depicted how radiation can effect the activiny of mutant forms of p53 which interm effects how succesful radiation is in treating cancer. After addition research, I unearthed some intersting facts about the P53 gene.
Intresting facts
1. If a person inherits only one functional copy of the p53 gene from their parents, they are predisposed to cancer and usually develop several independent tumors in a variety of tissues in early adulthood, a condition known as Li-Fraumeni syndrome.
2. How cancer starts?
When there is DNA damage, the p53 gene suspends the cell cycle until the damage can be repaired. If there is a mutation in p53, the cell cycle continues unrestrained and reproduces the damaged DNA, leading to uncontrolled cell proliferation and cancer tumors. Cancer develops as a result of the cell with damaged DNA dividing, the damaged DNA being replicated and passed to each newly produced daughter cell.
3. p53 becomes activated in response to a variety of factors which include but is not limited to DNA damage (induced by either UV, IR or chemical agents,such as hydrogen peroxide). Other inducive factors are ribonucleotide depletion and deregulated oncogene expression. This activation is marked by two major events. Firstly, the half-life of the p53 protein is increased drastically, leading to a quick accumulation of p53 in stressed cells. Secondly, a conformational change forces p53 to take on an active role as a transcription regulator.
The P53 gene is thought to play an important role in neoplastic development. It is thought to function as a cell cycle marker after irradiation, suggesting that mutant forms of p53 gene significantly increaces cellular resistance to a variety of hemtapoietic cell lineages(p53-2,p53-3,pL53-2). Researchers believe that p53 acts in a dominant negative manner to suppress the activity of the wild type p53 protein. Wild type p53 has been postulated to play a role in DNA repair. In this particular article, transgenic mice expressing mutant alleles of p53 were used to measure the resistance of hematopoietic cells to radition. to assess the effects of the mutant allele, the ability of radiatioon to prevent colony formation of cancer cells in a variety of tissues were observed(spleen, liver, lung, thymus). Results showed that mice that were hemizygous or either transgene showed no abnormatlities but infactt ad high incidence of lymphiod tumors. This research depicted how radiation can effect the activiny of mutant forms of p53 which interm effects how succesful radiation is in treating cancer. After addition research, I unearthed some intersting facts about the P53 gene.
Intresting facts
1. If a person inherits only one functional copy of the p53 gene from their parents, they are predisposed to cancer and usually develop several independent tumors in a variety of tissues in early adulthood, a condition known as Li-Fraumeni syndrome.
2. How cancer starts?
When there is DNA damage, the p53 gene suspends the cell cycle until the damage can be repaired. If there is a mutation in p53, the cell cycle continues unrestrained and reproduces the damaged DNA, leading to uncontrolled cell proliferation and cancer tumors. Cancer develops as a result of the cell with damaged DNA dividing, the damaged DNA being replicated and passed to each newly produced daughter cell.
3. p53 becomes activated in response to a variety of factors which include but is not limited to DNA damage (induced by either UV, IR or chemical agents,such as hydrogen peroxide). Other inducive factors are ribonucleotide depletion and deregulated oncogene expression. This activation is marked by two major events. Firstly, the half-life of the p53 protein is increased drastically, leading to a quick accumulation of p53 in stressed cells. Secondly, a conformational change forces p53 to take on an active role as a transcription regulator.
Wednesday, March 26, 2008
Questions
Questions – p53 and Cancer
1.The p53 gene is one of the most widely mutated genes in human cancers resulting in a protein with a sufficient function as a transcription factor resulting in a cancer cell with an enhanced survival potential when mutated. The transcription function of p53 is stress activated resulting in is an inducible activity that responds to the evolving microenvironment of the cancer cell. They are also regulatory genes whose products do control the expression of other genes. It is so that changes in p53 and its related transcription factors can lead to cascading consequences because they can induce mutations. These mutations can lead to transformation of normal cells to cancerous cells. According to the article, p53 also functions as a tumor suppressor as well as play a vital role in neoplastic development. To sum up, with p53 playing such a significant role any mutation could and or would result it a chain of consequences.
2. It is quite informative to study cancer and its implications in mice because the p53 gene and its isoforms are apparent in mice as well as humans. P53 is important because it is thought to play a role in neoplastic development. The mutation of the p53 germ line can be seen in Li-Fraumeni human patients. Mice are transgenic for p53 and have short generations, which aids in research development for humans.
3. The p53 gene family members express multiple mRNA variants due to multiple splicing and alternative promoters. This gene family is paralogous, meaning that they are from the same family of genes. The isoforms of p53, p63 and p73, gained different functions from expressing different p53 proteins, which require a different domain of protein. The different domain accounts for the different function of the isoform.
4. Protein folding and mis-folding are important to study because they help in determining relationships of different folding mechanisms and their results. Different folding sequences can lead to a deeper understanding of the way a disease, such as cancer, work and can ultimately provide a pathway to treatment or a cure. The shape of the folded protein can also be used to understand its function and design drugs to influence the processes that it is involved in. Nevertheless, proper protein folding is essential to function; mis-folding or failure to fold is essential in research of diseases as well as the genes that are involved.
5. Typically, p53 is a “tumor-suppressor gene” which indicates that if it loses function, tumors will result. However, expression of some of the isoforms of p53 can actually contribute to tumor formation. Nevertheless, not all mutations in p53 result in a loss of function. Consequently, making it incredibly difficult to understand the clinical role of p53. Considering our interviewee Norma, it is significant to determine the status of p53 because it assists in being able to keep the cancer in remission and maintain no sudden mutations and or spread of the pancreatic cancer. Being that the p53 has so many functions, keeping in mind of it experimentally and biologically assessing gene expression in relation to p53 status may provide prognostic and biologically relevant consequences.
Expression of p53 in Pancreatic Cancer Cells
Overexpression of Pancreatic Cancer in pancreas due to mutations of p53 gene
1.The p53 gene is one of the most widely mutated genes in human cancers resulting in a protein with a sufficient function as a transcription factor resulting in a cancer cell with an enhanced survival potential when mutated. The transcription function of p53 is stress activated resulting in is an inducible activity that responds to the evolving microenvironment of the cancer cell. They are also regulatory genes whose products do control the expression of other genes. It is so that changes in p53 and its related transcription factors can lead to cascading consequences because they can induce mutations. These mutations can lead to transformation of normal cells to cancerous cells. According to the article, p53 also functions as a tumor suppressor as well as play a vital role in neoplastic development. To sum up, with p53 playing such a significant role any mutation could and or would result it a chain of consequences.
2. It is quite informative to study cancer and its implications in mice because the p53 gene and its isoforms are apparent in mice as well as humans. P53 is important because it is thought to play a role in neoplastic development. The mutation of the p53 germ line can be seen in Li-Fraumeni human patients. Mice are transgenic for p53 and have short generations, which aids in research development for humans.
3. The p53 gene family members express multiple mRNA variants due to multiple splicing and alternative promoters. This gene family is paralogous, meaning that they are from the same family of genes. The isoforms of p53, p63 and p73, gained different functions from expressing different p53 proteins, which require a different domain of protein. The different domain accounts for the different function of the isoform.
4. Protein folding and mis-folding are important to study because they help in determining relationships of different folding mechanisms and their results. Different folding sequences can lead to a deeper understanding of the way a disease, such as cancer, work and can ultimately provide a pathway to treatment or a cure. The shape of the folded protein can also be used to understand its function and design drugs to influence the processes that it is involved in. Nevertheless, proper protein folding is essential to function; mis-folding or failure to fold is essential in research of diseases as well as the genes that are involved.
5. Typically, p53 is a “tumor-suppressor gene” which indicates that if it loses function, tumors will result. However, expression of some of the isoforms of p53 can actually contribute to tumor formation. Nevertheless, not all mutations in p53 result in a loss of function. Consequently, making it incredibly difficult to understand the clinical role of p53. Considering our interviewee Norma, it is significant to determine the status of p53 because it assists in being able to keep the cancer in remission and maintain no sudden mutations and or spread of the pancreatic cancer. Being that the p53 has so many functions, keeping in mind of it experimentally and biologically assessing gene expression in relation to p53 status may provide prognostic and biologically relevant consequences.
Tuesday, March 18, 2008
Interview
Intro . . .
Norma Tibbetts is a pancreatic cancer survivor who battled this treacherous cancer for eighteen years. When first diagnosed in 1990, her doctor gave her three months to live. Determine to not let it conquer her, she did everything in her power to conquer it and won her battle with cancer in 2008. Being the first to receive the Whipple surgery at the Shawnee Mission Medical Center, her pancreatic cancer was treated. Today Norma is helping to change the view of pancreatic cancer and raise awareness to the public. It is currently the lowest funded type of cancer research but has the second highest mortality rate. Norma Tibbetts helps to do her part by working in affiliation with the Bloch Cancer Society, where she takes calls and talks to people have been diagnosed with the condition that she once battled.
When were you diagnosed?
In 1990.
How were you diagnosed?
By a doctor who did a CT scan. Usually there are no tale-tell signs of pancreatic cancer until large amounts of pain are experienced due to the cancer infested pancreas.
What are the distinct symptoms that caught your attention?
Very specific stomach area pains. Not very many tests for pancreatic cancer, usually not caught until the cancer spreads to other parts of the body causing problems to be noticed in these regions of body.
How long did you battle cancer?
Battled cancer from 1990-2008
Which form of therapy did you use and why?
Whipple surgery. Whipple surgery is a radical surgery in which as much as 95% of the pancreas is removed to cease cancer production in the organ. In addition 75% of stomach is removed, constituting 14-16 inches of small intestine as well as the entire spleen being taken from the body. Because her pancreatic cancer involved islet cells, the cancer was very slow growing and the lymph nodes were not involved. Therefore, chemotherapy was not necessary. She had surgical therapy every three months for first 3 years, then every six months for the next 5 years. Now she is being evaluated once yearly and free of pancreatic cancer.
Before treatment what obstacles did doctors say would cause much difficulty?
Due to slow growing nature there would be no option for chemotherapy. Once the digestive system would be removed she would be limited in food consumption and become diabetic due to removal of majority of pancreas. She cannot consume foods high in fat content or that are difficult to digest such as fresh fruits and vegetables as well as whole wheat.
How did your body respond to treatment?
Took much recovery time. Trail-and-error when it came to fine tuning what could and could not be eaten when trying to establish a new diet. This is due to the fact that digestive enzymes are not being produced due to removal of the pancreas. Specific pills help to balance the problem. General feelings of nausea, discomfort and flashing were all side affects of the surgery.
Did physiological changes cause you to stop responding to treatments that you initially responded to?
No, continued response throughout treatment.
Have you heard of immunotherapy (body gets rid of cancer cells by ingesting them)?
Yes
Was immunotherapy offered as a treatments source?
No available or developed enough in pancreatic cancer field at time.
Were you offered any experimental drugs, such as recently diagnosed actor Patrick Swayze was?
No. Only some experimental drugs to help with general side affects of surgical therapy.
Why is pancreatic cancer often thought of as one of the most terminal forms of cancer?
People who suffer from pancreatic cancer are most often diagnosed late because there are no real tests for this type of cancer as well as not many symptoms. By the common time of diagnosis the cancer has already spread throughout the body causing even more damage. For thus reason many people don’t get treated and unfortunately leads to the second highest mortality rate. Pancreatic cancer is also the lowest funded type of cancer research.
Norma Tibbetts is a pancreatic cancer survivor who battled this treacherous cancer for eighteen years. When first diagnosed in 1990, her doctor gave her three months to live. Determine to not let it conquer her, she did everything in her power to conquer it and won her battle with cancer in 2008. Being the first to receive the Whipple surgery at the Shawnee Mission Medical Center, her pancreatic cancer was treated. Today Norma is helping to change the view of pancreatic cancer and raise awareness to the public. It is currently the lowest funded type of cancer research but has the second highest mortality rate. Norma Tibbetts helps to do her part by working in affiliation with the Bloch Cancer Society, where she takes calls and talks to people have been diagnosed with the condition that she once battled.
When were you diagnosed?
In 1990.
How were you diagnosed?
By a doctor who did a CT scan. Usually there are no tale-tell signs of pancreatic cancer until large amounts of pain are experienced due to the cancer infested pancreas.
What are the distinct symptoms that caught your attention?
Very specific stomach area pains. Not very many tests for pancreatic cancer, usually not caught until the cancer spreads to other parts of the body causing problems to be noticed in these regions of body.
How long did you battle cancer?
Battled cancer from 1990-2008
Which form of therapy did you use and why?
Whipple surgery. Whipple surgery is a radical surgery in which as much as 95% of the pancreas is removed to cease cancer production in the organ. In addition 75% of stomach is removed, constituting 14-16 inches of small intestine as well as the entire spleen being taken from the body. Because her pancreatic cancer involved islet cells, the cancer was very slow growing and the lymph nodes were not involved. Therefore, chemotherapy was not necessary. She had surgical therapy every three months for first 3 years, then every six months for the next 5 years. Now she is being evaluated once yearly and free of pancreatic cancer.
Before treatment what obstacles did doctors say would cause much difficulty?
Due to slow growing nature there would be no option for chemotherapy. Once the digestive system would be removed she would be limited in food consumption and become diabetic due to removal of majority of pancreas. She cannot consume foods high in fat content or that are difficult to digest such as fresh fruits and vegetables as well as whole wheat.
How did your body respond to treatment?
Took much recovery time. Trail-and-error when it came to fine tuning what could and could not be eaten when trying to establish a new diet. This is due to the fact that digestive enzymes are not being produced due to removal of the pancreas. Specific pills help to balance the problem. General feelings of nausea, discomfort and flashing were all side affects of the surgery.
Did physiological changes cause you to stop responding to treatments that you initially responded to?
No, continued response throughout treatment.
Have you heard of immunotherapy (body gets rid of cancer cells by ingesting them)?
Yes
Was immunotherapy offered as a treatments source?
No available or developed enough in pancreatic cancer field at time.
Were you offered any experimental drugs, such as recently diagnosed actor Patrick Swayze was?
No. Only some experimental drugs to help with general side affects of surgical therapy.
Why is pancreatic cancer often thought of as one of the most terminal forms of cancer?
People who suffer from pancreatic cancer are most often diagnosed late because there are no real tests for this type of cancer as well as not many symptoms. By the common time of diagnosis the cancer has already spread throughout the body causing even more damage. For thus reason many people don’t get treated and unfortunately leads to the second highest mortality rate. Pancreatic cancer is also the lowest funded type of cancer research.
Wednesday, February 27, 2008
Pre-Interview
Our interview process for our Service Learning Project has been deemed a little bit more difficult than we expected. After several emails and phone calls to prospective candidates for the interview, we finally received a response from a Pancreatic Cancer survivor. Our interview isn’t for a few more weeks, so we thought we would leave some brief information about Pancreatic Cancer.
Pancreatic cancer is relatively rare but deadly; most patients die within a year of diagnosis, and it is the fourth leading cause of cancer deaths in the US. At least 10% of pancreatic cancers is thought to be caused by inherited genetic mutations.
Pancreatic Cancer: A disease in which malignant cells are found in the tissues of the pancreas. Also called exocrine cancer.
It is estimated for 2008, that out of 37, 700 new cases of pancreatic cancer patients, over 34,000 of them will die. In up to 95% of cases, pancreatic cancer arises from the exocrine portion of the organ. The least common exocrine cancer comes from acinar cells. Most of the exocrine tumors are from ductal cells those of which line the pancreatic ducts. These tumors are classified as carcinomas, a word that refers to tumors arising from a lining cell.
Treatment:
Pancreatic cancer can be cured only when it is found at an early stage, before it has spread. Surgery for cancer of the pancreas is only offered to patients whose tumor is localized. Only about 15-20% of those individuals with pancreatic cancer will be found to be eligible for surgery. In these cases, surgical removal of the tumor from the pancreas gives the best chance for a cure and generally confers a better overall prognosis in contrast to medical therapy. However, other treatments may be able to control the disease and help patients live a little bit longer and feel better. When a cure or control of the disease is not possible, some patients and their doctors choose palliative therapy. Palliative therapy aspires to improve quality of life by controlling pain and other problems caused by this disease.
References:
http://www.mayoclinic.com/health/pancreatic-cancer/DS00357
http://www.cancer.org/docroot/home/index.asp?level=0
http://www.pancreatica.org/
http://www.oncolink.com/types/article.cfm?c=4&s=7&ss=49&id=1739
http://www.nlm.nih.gov/medlineplus/pancreaticcancer.html
http://www.pancan.org/
http://www.cancer.org/docroot/CRI/content/CRI_2_4_1X_What_is_pancreatic_cancer_34.asp
Cancer
According to the American Cancer Society, in 2007 7.6 million people died from cancer. Cancer is a term for deadly diseases in which abnormal cells divide uncontrollably. There are many instances when these cells are metastatic, in which it spreads to other locations in the body, as well as invasive, in which these abnormal cells invade and destroy nearby tissue.
There are several core types of cancer. They are divided into three groups, carcinoma, sarcoma, and lymphoma. Carcinoma is cancer that begins in the skin or in tissues that line or cover internal organs. Sarcoma is cancer that begins in bone, cartilage, fat, muscle, blood vessels, or other connective or supportive tissue. Leukemia is cancer that starts in blood-forming tissue such as the bone marrow, and causes large numbers of abnormal blood cells to be produced and enter the bloodstream. Lymphoma is cancer that begins in the cells of the immune system.
Cancer is usually differentiated according to the tissue from which the cancerous cells originate along with the normal cell type they most resemble. Most cancers can be treated and some cured, depending on the specific type, location, and stage. Once diagnosed, cancer is usually treated with a combination of radiotherapy, chemotherapy and or surgery, depending on the extremity of the cancer. However, as research progresses, treatments are becoming more specific for different varieties of cancer.
Cancer Cells Dividing
Breast Cancer Cells
References:
http://www.cancer.org/docroot/home/index.asp
http://www.cancer.gov/
http://www.nlm.nih.gov/medlineplus/cancer.html
http://cancer.about.com/
http://familydoctor.org/online/famdocen/home/common/cancer/treatment/721.html
There are several core types of cancer. They are divided into three groups, carcinoma, sarcoma, and lymphoma. Carcinoma is cancer that begins in the skin or in tissues that line or cover internal organs. Sarcoma is cancer that begins in bone, cartilage, fat, muscle, blood vessels, or other connective or supportive tissue. Leukemia is cancer that starts in blood-forming tissue such as the bone marrow, and causes large numbers of abnormal blood cells to be produced and enter the bloodstream. Lymphoma is cancer that begins in the cells of the immune system.
Cancer is usually differentiated according to the tissue from which the cancerous cells originate along with the normal cell type they most resemble. Most cancers can be treated and some cured, depending on the specific type, location, and stage. Once diagnosed, cancer is usually treated with a combination of radiotherapy, chemotherapy and or surgery, depending on the extremity of the cancer. However, as research progresses, treatments are becoming more specific for different varieties of cancer.
References:
http://www.cancer.org/docroot/home/index.asp
http://www.cancer.gov/
http://www.nlm.nih.gov/medlineplus/cancer.html
http://cancer.about.com/
http://familydoctor.org/online/famdocen/home/common/cancer/treatment/721.html
Monday, February 4, 2008
Day One
We decided on our topic of interest today and thought cancer would be most interesting. Though we are a little bit overwhelmed, we are taking it one day at a time. With our grid projects already running, our next task at hand is deciding who we are going to interview as well as the questions we are going to ask. Until then...
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