by CharlesC
Posted by Christina
News Article:Health Day (Apr 26, 2007)"Scientists spot mechanism behind lung cancer drug resistance.
"Primary Scientific News Article:Science (May18, 2007) Vol.316.no.5827,pp1039-1043
Posted by cadeta
News Article:Impaired gene helps non-small cell lung cancer resist drug, Biotech Business Week 2006.
Primary ArticleFunctional characterization of the candidate tumor suppressor gene NPRL2/G21 located in 3p21.C3. Cancer research 64, 438-6433, September 15, 2004. American Association for Cancer Research.
After reviewing everyone blogs i noticed a similarity between cell proliferation and the discovery of a new therapuetic drug being studied for a particular type of cancer . But their were two articles in the blog that caught my attention . One was titled "Drug Resistant Lung Cancer" by Christina and the other "Genes give clue to lung Cancer" by cadeta. Instead of stating that reaserchers are coming up with a development for a therapuetic drug on cancer, this article discusses how a drug to treat lung cancer can be resistant. In the blog written by christina, it states how researchers developed to understand that a MET amplification was found in lung cancer patients that had developed a drug resistance to the two growth factor receptor kinase inhibitors. These kinase inhibitors have shown in recent studies that they may help with the treatment in lung cancer.
The common molecular event occurs in "Genes give a clue to lung cancer". just like how reaserachers found MET amplification in patients with EGFR, which are becoming resistant to growth factor receptor Kinases inhibitors, the occurance of cell amplification, and resistance to a drug for the treatment in lung cancer but was found in genes. Both of the articles discussses the cell proliferation within tumor supressor genes and the effect on how growth factor receptors play a key role on how the treatment for cancer responds to to them.
After the discovery of a certain gene like NPRL2 having to do with the resistant to lung cancer therapy, will this help with other cancer treatments?
Are their particular growth factor kinases inhibitors, like the ones Gefitinib and erlotinib naturally found in most diagnosed with cancer?
Tuesday, February 19, 2008
Monday, February 18, 2008
BLOG COMPARISONS
Blog Post1:
IKBKE gene amplification is seen loud and clear in breast cancer tumors!
Primary Article:
Boehm, Jesse S. et. al (2007). Integrative Genomic Approaches Identify IKBKE as a Breast Cancer Oncogene. Cell Press Vol. 129, pp. 1065-1079
Blog Post 2:
Can we finally stop breast cancer from spreading?!
Primary Article:
Xiaoming Ju, Sanjay Katiyar, Chenguang Wang, Manran Liu, Xuanmao Jiao, Shengwen Li, Jie Zhou, Jacob Turner, Michael P. Lisanti, Robert G. Russell, Susette C. Mueller, John Ojeifo, William S. Chen, Nissim Hay, and Richard G. Pestell. (2007, May). Akt1 Governs Breast Cancer Progression In Vivo. Proceedings of the National Academy of Sciences, 104: 7438 – 7443.
Summary:
These two blog posts stood out to me the most because of the way they were so closely related. When I was reading the summaries it seemed as if the two articles could have both sited the other article as a secondary source. The first blog post talks about breast cancer and how the survival of breast cancer was due to the mutation of the gene IKBE. It describes the experiment that the researchers conducted to search the pathway of the IKBE gene and find out where the mutation occurs that leads to the vitality of breast cancer in general.
The second blog post talks about there ever being a cure for cancer. It mainly discussed the fact that researchers found that AKT1 which is involved in the pathway of IKBE was the key to finding a way to sustain breast cancer so that not as may women were dying from the disease. It also talks about how breast cancer is one of leading cancers in America which is also true. It was basically extremely interesting to me how the two articles went hand in hand with one another.
Questions:
1. Did these two articles ever site each other as sources?
2. What new research is being done in breast cancer research?
3. What is the connection between IKBE and AKT1?
IKBKE gene amplification is seen loud and clear in breast cancer tumors!
Primary Article:
Boehm, Jesse S. et. al (2007). Integrative Genomic Approaches Identify IKBKE as a Breast Cancer Oncogene. Cell Press Vol. 129, pp. 1065-1079
Blog Post 2:
Can we finally stop breast cancer from spreading?!
Primary Article:
Xiaoming Ju, Sanjay Katiyar, Chenguang Wang, Manran Liu, Xuanmao Jiao, Shengwen Li, Jie Zhou, Jacob Turner, Michael P. Lisanti, Robert G. Russell, Susette C. Mueller, John Ojeifo, William S. Chen, Nissim Hay, and Richard G. Pestell. (2007, May). Akt1 Governs Breast Cancer Progression In Vivo. Proceedings of the National Academy of Sciences, 104: 7438 – 7443.
Summary:
These two blog posts stood out to me the most because of the way they were so closely related. When I was reading the summaries it seemed as if the two articles could have both sited the other article as a secondary source. The first blog post talks about breast cancer and how the survival of breast cancer was due to the mutation of the gene IKBE. It describes the experiment that the researchers conducted to search the pathway of the IKBE gene and find out where the mutation occurs that leads to the vitality of breast cancer in general.
The second blog post talks about there ever being a cure for cancer. It mainly discussed the fact that researchers found that AKT1 which is involved in the pathway of IKBE was the key to finding a way to sustain breast cancer so that not as may women were dying from the disease. It also talks about how breast cancer is one of leading cancers in America which is also true. It was basically extremely interesting to me how the two articles went hand in hand with one another.
Questions:
1. Did these two articles ever site each other as sources?
2. What new research is being done in breast cancer research?
3. What is the connection between IKBE and AKT1?
Oncogenes at it Again
Posts:
IKBKE gene amplification is seen loud and clear in breast cancer tumors!
Primary paper:
Boehm, Jesse S. et al (2007). Integrative Genomic Approaches Identify IKBKE as a Breast Cancer Oncogene. Cell Press Vol.129, pp.1065-1079
Leukemia Patients with KIT-D816 Mutations.
Primary Paper:
Schnittger, S. et al (2006). KIT-D816 Mutations in AML1-ETO-Positive AML are associated with impaired event-free and overall survival.
At face value, what sparked the interest on reflecting on these two articles was the fact that they are both not only caused by mutations, which we know is what gives rise to cancer, but they both can be linked to specific oncogenes. These particular mutations give rise to types of breast cancer and acute myeloid leukemia that can be categorized as “gain-of-function” mutations as opposed to “loss-of-function” which is the category that for instance a tumor suppressor gene would fall under because the gene can no longer suppress the growth or development of tumors. In studying any type of cancer it is important to maybe make this a primary distinction in order to conduct more focused research.
The mutation being examined in breast cancer occurs in the IKBKE caused by gene amplification leading it to function as an oncogene. In terms of acute myeloid leukemia, KIT is a proto-oncogene that when converted causes the D816 which becomes KIT –D816. It is important to note that both IKBKE and KIT-D816 starts off as normal genes. Mutations cause for these once normal genes to become oncogenes which are directly linked to development of any type of cancer. This is one of the first points emphasized in Cancer Biology.
After reading both these blogs a few questions did rise such as if these mutations are only specific to specific forms of breast cancer and leukemia? This then leads me to wonder how many types of these cancers exist. Are there any studies that are looking at the factors that contribute to the occurrence of these mutations; are they environmental or genetic or both?
IKBKE gene amplification is seen loud and clear in breast cancer tumors!
Primary paper:
Boehm, Jesse S. et al (2007). Integrative Genomic Approaches Identify IKBKE as a Breast Cancer Oncogene. Cell Press Vol.129, pp.1065-1079
Leukemia Patients with KIT-D816 Mutations.
Primary Paper:
Schnittger, S. et al (2006). KIT-D816 Mutations in AML1-ETO-Positive AML are associated with impaired event-free and overall survival.
At face value, what sparked the interest on reflecting on these two articles was the fact that they are both not only caused by mutations, which we know is what gives rise to cancer, but they both can be linked to specific oncogenes. These particular mutations give rise to types of breast cancer and acute myeloid leukemia that can be categorized as “gain-of-function” mutations as opposed to “loss-of-function” which is the category that for instance a tumor suppressor gene would fall under because the gene can no longer suppress the growth or development of tumors. In studying any type of cancer it is important to maybe make this a primary distinction in order to conduct more focused research.
The mutation being examined in breast cancer occurs in the IKBKE caused by gene amplification leading it to function as an oncogene. In terms of acute myeloid leukemia, KIT is a proto-oncogene that when converted causes the D816 which becomes KIT –D816. It is important to note that both IKBKE and KIT-D816 starts off as normal genes. Mutations cause for these once normal genes to become oncogenes which are directly linked to development of any type of cancer. This is one of the first points emphasized in Cancer Biology.
After reading both these blogs a few questions did rise such as if these mutations are only specific to specific forms of breast cancer and leukemia? This then leads me to wonder how many types of these cancers exist. Are there any studies that are looking at the factors that contribute to the occurrence of these mutations; are they environmental or genetic or both?
WNT signaling pathway
Posted By: Minerva B
Primary Scientific Article:
Gumz, M.L. et al. (2007) Secreted Frizzled-Related Protein 1 Loss Contributes to Tumor Phenotype of Clear Cell Renal Cell Carcinoma. Clinical Cancer Research; 13(16)
Gumz, M.L. et al. (2007) Secreted Frizzled-Related Protein 1 Loss Contributes to Tumor Phenotype of Clear Cell Renal Cell Carcinoma. Clinical Cancer Research; 13(16)
Blog Post #2 GPRC5A Can Be the Key to Lung Cancer
Posted By: MON
Primary Scientific Article:
Primary scientific article:Tao, Q., Fujimoto, J., Men, T., Ye, X., Deng, J., Lacroix, L. & et al. (2007, November 13 ). Identification of the Retinoic Acid – Inducible Gprc5aAs a New Lung Tumor Suppressor Gene. Journal of the National Cancer Institute, 99(22), 1668-1682.
Blog Comments
From a molecular biology standpoint, the blog that I particularly find to be interesting is Minerva B’s blog on clear cell renal carcinoma (ccRCC). I decided to comment on this blog because ccRCC is a cancer located in the kidney’s that’s on the rise. Like Minerva said in her blog, it has resistance to radiation and chemotherapy which makes it very expensive and difficult to treat. It’s a challenge to conduct studies and tests on difficult cancers like ccRCC. This post explains the studies that researchers conducted and the results that they were able to prove about the sFrP1 (Secreted Frizzled-Related Protein 1), which is a tumor suppressor gene. What I found interesting is that when the gene is turned off transcription factors are blocked. Scientist made the educated guess that if the sFRP1 gene activated by turning it on. Activating it will lessen the growth of the tumor and can even get rid of it. I find that to be a tremendous discovery, thats one of the cancers that we can possibly treat if detected early.
Primary scientific article:Tao, Q., Fujimoto, J., Men, T., Ye, X., Deng, J., Lacroix, L. & et al. (2007, November 13 ). Identification of the Retinoic Acid – Inducible Gprc5aAs a New Lung Tumor Suppressor Gene. Journal of the National Cancer Institute, 99(22), 1668-1682.
Blog Comments
From a molecular biology standpoint, the blog that I particularly find to be interesting is Minerva B’s blog on clear cell renal carcinoma (ccRCC). I decided to comment on this blog because ccRCC is a cancer located in the kidney’s that’s on the rise. Like Minerva said in her blog, it has resistance to radiation and chemotherapy which makes it very expensive and difficult to treat. It’s a challenge to conduct studies and tests on difficult cancers like ccRCC. This post explains the studies that researchers conducted and the results that they were able to prove about the sFrP1 (Secreted Frizzled-Related Protein 1), which is a tumor suppressor gene. What I found interesting is that when the gene is turned off transcription factors are blocked. Scientist made the educated guess that if the sFRP1 gene activated by turning it on. Activating it will lessen the growth of the tumor and can even get rid of it. I find that to be a tremendous discovery, thats one of the cancers that we can possibly treat if detected early.
As I red up on other blog posts, there was a common thread between Kidney Cancer Caused by "Sleeping Gene"? Rise and Shine!!!! Posted by: MinervaB and GPRC5A Can Be the Key to Lung Cancer Posted by: MON. Both of the post were written and researched by using primary articles pertaining to these cancers and their tumor suppressor gene’s. The genes that are involved are GPRC5A and sFRP1. sFRP1 functions as a tumor suppressor gene and GPRc5A is a gene is that is key to developing cancer. Both of these genes, Inhibit uncontrolled proliferation by affecting WNT, which is a signaling pathway. So far in my senior semior seminar class we have studied signaling pathways and tsg's. The common thread I see in both blogs is the signaling pathways and the tsg's that supress or inhibit uncontrolled cell proliferation.
Remaining Questions:
1.)In what way moelcularly does both tsg inhibit proiferation by affecting WNT?
2.)Sine I found a common relationship between the two blogs. Does the primary articles cite one another?
Now the metastasize of cancers can be prevented!!!
Can we finally stop breast cancer from spreading?! Blog by Kaz Ju, X., Katiyar, S., Wang, C., Liu, M., Jiao, X., Li, S., et al. (2007, May). Akt1 Governs Breast Cancer Progression In Vivo. Proceedings of the National Academy of Sciences, 104: 7438 – 7443.
“What’s the Bladder? A Look into Bladder Cancer and the Tumor Suppressor Gene RhoGD12” blog by PattyP13 Titus, B., Frierson, H.F., Conaway, M., Ching, K., Guise, T., Chirgwin, J., Hampton, G., Theodorescu, D. (2005). Endothelin Axis Is a Target of the Lung Metastasis Suppressor Gene Rho GD12. Clinical Cancer Research 65, (16).
Breast cancer is one of the most common cancers in women living in the United States. As years go by, researchers are trying their best to fine a cure for breast cancer. They are trying to find the cause of breast cancer as well as a therapeutic drug to block the cancer from traveling through the other parts of the body a process called metastasis. Instead of just removing a women’s breast, medical researchers are trying to figure out a way to just stop the cancer from metastasizing through the body. Since nowadays the researchers are getting closer and closer to find the cure for breast cancer fewer women are dying from this cancer each year. I found the article by Ju, X., Katiyar, S., Wang, C., Liu, M., Jiao, X., Li, S., et al.to be very important because the result the scientist discovered pave the way for a new therapeutic drug for breast cancer. The drug that the scientists are studying is an anti-Akt which would be a good treatment for women who are at the earlier stage of breast cancer. I was amazed when I discovered that the researcher had found the protein that enables the breast cancer to proliferate. The mice that did not have two copies of the Akt1gene did not develop cancer, but the mice that had one copy had a small tumor which was growing slowly. The mice who had two copies of Akt1 had the cancer, which grew extremely fast. This article is novel because researchers are getting closer in finding what causes breast cancer. They are also trying to find a new drug that can block breast cancer metastasizing throughout the body or a treatment for it. The scientist found the protein that helped beast cancer to spread all over the body.
The two article I have chosen to comment on are Can we finally stop breast cancer from spreading by Kaz B and “What’s the Bladder? A Look into Bladder Cancer and the Tumor Suppressor Gene RhoGD12 by PattyP3.
The two articles did not have any molecular event in common expect they both are trying to prevent proliferation of cancer cells. The articles were related to what I have studied in class so far: a cell that has the ability to metastasize is a cell that is not functioning properly and has a mutation in its DNA. In class I studied that an ocogene is a mutated or abnormal form of proto-ocongene. In class I have learned that Akt1 is a kinase (adding of phosphate groups) that takes parts in normal pro-growth signaling pathways in the cell and it encodes for proteins.
As I was reading and learning about my classmate’s blog, the two articles that I choose to comment on are Kaz and Patty. I found these two blogs to be very significant because both of these articles explain how it is important for scientist to come up with a new strategy to prevent the spreading of cancer in other part of the body, and how to stop it from the first place that it began. On Kaz’s article the scientist were trying to find the protein that helps with the spreading of tumor cells in breast cancer. During the research in both article the scientist used mice to perform their experiment. On Kaz’s article the researcher raised a few mice that had no Akt1 gene with other mice with ErbB2 onocogen. After the experiment was done the researchers found the protein in some of the mice. The mice that did not have two copy of Akt1 gene did not develop cancer.
The other mice that had one copy of the gene had a small tumor that was slow growing. The mice with two copy of the gene had cancer that was spreading fast. Patty’s article it emphasized that patients that had late stage bladder cancer relapse with fatal lung cancer. RhoGD12 gene is a tumor suppressor gene that is found in bladder cancers, whenever the RhoGd12 expression is not working, the genes ET-1 is present which encodes for endotheline and is controlled by RhoGd12. When the gene RhoGD12 is present, ET-1 turns “off”. Endothelin which is an amino acid helps tumor cells metastasize, the gene RhoGD12 make ET-1 stay of so the cancer will not proliferate.
The research did a DNA microarrays and an RNA isolation they study a metastasis and a non-metastasis bladder cancer cells. They gave a group of mice ET-1 suppress in the mice’s drinking water this would of give them the role of ET-1 cancer metastasis. They watch the mice for twelve weeks and while the cancer spread through their lungs. The mice that were DNA microarray had many genes including RhoGD12 that were not express.
Questions
1. When a gene loses its function is it possible for it to regain?
2. Why did the researchers do a DNA microarray and an RNA islocation?
“What’s the Bladder? A Look into Bladder Cancer and the Tumor Suppressor Gene RhoGD12” blog by PattyP13 Titus, B., Frierson, H.F., Conaway, M., Ching, K., Guise, T., Chirgwin, J., Hampton, G., Theodorescu, D. (2005). Endothelin Axis Is a Target of the Lung Metastasis Suppressor Gene Rho GD12. Clinical Cancer Research 65, (16).
Breast cancer is one of the most common cancers in women living in the United States. As years go by, researchers are trying their best to fine a cure for breast cancer. They are trying to find the cause of breast cancer as well as a therapeutic drug to block the cancer from traveling through the other parts of the body a process called metastasis. Instead of just removing a women’s breast, medical researchers are trying to figure out a way to just stop the cancer from metastasizing through the body. Since nowadays the researchers are getting closer and closer to find the cure for breast cancer fewer women are dying from this cancer each year. I found the article by Ju, X., Katiyar, S., Wang, C., Liu, M., Jiao, X., Li, S., et al.to be very important because the result the scientist discovered pave the way for a new therapeutic drug for breast cancer. The drug that the scientists are studying is an anti-Akt which would be a good treatment for women who are at the earlier stage of breast cancer. I was amazed when I discovered that the researcher had found the protein that enables the breast cancer to proliferate. The mice that did not have two copies of the Akt1gene did not develop cancer, but the mice that had one copy had a small tumor which was growing slowly. The mice who had two copies of Akt1 had the cancer, which grew extremely fast. This article is novel because researchers are getting closer in finding what causes breast cancer. They are also trying to find a new drug that can block breast cancer metastasizing throughout the body or a treatment for it. The scientist found the protein that helped beast cancer to spread all over the body.
The two article I have chosen to comment on are Can we finally stop breast cancer from spreading by Kaz B and “What’s the Bladder? A Look into Bladder Cancer and the Tumor Suppressor Gene RhoGD12 by PattyP3.
The two articles did not have any molecular event in common expect they both are trying to prevent proliferation of cancer cells. The articles were related to what I have studied in class so far: a cell that has the ability to metastasize is a cell that is not functioning properly and has a mutation in its DNA. In class I studied that an ocogene is a mutated or abnormal form of proto-ocongene. In class I have learned that Akt1 is a kinase (adding of phosphate groups) that takes parts in normal pro-growth signaling pathways in the cell and it encodes for proteins.
As I was reading and learning about my classmate’s blog, the two articles that I choose to comment on are Kaz and Patty. I found these two blogs to be very significant because both of these articles explain how it is important for scientist to come up with a new strategy to prevent the spreading of cancer in other part of the body, and how to stop it from the first place that it began. On Kaz’s article the scientist were trying to find the protein that helps with the spreading of tumor cells in breast cancer. During the research in both article the scientist used mice to perform their experiment. On Kaz’s article the researcher raised a few mice that had no Akt1 gene with other mice with ErbB2 onocogen. After the experiment was done the researchers found the protein in some of the mice. The mice that did not have two copy of Akt1 gene did not develop cancer.
The other mice that had one copy of the gene had a small tumor that was slow growing. The mice with two copy of the gene had cancer that was spreading fast. Patty’s article it emphasized that patients that had late stage bladder cancer relapse with fatal lung cancer. RhoGD12 gene is a tumor suppressor gene that is found in bladder cancers, whenever the RhoGd12 expression is not working, the genes ET-1 is present which encodes for endotheline and is controlled by RhoGd12. When the gene RhoGD12 is present, ET-1 turns “off”. Endothelin which is an amino acid helps tumor cells metastasize, the gene RhoGD12 make ET-1 stay of so the cancer will not proliferate.
The research did a DNA microarrays and an RNA isolation they study a metastasis and a non-metastasis bladder cancer cells. They gave a group of mice ET-1 suppress in the mice’s drinking water this would of give them the role of ET-1 cancer metastasis. They watch the mice for twelve weeks and while the cancer spread through their lungs. The mice that were DNA microarray had many genes including RhoGD12 that were not express.
Questions
1. When a gene loses its function is it possible for it to regain?
2. Why did the researchers do a DNA microarray and an RNA islocation?
Oncogenes at it Again
Posts:
IKBKE gene amplification is seen loud and clear in breast cancer tumors!
Primary paper:
Boehm, Jesse S. et al (2007). Integrative Genomic Approaches Identify IKBKE as a Breast Cancer Oncogene. Cell Press Vol.129, pp.1065-1079
Leukemia Patients with KIT-D816 Mutations.
Primary Paper:
Schnittger, S. et al (2006). KIT-D816 Mutations in AML1-ETO-Positive AML are associated with impaired event-free and overall survival.
At face value, what sparked the interest on reflecting on these two articles was the fact that they are both not only caused by mutations, which we know is what gives rise to cancer, but they both can be linked to specific oncogenes. These particular mutations give rise to types of breast cancer and acute myeloid leukemia that can be categorized as “gain-of-function” mutations as opposed to “loss-of-function” which is the category that for instance a tumor suppressor gene would fall under because the gene can no longer suppress the growth or development of tumors. In studying any type of cancer it is important to maybe make this a primary distinction in order to conduct more focused research.
The mutation being examined in breast cancer occurs in the IKBKE caused by gene amplification leading it to function as an oncogene. In terms of acute myeloid leukemia, KIT is a proto-oncogene that when converted causes the D816 which becomes KIT –D816. It is important to note that both IKBKE and KIT-D816 starts off as normal genes. Mutations cause for these once normal genes to become oncogenes which are directly linked to development of any type of cancer. This is one of the first points emphasized in Cancer Biology.
After reading both these blogs a few questions did rise such as if these mutations are only specific to specific forms of breast cancer and leukemia? This then leads me to wonder how many types of these cancers exist. Are there any studies that are looking at the factors that contribute to the occurrence of these mutations; are they environmental or genetic or both?
IKBKE gene amplification is seen loud and clear in breast cancer tumors!
Primary paper:
Boehm, Jesse S. et al (2007). Integrative Genomic Approaches Identify IKBKE as a Breast Cancer Oncogene. Cell Press Vol.129, pp.1065-1079
Leukemia Patients with KIT-D816 Mutations.
Primary Paper:
Schnittger, S. et al (2006). KIT-D816 Mutations in AML1-ETO-Positive AML are associated with impaired event-free and overall survival.
At face value, what sparked the interest on reflecting on these two articles was the fact that they are both not only caused by mutations, which we know is what gives rise to cancer, but they both can be linked to specific oncogenes. These particular mutations give rise to types of breast cancer and acute myeloid leukemia that can be categorized as “gain-of-function” mutations as opposed to “loss-of-function” which is the category that for instance a tumor suppressor gene would fall under because the gene can no longer suppress the growth or development of tumors. In studying any type of cancer it is important to maybe make this a primary distinction in order to conduct more focused research.
The mutation being examined in breast cancer occurs in the IKBKE caused by gene amplification leading it to function as an oncogene. In terms of acute myeloid leukemia, KIT is a proto-oncogene that when converted causes the D816 which becomes KIT –D816. It is important to note that both IKBKE and KIT-D816 starts off as normal genes. Mutations cause for these once normal genes to become oncogenes which are directly linked to development of any type of cancer. This is one of the first points emphasized in Cancer Biology.
After reading both these blogs a few questions did rise such as if these mutations are only specific to specific forms of breast cancer and leukemia? This then leads me to wonder how many types of these cancers exist. Are there any studies that are looking at the factors that contribute to the occurrence of these mutations; are they environmental or genetic or both?
What can a mutation in the BRAF protein do to me????
Possible Cure for Skin Cancer????? Blog by Charlene C.
Futreal, Andy. June 10. 2002. “ British Scientist Identify Skin Cancer Gene”. The New York Times. June11.2002. http://ww.nytimes.com/
Turn off the switch for thyroid papillary carcinoma cancer!!! Blog by Tanya M.
Cohen,Y., Xing, M., Mambo, E., Guo., Z., Wu. G., Trink, B., et al. (2003 April) BRAF mutation in papillary thyroid carcinoma. Journal of the National Cancer Institute, vol. 95, No.8.
I believe that developing a possible cure for skin cancer is vital because this disease is very common; everybody who is exposed to UV light is at risk of getting skin cancer. Although skin cancer may be dormant for years, one has to remember that cancer is a work in progress, which means it takes time for symptoms to occur. Finding a drug that could inhibit the mutant BRAF in cancer cells would save lives; that way, we can at least stop the tumor cells from proliferating. When BRAF proto-oncoprotein is constantly activated that leads to uncontrollable growth. BRAF protein is similar to RAF which is in the RAS-MAPK pathway. BRAF is activated when an adaptor protein helped Ras become activated by binding GTP to it instead of GDP, then activated Ras would then bind BRAF, which would become phosphorylated, and it would become active. BRAF is a kinase (an enzyme that catalyzes protein phosphorylation), and when it is active, it phosphorylates other proteins, like MEK and MAPK and then pass on the pro-growth signal to the nucleus. This article is extremely important because not only did the results of the experiment pave the way for future research about skin cancer, they also discovered a way to create an inhibitor that slowed down the kinase for a similar protein to BRAF called the ABL protein. ABL protein acts as a proto-oncoprotein in most normal cells. However, the finding states that ABL was present in patients diagnosed with leukemia. It is unknown to me whether what the researchers found in the patient diagnosed with leukemia was a mass of ABL protein or a mutated ABL protein.
While reading these fascinating blogs, I discovered a common molecular event between these two articles: Possible Cure for Skin Cancer????? and Turn off the switch for thyroid papillary carcinoma cancer!!! discussed by Charlene C. and Tanya M. I found these two articles interesting because they both examine the relationship between BRAF in cancer; in fact the research in Charlene C’s article was the basis for the scientists to see if the mutated gene BRAF was present in papillary thyroid cancer. Both papers explored the BRAF gene which is found in normal cell types as well as cancerous cell types. What is fascinating is that Cohen et al knew that BRAF mutation was involved in thyroid cancer and that BRAF has a connection with melanoma through the experiment that they did in June2002. Therefore, with this knowledge they were able to make new hypothesis and did further experiment. The result of their new experiment showed that there was a mutation in the BRAF gene (T1796A) in 69% of papillary thyroid cancers. They discovered that nucleotide 1796 in BRAF was changed from thymine (T) to adenine (A), and this single change was enough to contribute to BRAF always being “on” which then causes the thyroid cells to proliferate and then eventually become cancer cells. Both these findings may pave the way for chemotherapy to deactivate the mutated BRAF protein. While reading these articles, I noticed a lot of similarity to what we have learned in class especially knowing that when something that should not always be turned on is on. We know that then chaos will happen; there will be uncontrollable growth which in turn becomes malignant tumor. The similar research Cohen et al did was that even though they knew that a mutation in BRAF can be labeled as an oncogene in cancer patients, they could not identify the specific point mutation in the most malignant melanomas. The scientists then created a study in which they can separate the normal cells from the tumor cells and did an experiment to figure out in which cell types BRAF is most active and found that BRAF was present in the patient’s DNA who had cancer. They screened the BRAF gene mutation in different type of cancers. There were no differences in the results described about the on and off switch.
I have several questions I would like to pose regarding this information: besides the spontaneous changes that can happen within the cells when proliferating and mutation, what is the main thing that can distract a gene which stops it from doing what it’s supposed to do? For example, why would the BRAF gene in T1796A change T to A? How do these genes get activated? In addition, I am curious about environmental triggers: can the environment cause the mutations to be turned on? Or can an individual’s life style such as obesity set off the gene?
Futreal, Andy. June 10. 2002. “ British Scientist Identify Skin Cancer Gene”. The New York Times. June11.2002. http://ww.nytimes.com/
Turn off the switch for thyroid papillary carcinoma cancer!!! Blog by Tanya M.
Cohen,Y., Xing, M., Mambo, E., Guo., Z., Wu. G., Trink, B., et al. (2003 April) BRAF mutation in papillary thyroid carcinoma. Journal of the National Cancer Institute, vol. 95, No.8.
I believe that developing a possible cure for skin cancer is vital because this disease is very common; everybody who is exposed to UV light is at risk of getting skin cancer. Although skin cancer may be dormant for years, one has to remember that cancer is a work in progress, which means it takes time for symptoms to occur. Finding a drug that could inhibit the mutant BRAF in cancer cells would save lives; that way, we can at least stop the tumor cells from proliferating. When BRAF proto-oncoprotein is constantly activated that leads to uncontrollable growth. BRAF protein is similar to RAF which is in the RAS-MAPK pathway. BRAF is activated when an adaptor protein helped Ras become activated by binding GTP to it instead of GDP, then activated Ras would then bind BRAF, which would become phosphorylated, and it would become active. BRAF is a kinase (an enzyme that catalyzes protein phosphorylation), and when it is active, it phosphorylates other proteins, like MEK and MAPK and then pass on the pro-growth signal to the nucleus. This article is extremely important because not only did the results of the experiment pave the way for future research about skin cancer, they also discovered a way to create an inhibitor that slowed down the kinase for a similar protein to BRAF called the ABL protein. ABL protein acts as a proto-oncoprotein in most normal cells. However, the finding states that ABL was present in patients diagnosed with leukemia. It is unknown to me whether what the researchers found in the patient diagnosed with leukemia was a mass of ABL protein or a mutated ABL protein.
While reading these fascinating blogs, I discovered a common molecular event between these two articles: Possible Cure for Skin Cancer????? and Turn off the switch for thyroid papillary carcinoma cancer!!! discussed by Charlene C. and Tanya M. I found these two articles interesting because they both examine the relationship between BRAF in cancer; in fact the research in Charlene C’s article was the basis for the scientists to see if the mutated gene BRAF was present in papillary thyroid cancer. Both papers explored the BRAF gene which is found in normal cell types as well as cancerous cell types. What is fascinating is that Cohen et al knew that BRAF mutation was involved in thyroid cancer and that BRAF has a connection with melanoma through the experiment that they did in June2002. Therefore, with this knowledge they were able to make new hypothesis and did further experiment. The result of their new experiment showed that there was a mutation in the BRAF gene (T1796A) in 69% of papillary thyroid cancers. They discovered that nucleotide 1796 in BRAF was changed from thymine (T) to adenine (A), and this single change was enough to contribute to BRAF always being “on” which then causes the thyroid cells to proliferate and then eventually become cancer cells. Both these findings may pave the way for chemotherapy to deactivate the mutated BRAF protein. While reading these articles, I noticed a lot of similarity to what we have learned in class especially knowing that when something that should not always be turned on is on. We know that then chaos will happen; there will be uncontrollable growth which in turn becomes malignant tumor. The similar research Cohen et al did was that even though they knew that a mutation in BRAF can be labeled as an oncogene in cancer patients, they could not identify the specific point mutation in the most malignant melanomas. The scientists then created a study in which they can separate the normal cells from the tumor cells and did an experiment to figure out in which cell types BRAF is most active and found that BRAF was present in the patient’s DNA who had cancer. They screened the BRAF gene mutation in different type of cancers. There were no differences in the results described about the on and off switch.
I have several questions I would like to pose regarding this information: besides the spontaneous changes that can happen within the cells when proliferating and mutation, what is the main thing that can distract a gene which stops it from doing what it’s supposed to do? For example, why would the BRAF gene in T1796A change T to A? How do these genes get activated? In addition, I am curious about environmental triggers: can the environment cause the mutations to be turned on? Or can an individual’s life style such as obesity set off the gene?
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