› Forums › Mucosal Melanoma Community › Great News!
- This topic has 15 replies, 4 voices, and was last updated 12 years, 2 months ago by
JerryfromFauq.
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- September 28, 2012 at 3:37 am
My husband had his 3rd round of carbo/taxol for his stage 3 mucosal melanoma today. Before the treatment, they did a scan and his tumors have shrunk 75% plus a second primary lung cancer is shrinking before they got to the radiation they are going to do! The doctor is very happy and said that sometimes, with mucosal, they can get a durable response with chemo.
My husband had his 3rd round of carbo/taxol for his stage 3 mucosal melanoma today. Before the treatment, they did a scan and his tumors have shrunk 75% plus a second primary lung cancer is shrinking before they got to the radiation they are going to do! The doctor is very happy and said that sometimes, with mucosal, they can get a durable response with chemo. Anybody here have mucosal? I'd like to hear of your expeeriences. He will have at least two more rounds of chemo and another scan in 6 weeks to see how things are. So many people are praying for him and our prayers are being answered.
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- September 28, 2012 at 1:52 pm
Really Great posts.That is news that we all love reading.You both are in my prayers .Beat the Beast. Al
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- September 28, 2012 at 1:52 pm
Really Great posts.That is news that we all love reading.You both are in my prayers .Beat the Beast. Al
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- September 28, 2012 at 1:52 pm
Really Great posts.That is news that we all love reading.You both are in my prayers .Beat the Beast. Al
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- September 30, 2012 at 9:01 pm
I have mucousal with the c-kit oncoprotein and have been on Gleevec for over three years now. I have not read about carbo/taxol having a high success rate for mucousal. Will have to research that. Do you know which oncoproteins and DNA mutations your husbands melanoma has?
While carbo/taxol does not have a high across the board success rate on general melanoma, it has been very successful on some individuals. Do I read correctly that the tumors in his lungs are not a metastisis from the mucousal melanoma, but a completely different cancer type?
Praying for continued tumor clearing.
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- September 30, 2012 at 10:08 pm
My husband has two primary cancers: nasal mucosal melanama stage 3c and non small cell lung cancer. It is thought that he will overcome the lung cancer just fine but the melanoma is the problem. Nothing had been done between the time he had surgery on his nose and neck on May8 until August 13, when a large tumor and a chain of bumps on his neck showed up literally overnight and continued to grow at an alarming rate. By the time they began the carbo/taxol, the largest one was pressing on a nerve, causing pain, pressing on an artery, making the blood pressure go up, and was close to affecting his swollowiing and breathing. He is cKit and B-RAF negative, unable to go through a clinical trial because of the lung cancer, and was told that he could not tolerate IL2. Yerevoy was mentioned as an option but they went with carbo/taxol because the things were growing so fast. He had an immediate response. After the first treatment, I watched them shrink as fast as they had grown. After the second, things went down even more to the 75% response rate. They said they don't usually see this good of a response. Initially they said there would be no durable response with this but now they said there is a chance. If he becomes NED, they said they will just watch and scan. I don't know what other options are out there for him. They talked about interferon for a year and radiation but that plan got thrown out the window when everything popped up and took off.
It's been a heck of a ride so far. I've had to push and ask for the cKit mutation to be checked, then push again when I was told that the doctor has requested it but it hadn't been done, then push again after they said they did it the second time. They don't tell us anything unless I ask and then they said I ask a lot of questions and most people don't do that! What do you mean by oncoproteins and DNA mutations? My husband is seeing a melanoma specialist at the Hillman Cancer Center in Pittsburgh.
The long delay on the melanoma treatment was because they were trying to figure out what was in the lung and what to do about it. He's supposed to have cyberknife radation but that is another story. Two tries and they couldn't do it because they don't have the cooridinates right. They've redone the plan and they will try again this week. That's being done by our local doctor.
Anyway, my husband feels good and has had very little side affects with the chemo. He missed a day and a half of work because of the fatigue after the first treatment but handled the second one better and is doing better yet this time around. Has a little joint pain now and then and some neuropathy but nothing bad. Thanks for the prayer. I truly believe that God is at work here.
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- October 1, 2012 at 6:03 am
http://en.wikipedia.org/wiki/Oncogene
An oncogene is a gene that has the potential to cause cancer.[1] In tumor cells, they are often mutated or expressed at high levels.[2]
Most normal cells undergo a programmed form of death (apoptosis). Activated oncogenes can cause those cells that ought to die to survive and proliferate instead.[3] Most oncogenes require an additional step, such as mutations in another gene, or environmental factors, such as viral infection, to cause cancer. Since the 1970s, dozens of oncogenes have been identified in human cancer. Many cancer drugs target the proteins encoded by oncogenes.
Proto-oncogene
A proto-oncogene is a normal gene that can become an oncogene due to mutations or increased expression. The resultant protein may be termed an oncoprotein.[7] Proto-oncogenes code for proteins that help to regulate cell growth and differentiation. Proto-oncogenes are often involved in signal transduction and execution of mitogenic signals, usually through their protein products. Upon activation, a proto-oncogene (or its product) becomes a tumor-inducing agent, an oncogene.[8] Examples of proto-oncogenes include RAS, WNT, MYC, ERK, and TRK. The MYC gene is implicated in Burkitt's Lymphoma, which starts when a chromosomal translocation moves an enhancer sequence within the vicinity of the MYC gene. The MYC gene codes for widely used transcription factors. When the enhancer sequence is wrongly placed, these transcription factors are produced at much higher rates. Another example of an oncogene is the Bcr-Abl gene found on the Philadelphia Chromosome, a piece of genetic material seen in Chronic Myelogenous Leukemia caused by the translocation of pieces from chromosomes 9 and 22. Bcr-Abl codes for a receptor tyrosine kinase, which is constitutively active, leading to uncontrolled cell proliferation.
An oncogene (Oncoprotein) may cause a cell to secrete growth factors even though it does not normally do so.
(C-kit & BRAF are both oncoproteins and resulting DNA mutations.)
****************************************
http://www.ncbi.nlm.nih.gov/pubmed/22671702
Abstract
Tumor-derived mutant KRAS (v-Ki-ras-2 Kirsten rat sarcoma viral oncogene) oncoprotein is a critical driver of cancer phenotypes and a potential biomarker for many epithelial cancers.
******************************************
In the case of my c-kit oncoproteins and DNA mutations, they first check to see if the tumor cells have the c-kit oncoprotein on their surface, If the c-kit Oncoprotein is there, they then need to determine which of the DNA mutations may exist in the chromosomes. They are working to determine which drug will have what effect on each of the different DNA mutations. If just C-kit melanoma is this bad, think how complex the whole field of cancer is. How many types of melanoma are there? Who actually knows?
-
- October 1, 2012 at 6:03 am
http://en.wikipedia.org/wiki/Oncogene
An oncogene is a gene that has the potential to cause cancer.[1] In tumor cells, they are often mutated or expressed at high levels.[2]
Most normal cells undergo a programmed form of death (apoptosis). Activated oncogenes can cause those cells that ought to die to survive and proliferate instead.[3] Most oncogenes require an additional step, such as mutations in another gene, or environmental factors, such as viral infection, to cause cancer. Since the 1970s, dozens of oncogenes have been identified in human cancer. Many cancer drugs target the proteins encoded by oncogenes.
Proto-oncogene
A proto-oncogene is a normal gene that can become an oncogene due to mutations or increased expression. The resultant protein may be termed an oncoprotein.[7] Proto-oncogenes code for proteins that help to regulate cell growth and differentiation. Proto-oncogenes are often involved in signal transduction and execution of mitogenic signals, usually through their protein products. Upon activation, a proto-oncogene (or its product) becomes a tumor-inducing agent, an oncogene.[8] Examples of proto-oncogenes include RAS, WNT, MYC, ERK, and TRK. The MYC gene is implicated in Burkitt's Lymphoma, which starts when a chromosomal translocation moves an enhancer sequence within the vicinity of the MYC gene. The MYC gene codes for widely used transcription factors. When the enhancer sequence is wrongly placed, these transcription factors are produced at much higher rates. Another example of an oncogene is the Bcr-Abl gene found on the Philadelphia Chromosome, a piece of genetic material seen in Chronic Myelogenous Leukemia caused by the translocation of pieces from chromosomes 9 and 22. Bcr-Abl codes for a receptor tyrosine kinase, which is constitutively active, leading to uncontrolled cell proliferation.
An oncogene (Oncoprotein) may cause a cell to secrete growth factors even though it does not normally do so.
(C-kit & BRAF are both oncoproteins and resulting DNA mutations.)
****************************************
http://www.ncbi.nlm.nih.gov/pubmed/22671702
Abstract
Tumor-derived mutant KRAS (v-Ki-ras-2 Kirsten rat sarcoma viral oncogene) oncoprotein is a critical driver of cancer phenotypes and a potential biomarker for many epithelial cancers.
******************************************
In the case of my c-kit oncoproteins and DNA mutations, they first check to see if the tumor cells have the c-kit oncoprotein on their surface, If the c-kit Oncoprotein is there, they then need to determine which of the DNA mutations may exist in the chromosomes. They are working to determine which drug will have what effect on each of the different DNA mutations. If just C-kit melanoma is this bad, think how complex the whole field of cancer is. How many types of melanoma are there? Who actually knows?
-
- October 1, 2012 at 6:03 am
http://en.wikipedia.org/wiki/Oncogene
An oncogene is a gene that has the potential to cause cancer.[1] In tumor cells, they are often mutated or expressed at high levels.[2]
Most normal cells undergo a programmed form of death (apoptosis). Activated oncogenes can cause those cells that ought to die to survive and proliferate instead.[3] Most oncogenes require an additional step, such as mutations in another gene, or environmental factors, such as viral infection, to cause cancer. Since the 1970s, dozens of oncogenes have been identified in human cancer. Many cancer drugs target the proteins encoded by oncogenes.
Proto-oncogene
A proto-oncogene is a normal gene that can become an oncogene due to mutations or increased expression. The resultant protein may be termed an oncoprotein.[7] Proto-oncogenes code for proteins that help to regulate cell growth and differentiation. Proto-oncogenes are often involved in signal transduction and execution of mitogenic signals, usually through their protein products. Upon activation, a proto-oncogene (or its product) becomes a tumor-inducing agent, an oncogene.[8] Examples of proto-oncogenes include RAS, WNT, MYC, ERK, and TRK. The MYC gene is implicated in Burkitt's Lymphoma, which starts when a chromosomal translocation moves an enhancer sequence within the vicinity of the MYC gene. The MYC gene codes for widely used transcription factors. When the enhancer sequence is wrongly placed, these transcription factors are produced at much higher rates. Another example of an oncogene is the Bcr-Abl gene found on the Philadelphia Chromosome, a piece of genetic material seen in Chronic Myelogenous Leukemia caused by the translocation of pieces from chromosomes 9 and 22. Bcr-Abl codes for a receptor tyrosine kinase, which is constitutively active, leading to uncontrolled cell proliferation.
An oncogene (Oncoprotein) may cause a cell to secrete growth factors even though it does not normally do so.
(C-kit & BRAF are both oncoproteins and resulting DNA mutations.)
****************************************
http://www.ncbi.nlm.nih.gov/pubmed/22671702
Abstract
Tumor-derived mutant KRAS (v-Ki-ras-2 Kirsten rat sarcoma viral oncogene) oncoprotein is a critical driver of cancer phenotypes and a potential biomarker for many epithelial cancers.
******************************************
In the case of my c-kit oncoproteins and DNA mutations, they first check to see if the tumor cells have the c-kit oncoprotein on their surface, If the c-kit Oncoprotein is there, they then need to determine which of the DNA mutations may exist in the chromosomes. They are working to determine which drug will have what effect on each of the different DNA mutations. If just C-kit melanoma is this bad, think how complex the whole field of cancer is. How many types of melanoma are there? Who actually knows?
-
- September 30, 2012 at 10:08 pm
My husband has two primary cancers: nasal mucosal melanama stage 3c and non small cell lung cancer. It is thought that he will overcome the lung cancer just fine but the melanoma is the problem. Nothing had been done between the time he had surgery on his nose and neck on May8 until August 13, when a large tumor and a chain of bumps on his neck showed up literally overnight and continued to grow at an alarming rate. By the time they began the carbo/taxol, the largest one was pressing on a nerve, causing pain, pressing on an artery, making the blood pressure go up, and was close to affecting his swollowiing and breathing. He is cKit and B-RAF negative, unable to go through a clinical trial because of the lung cancer, and was told that he could not tolerate IL2. Yerevoy was mentioned as an option but they went with carbo/taxol because the things were growing so fast. He had an immediate response. After the first treatment, I watched them shrink as fast as they had grown. After the second, things went down even more to the 75% response rate. They said they don't usually see this good of a response. Initially they said there would be no durable response with this but now they said there is a chance. If he becomes NED, they said they will just watch and scan. I don't know what other options are out there for him. They talked about interferon for a year and radiation but that plan got thrown out the window when everything popped up and took off.
It's been a heck of a ride so far. I've had to push and ask for the cKit mutation to be checked, then push again when I was told that the doctor has requested it but it hadn't been done, then push again after they said they did it the second time. They don't tell us anything unless I ask and then they said I ask a lot of questions and most people don't do that! What do you mean by oncoproteins and DNA mutations? My husband is seeing a melanoma specialist at the Hillman Cancer Center in Pittsburgh.
The long delay on the melanoma treatment was because they were trying to figure out what was in the lung and what to do about it. He's supposed to have cyberknife radation but that is another story. Two tries and they couldn't do it because they don't have the cooridinates right. They've redone the plan and they will try again this week. That's being done by our local doctor.
Anyway, my husband feels good and has had very little side affects with the chemo. He missed a day and a half of work because of the fatigue after the first treatment but handled the second one better and is doing better yet this time around. Has a little joint pain now and then and some neuropathy but nothing bad. Thanks for the prayer. I truly believe that God is at work here.
-
- September 30, 2012 at 10:08 pm
My husband has two primary cancers: nasal mucosal melanama stage 3c and non small cell lung cancer. It is thought that he will overcome the lung cancer just fine but the melanoma is the problem. Nothing had been done between the time he had surgery on his nose and neck on May8 until August 13, when a large tumor and a chain of bumps on his neck showed up literally overnight and continued to grow at an alarming rate. By the time they began the carbo/taxol, the largest one was pressing on a nerve, causing pain, pressing on an artery, making the blood pressure go up, and was close to affecting his swollowiing and breathing. He is cKit and B-RAF negative, unable to go through a clinical trial because of the lung cancer, and was told that he could not tolerate IL2. Yerevoy was mentioned as an option but they went with carbo/taxol because the things were growing so fast. He had an immediate response. After the first treatment, I watched them shrink as fast as they had grown. After the second, things went down even more to the 75% response rate. They said they don't usually see this good of a response. Initially they said there would be no durable response with this but now they said there is a chance. If he becomes NED, they said they will just watch and scan. I don't know what other options are out there for him. They talked about interferon for a year and radiation but that plan got thrown out the window when everything popped up and took off.
It's been a heck of a ride so far. I've had to push and ask for the cKit mutation to be checked, then push again when I was told that the doctor has requested it but it hadn't been done, then push again after they said they did it the second time. They don't tell us anything unless I ask and then they said I ask a lot of questions and most people don't do that! What do you mean by oncoproteins and DNA mutations? My husband is seeing a melanoma specialist at the Hillman Cancer Center in Pittsburgh.
The long delay on the melanoma treatment was because they were trying to figure out what was in the lung and what to do about it. He's supposed to have cyberknife radation but that is another story. Two tries and they couldn't do it because they don't have the cooridinates right. They've redone the plan and they will try again this week. That's being done by our local doctor.
Anyway, my husband feels good and has had very little side affects with the chemo. He missed a day and a half of work because of the fatigue after the first treatment but handled the second one better and is doing better yet this time around. Has a little joint pain now and then and some neuropathy but nothing bad. Thanks for the prayer. I truly believe that God is at work here.
-
- September 30, 2012 at 9:01 pm
I have mucousal with the c-kit oncoprotein and have been on Gleevec for over three years now. I have not read about carbo/taxol having a high success rate for mucousal. Will have to research that. Do you know which oncoproteins and DNA mutations your husbands melanoma has?
While carbo/taxol does not have a high across the board success rate on general melanoma, it has been very successful on some individuals. Do I read correctly that the tumors in his lungs are not a metastisis from the mucousal melanoma, but a completely different cancer type?
Praying for continued tumor clearing.
-
- September 30, 2012 at 9:01 pm
I have mucousal with the c-kit oncoprotein and have been on Gleevec for over three years now. I have not read about carbo/taxol having a high success rate for mucousal. Will have to research that. Do you know which oncoproteins and DNA mutations your husbands melanoma has?
While carbo/taxol does not have a high across the board success rate on general melanoma, it has been very successful on some individuals. Do I read correctly that the tumors in his lungs are not a metastisis from the mucousal melanoma, but a completely different cancer type?
Praying for continued tumor clearing.
Tagged: mucosal melanoma
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