glioma tumor

momatabor

first Id like to ty all for letting me know Were not alone.my brother has a glioma tumor and has had surgery and is starting chemo,radiation the cancer is very aggresive 3/6 mon without therp, and less than a year with .my question is how will the chemo and rad affect his time left ? Please help

oneagleswings

my husband had a different kind of cancer but during the time he was on chemo it extended his life span and gave him a better quality of life..don't focus on the "time" stats and instead focus day to day how he feels...take care\ Bev

Felixthecat

I worry a little about the coadministration of corticosteroids with chemo for gliomas. They are generally used to prevent nausea but can cause some glioma cell types to become chemo resistant. While the drug referred to below (which is a progesterone antagonist with an antiglucocorticoid activity is a little difficult to get it could possible be helpful but he'd have to discuss further with an oncologist):

1993: Inhibition of growth of the human malignant glioma cell line (U87MG) by the steroid hormone antagonist RU486
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8077338&dopt=Abstract

• “These results indicate that the growth of U87MG human malignant glioma is dependent on corticoids. The antiproliferative effect of RU486 appears to be due to the inhibition of binding of glucocorticoid hormones to their receptor proteins. Our results suggest a new therapy for some brain tumors, such as malignant gliomas based on the steroid hormone antagonist RU486.”

1997: Dexamethasone inhibits apoptosis in C6 glioma cells through increased expression of Bcl-XL
http://www.springerlink.com/content/7r22113065664351/
“.... The glucocorticoid dexamethasone (Dex) has been reported to modulate a number of signaling pathways and physiological processes, including apoptosis. This study was carried out to investigate the cytoprotective mechanism of Dex in C6 glioma cells. Pre-treatment of cells with Dex inhibited apoptosis induced by staurosporine, etoposide and thapsigargin. Apoptosis inhibition correlated with blockade of mitochondrial cytochrome c release, abolition of caspase-3 activity along with inhibition of caspase-9 and PARP cleavage. Dex-mediated cytoprotection coincided with the induction of the anti-apoptotic protein, Bcl-XL. The specific glucocorticoid receptor antagonist, RU486, reversed the anti-apoptotic effect of Dex and prevented Bcl-XL induction. Here, we show for the first time that knockdown of Bcl-XL expression with siRNA reversed the protective effects of the glucocorticoid in glioma cells. We conclude that Dex-mediated inhibition of apoptosis in C6 glioma cells is through induction of Bcl-XL. “

1994: The antiprogestatin drug RU 486 potentiates doxorubicin cytotoxicity in multidrug resistant cells through inhibition of P-glycoprotein function.
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=7982498&dopt=Abstract
• “These results thus demonstrate that RU 486 can downmodulate anticancer drug resistance through inhibition of P-gp function.”

1999: Ceramide toxicity and metabolism differ in wild-type and multidrug-resistant cancer cells.
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10427136&dopt=Abstract
• “The anti-progestine, RU486, also blocked glucosylceramide synthesis in cells; however, LY117018, a raloxifene analog, was without influence. We propose that an enhanced capacity to glycosylate ceramide as evidenced in MCF-7-AdrR cells, is a molecular determinant of drug resistance, particularly as regards resistance to ceramide-enhancing agents such as anthracyclines, ionizing radiation, and tumor necrosis factor-alpha.”


Corticosteroids induce chemotherapy resistance in the majority of tumour cells from bone, brain, breast, cervix, melanoma and neuroblastoma
http://histology1.med.uoc.gr/ijo/2006/volume29/number5/1295.pdf

ming59

Felixthecat said:

I worry a little about the coadministration of corticosteroids with chemo for gliomas. They are generally used to prevent nausea but can cause some glioma cell types to become chemo resistant. While the drug referred to below (which is a progesterone antagonist with an antiglucocorticoid activity is a little difficult to get it could possible be helpful but he'd have to discuss further with an oncologist):

1993: Inhibition of growth of the human malignant glioma cell line (U87MG) by the steroid hormone antagonist RU486
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8077338&dopt=Abstract

• “These results indicate that the growth of U87MG human malignant glioma is dependent on corticoids. The antiproliferative effect of RU486 appears to be due to the inhibition of binding of glucocorticoid hormones to their receptor proteins. Our results suggest a new therapy for some brain tumors, such as malignant gliomas based on the steroid hormone antagonist RU486.”

1997: Dexamethasone inhibits apoptosis in C6 glioma cells through increased expression of Bcl-XL
http://www.springerlink.com/content/7r22113065664351/
“.... The glucocorticoid dexamethasone (Dex) has been reported to modulate a number of signaling pathways and physiological processes, including apoptosis. This study was carried out to investigate the cytoprotective mechanism of Dex in C6 glioma cells. Pre-treatment of cells with Dex inhibited apoptosis induced by staurosporine, etoposide and thapsigargin. Apoptosis inhibition correlated with blockade of mitochondrial cytochrome c release, abolition of caspase-3 activity along with inhibition of caspase-9 and PARP cleavage. Dex-mediated cytoprotection coincided with the induction of the anti-apoptotic protein, Bcl-XL. The specific glucocorticoid receptor antagonist, RU486, reversed the anti-apoptotic effect of Dex and prevented Bcl-XL induction. Here, we show for the first time that knockdown of Bcl-XL expression with siRNA reversed the protective effects of the glucocorticoid in glioma cells. We conclude that Dex-mediated inhibition of apoptosis in C6 glioma cells is through induction of Bcl-XL. “

1994: The antiprogestatin drug RU 486 potentiates doxorubicin cytotoxicity in multidrug resistant cells through inhibition of P-glycoprotein function.
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=7982498&dopt=Abstract
• “These results thus demonstrate that RU 486 can downmodulate anticancer drug resistance through inhibition of P-gp function.”

1999: Ceramide toxicity and metabolism differ in wild-type and multidrug-resistant cancer cells.
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10427136&dopt=Abstract
• “The anti-progestine, RU486, also blocked glucosylceramide synthesis in cells; however, LY117018, a raloxifene analog, was without influence. We propose that an enhanced capacity to glycosylate ceramide as evidenced in MCF-7-AdrR cells, is a molecular determinant of drug resistance, particularly as regards resistance to ceramide-enhancing agents such as anthracyclines, ionizing radiation, and tumor necrosis factor-alpha.”


Corticosteroids induce chemotherapy resistance in the majority of tumour cells from bone, brain, breast, cervix, melanoma and neuroblastoma
http://histology1.med.uoc.gr/ijo/2006/volume29/number5/1295.pdf

Dear felixthecat, I am new in this chat line. I am italian and we live in Italy so sorry for my english. Unfortunately my wife was diagnosed on decenber 2006 of an high grade glioma. She is 37 yars old and we have 3 children. Her work was Flight Cabin attendant for alitalia airline. On january 2007 she underwent a surgery for peritonealventricle diversin with right ventricle access and after a while also at the left front horn. She began raditherapy on the thalamic site. this was combinated with Cyber-knife treatment on frontal site. She start also chemiotherapy involving cisplatino and temozolomide. She had repeat this kind of treatment other 5 times.
Now she is good at least and we are waiting for a new therapy based on receptors Monoclone.
In the last month she has some problems to her eyes concerning with sight field. Her sight field is reduced on the lateral side of an half. Now we have started again to take cortisone and she is going much better.
The question is: have you some suggestion regarding this new problem I mean her sight problem?
Thank you very much for your interest
Ming59

momatabor

up date
14 months and doing great, prays be to god

christinamw

momatabor said:

up date
14 months and doing great, prays be to god

glioma
my hope and prayers are with you my husband has stage 3 glioma we are six months tumor free there is hope stay strong

dana748

Your Husband
Hello, my name is Dana McDonald and I live in St. Louis, Missouri. I was just recently diagnosed with a stage 3 Glioma tumor and have since had most of it surgically removed. I came across your post and was wondering if you would mind sharing some of what your journey has been like to help me better understand my own situation? If it is too difficult to talk about I would understand, I am just trying to get a better idea of what I am dealing with.