Brain Tumour Survivor

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PostPosted: Tue Oct 31, 2006 1:23 pm 
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Joined: Mon Oct 30, 2006 3:14 pm
Posts: 1
Dear Friends,

I'm a brain tumour patient diagnosed with a Pinealoblastoma.
Can anyone provide me information on this?

Will i survive? :(

I don't want to die at this age.....


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PostPosted: Tue Oct 31, 2006 6:04 pm 
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Joined: Tue Oct 10, 2006 5:13 pm
Posts: 11
Location: goondiwindi
I am sorry I am only new at this game too - I haven't heard of this tumour but the site below is another great way to get help from people who are at the'chalk face' so to speak. Sending you prayers of hope Catherine

http://health.groups.yahoo.com/group/OzBrainTumour/


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PostPosted: Thu Apr 26, 2007 8:50 pm 
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Joined: Sat Nov 04, 2006 10:18 pm
Posts: 360
Location: Australia
Retinoblastomas (cones of the eye), medulloblastomas (cerebellum), pinealoblastomas (pineal), and adult neuroblastomas (lots of places) are related pediatric tumors that look like neuroblastomas microscopically.

Here is some info on the hormone treatment to use either monotherapy or in combination with radiation therapy.

Negative cross-talk between p53 and the glucocorticoid receptor and its role in neuroblastoma cells
http://www.pubmedcentral.nih.gov/articl ... tid=305812

• The tumour suppressor p53 and the glucocorticoid receptor (GR) respond to different types of stress. We found that dexamethasone-activated endogenous and exogenous GR inhibit p53-dependent functions, including transactivation, up- (Bax and p21WAF1/CIP1) and down- (Bcl2) regulation of endogenous genes, cell cycle arrest and apoptosis. GR forms a complex with p53 in vivo, resulting in cytoplasmic sequestration of both p53 and GR. In neuroblastoma (NB) cells, cytoplasmic retention and inactivation of wild-type p53 involves GR. p53 and GR form a complex that is dissociated by GR antagonists, resulting in accumulation of p53 in the nucleus, activation of p53-responsive genes, growth arrest and apoptosis. These results suggest that molecules that efficiently disrupt GR–p53 interactions would have a therapeutic potential for the treatment of neuroblastoma and perhaps other diseases in which p53 is sequestered by GR.


2003: Glucocorticoid Cotreatment Induces Apoptosis Resistance toward Cancer Therapy in Carcinomas1
http://cancerres.aacrjournals.org/cgi/c ... 63/12/3112

• In conclusion, GCs are widely used in high doses in the therapy of leukemias and lymphomas and are also used as antiemetics or preservatives for normal cells during chemotherapy of solid tumors. In addition, GCs are among the most widely used anti-inflammatory drugs. In this study, we have shown that application of GCs renders certain tumors resistant or less susceptible to apoptosis after cancer therapy. This finding urges to carefully reconsider the widespread use of GCs in almost all treatment protocols for patients with solid cancers. In the clinical setting of cancer therapy, e.g., in antiemetic regimens, corticosteroids are usually given transiently to suppress acute side effects of cancer therapy. Although our experiments did not mimic precisely the clinical situation because we administered DEX daily to achieve steady-state levels, short-term exposure to DEX may nevertheless be sufficient to abrogate or diminish the efficacy of concomitant chemotherapy in cancer patients in vivo. This is suggested by our experiments where DEX was found to down-regulate basal and cisplatin-induced expression of apoptosis effectors within 24 h in vitro. Also, endogenous levels of GCs and those existing as a consequence of administered hormones may render solid tumors less susceptible to apoptosis after cancer therapy. The administration of steroid/receptor agonists such as RU486 might be beneficial before chemotherapy and radiotherapy to enhance cell death of solid tumor cells.


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