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Finally, a response


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After two and a half years of being diagnosed with lung cancer, to day my oncologist said there was a change. As y'all know I was misdiagnosed with nsclc in Dec. 2000 and all the chemo had no effect on my cancer. In the meantime I developed a crippling type of arthritis that was getting worse. Then in Feb. I was rediagnosed with atypical carcinoid. I started taking 3 shots a day of sandostatin. I have been on this for 6 weeks and when I went for my 3 month check up today I was told that the 24 hour urine test showed that the seratonin level had dropped from 70 to 14. This is what the tumor secretes that causes the side effects like flushing and diarhhea. My doctor says it is very rare for the cancer to cause the arthritis I have but not out of the question. I have been feeling some relief from the arthritis but was afraid to jump to any conclusions. Maybe,

just maybe, this drug will help and I can enjoy a better qualityof life.

My onc. wants to start with the LAR sandostatin which is a long acting release shot that I will get once a month. He was enthusiastic about it so I guess I can be too.

Please, don't get me wrong. I was happy to hear that I had a stable disease when I went for check-ups....But after all I've been through I at least wanted to put a DENT in that old nasty cancer.

My grandbaby is coming for Mother's Day. I haven't seen her since she was 1 month old. She will be almost 6 months next week. :D:D

So it's "two" good newses"

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WOW what great news!! I, too, hope you have a wonderful Mother's Day with your little grandbaby!! Do you mind if I ask how you were diagnosed with your atypical carcinoid? Originally I see you were misdiagnosed - so was I with squamous cell. I was just curious as to how they changed that diagnosis for you. They found my typical carcinoid after they removed my lung. God bless!


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  • 1 month later...


Here is some research info. It happens to come from New Orleans :)

Glad you enjoyed your visit with the grandchild. Wishing you many more visits

Effective treatment of H838 human non-small cell lung carcinoma with a targeted cytotoxic somatostatin analog, AN-238.

Szereday Z, Schally AV, Szepeshazi K, Bajo AM, Hebert F, Halmos G, Nagy A.

Endocrine, Polypeptide and Cancer Institute, Veterans Affairs Medical Center, New Orleans, LA 70112-1262, USA.

The accumulation of radioactive somatostatin analog [111In]pentetreotide in non-small cell lung cancer (non-SCLC) during scintigraphy of patients provides a rationale for investigating the efficacy of somatostatin receptor-based chemotherapy in non-SCLC. Consequently, in this study, we evaluated the antitumor effects of cytotoxic somatostatin analog AN-238 on H838 human non-SCLC xenografted into nude mice in comparison with its cytotoxic radical, 2-pyrrolinodoxorubicin (AN-201). The expression of messenger RNA (mRNA) for human somatostatin receptor subtypes 2 (hsst2) and 5 (hsst5) in H838 cells, and tumors was also investigated using reverse-transcription polymerase chain reaction (RT-PCR). Somatostatin receptors on H838 tumors were characterized by ligand competition assay using radiolabeled somatostatin analog, RC-160. Three i.v. injections of AN-238 at 150 nmol/kg, given on days 1, 7 and 21, resulted in a significant (p<0.05) tumor growth inhibition, the final tumor volume being 60% smaller than in the controls. The tumor doubling time was also extended significantly (p<0.05) from 9.65+/-0.56 days in the controls to 17.52+/-3.3 days. Only one of 8 mice died due to toxicity. In contrast, cytotoxic radical AN-201 was ineffective and more toxic, killing 2 of 7 animals. mRNA for hsst2 was found in H838 xenografts, but not in H838 cells from which the xenografts originated. Interestingly, H838 cells grown in a special, serum-free medium did express mRNA for hsst2. mRNA for hsst5 was not found in any samples tested. Binding studies demonstrated the presence of high affinity (Kd = 7.3+/-1.2 nM) binding sites for RC-160 with a mean maximal binding capacity (Bmax) of 953.3+/-45.3 fmol/mg protein. AN-238 at 3.14+/-0.93 nM concentration displaced 50% of radiolabeled RC-160 binding to somatostatin receptors in H838 tumors. Our results indicate that patients with inoperable non-SCLC may benefit from chemotherapy targeted to somatostatin receptors based on AN-238.

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