Colon
Antiproliferative activity and induction of apoptosis in human colon cancer cells treated in vitro with constituents of a product derived from Pistacia ... Journal of Phytotherapy & Phytopharmacology [H] [T] [M]
Array (Digital) Thomson Gale 2007-04-01
Release date: 2007-05-21
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No. Cancer is not a contagious disease.
This is a colon cancer cell.
Hi every one, im sherwin from philippines, i just wana share to you guys my experience on this cancer matter. my mom is 48 yrs old and got a diagnosed colon CA last feb. 18 2006, and she run through operation to took off her large intestine and got s colostomy bag on her stomach. we got to knew that my mom was on her 3rd stage allready. after 2 or 3 months of operation she under go chemotherapy for about 6 monts. and her CEA was not decreasing instead it was i ncreasing its rate every month. after her chemo and decided to take a rest for a month, and make her CEA again our doc said that the cancer cells are spreading faster to her body that makes her liver afected a littlebit, and find out that it is on its 4th stage already, i would like to know that is there another chance fo my mom to survive? can my mom survive on her 4th stage cancer? Or is there another possible way to get through w/ this and make my mom live? thanks a lot guys. i am looikng forward to answer my question.
Patients with stage IV disease rarely live beyond 5 years, and the median survival (meaning half the patients live longer, and half shorter) with treatment is between 1 and 2 years.
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as i am in my late 30's only(?), my doctor is puzzled that i being younger to exhibit symptoms of the disease...am the youngest in the brood of 5 and the only one in the family to have it (or any cancer for that matter)..the rest of my siblings will follow suit w/ colonoscopy soon...any of them may be positive w/c worries me more...please help me clarify this notion medical people or not...thank you...
No one knows the answer to this question. It is possible that malignant cells can remain dormant in the body, this happens to cancer patients who experience relapse. So, it may not be a slow cancer you are describing but a dormant cancer cell that has not yet begun to grow. At some point, perhaps age . . or some carcingoen . . or hormones . . something triggers that dormant cell to begin growing uncontrollably. But, it is not clear why.
My son has a rare cancer that seemed to come out of nowhere. He actually had a well physical in December of that year so he could play sports. He had a complete physical and was found healthy. A month later in January he was not recovering from the flu. By early March he was diagnosed with stage IV sarcoma. I asked this same question . . could this have started when he was really little and been growing all along? And, I was told, probably not . . that the cancer can absolutely grow that aggressively and fast in only a few months. Since that time I have met other patients with this disease . . sometimes the cancer grows in as little as weeks . . but sometimes for unknown reasons it will sit dormant and not grow at all.
My dad has 1 in 10 cells showing cancer, they are recommending hormone shots every 3 months. Is this helful or not? He doesn't want to get the shots if it is not going to slow it down or stop the growth.
It would help greatly if you could tell us what specific hormonal agent is being recommended. There are many types of hormones that can be used clinically. Most are not generally used for adenocarcinoma of the colon.
And do you mean one in ten lymph nodes show cancer rather than "one in ten cells?" Has you dad had a colon resection?
Are you sure this isn't prostate cancer? Adenocarcinoma of the prostate that has spread to the colon might commonly be treated palliatively with hormonal agents.
If the doctor is recommending "adjuvant" (preventive) treatments, he or she should be providing you and your dad with the data regarding expected benefits verses risks of treatment. Ideally you would be present with him at the doctor visit when this treatment was recommended.
I would not recommend a treatment without explaining the chances for benefit based on experience reported in the medical literature with groups of similar patients. Sometimes there are no family members present, and the patients cannot recall all of the details regarding the explanation. Also, I suspect there are times when today's doctors are too busy to fully explain the rationale of treatments recommended.
Modern medical practice with the limits on reimbursement for time seems to force doctors to run people through faster leaving less time to explain things. I was fortunate to retire before I was forced by Medicare and other insurance carriers to see patients more quickly.
Here is an article that says so.
http://www.medsocial.com/blog.aspx?bloga ction=viewblog&show=280
Unlike the first answerer, I see great promise in stem cell treatment. Time will tell if the hope that many sufferers have been given by this possibility is fully justified, but it seems likely that many, many diseases can be treated more effectively with stem cells than with any current or "in process of development" therapies. It seems so much more hopeful to use a treatment that does not destroy healthy tissue and leave people with devastating side effects.
Colon cancer, however, will probably not be the first cancer to be evaluated for cure with stem cells. There is a current effective treatment for colon cancer--surgical removal of part or all of the colon. The pancreas, liver, and lungs cannot be as easily treated surgically, so I would imagine that those cancers would get priority in the search for cures with stem cells. A cure for colon cancer could follow quite quickly, however.
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Sphingosine Kinase Isoforms Regulate Oxaliplatin Sensitivity of ...
Abstract
The relationship between sphingosine kinase (SPHK), cellular ceramide concentration and chemosensitivity was investigated in human colon cancer cell lines. Among nine colon cancer cell lines, SPHK1 and SPHK2 activity and protein expression was highest in RKO cells and lowest in HCT116 cells. A viability assay revealed that HCT116 cells were sensitive to the effects of oxaliplatin ( -OHP was inhibited by fumonisin B1 but not myriocin, suggesting that ceramide formation was through the salvage pathway. Endogenous phosphorylated Akt levels were much higher in the resistant RKO cells than in the sensitive HCT116 cells. Either SPHK1 or SPHK2 silencing in RKO cells decreased phosphorylated Akt levels and increased p53 and p21 protein levels as well as poly(ADP-ribose) polymerase cleavage in response to
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Cell 75 (5) Dec. 3, 1993 Colon Cancer Gene