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חומרים טבעיים הגורמים להתמיינות מחדש (רה-דיפרנציאציה): CAPE, דיידזאין, אמודין, EPA, DHA, גניסטאין, מונוטרפנים, קוארצטין, רסברטרול. סלניום, ויטמין C, אלפה דהידרו-כולה-קלציפרול, ויטמין A. ד"ר יוסף ברנר www.sartan.co.il

בהמשך לתשובתי : 1. התאוריה על תאי אב שהופיעה בשאלה המקורית קיימת, אך זו תאוריה בלבד ואין לה עדין סימוכין מבוססים. להלן מאמר מסלובקיה המדבר על התאוריה הזאת. Neoplasma. 2005;52(6):435-40. Related Articles, Links Cancer stem cells. Soltysova A, Altanerova V, Altaner C. Cancer Research Institute, Slovak Academy of Sciences, Bratislava, Slovak Republic. There is an increasing evidence supporting the cancer stem cell hypothesis. Normal stem cells in the adult organism are responsible for tissue renewal AND repair of aged OR damaged tissue. A substantial characteristic of stem cells is their ability for self-renewal without loss of proliferation capacity with each cell division. The stem cells are immortal, AND rather resistant to action of drugs. They are able to differentiate AND form specific types of tissue due to the influence of microenvironmental AND some other factors. Stem cells divide asymmetrically producing two daughter cells -- one is a new stem cell AND the second is progenitor cell, which has the ability for differentiation AND proliferation, but not the capability for self-renewal. Cancer stem cells are in many aspects similar to the stem cells. It has been proven that tumor cells are heterogeneous comprising rare tumor initiating cells AND abundant non-tumor initiating cells. Tumor initiating cells -- cancer stem cells have the ability of self-renewal AND proliferation, are resistant to drugs, AND express typical markers of stem cells. It is not clear whether cancer stem cells originate from normal stem cells in consequence of genetic AND epigenetic changes and/or by redifferentiation from somatic tumor cells to the stem-like cells. Probably both mechanisms are involved in the origin of cancer stem cells. Dysregulation of stem cell self-renewal is a likely requirement for the development of cancer. Isolation AND identification of cancer stem cells in human tumors AND in tumor cell lines has been successful. To date, the existence of cancer stem cells has been proven in acute AND chronic myeloid leukemia, in breast cancer, in brain tumors, in lung cancer AND gastrointestinal tumors. Cancer stem cell model is also consistent with some clinical observations. Although standard chemotherapy kills most cells in a tumor, cancer stem cells remain viable. Despite the small number of such cells, they might be the cause of tumor recurrence, sometimes many years after the "successful" treatment of primary tumor. Growth of metastases in distinct areas of body AND their cellular heterogeneity might be consequence of cancer stem cell differentiation and/or dedifferentiation AND asymmetric division of cancer stem cells. Further characterization of cancer stem cells is needed in order to find ways to destroy them, which might contribute significantly to the therapeutic management of malignant tumors. 2. חומצה רטינואידית שהיא ניגזרת סינטטית של ויטמין A היא אחד מהחומרים החזקים ביותר עם תכונות של רה-דיפרנציאציה, כלומר זהו חומר אשר יכול להחזיר לתאים שאבדו את יכולת ההתמינות את היכולת הזאת. להלן מאמר אחד מבין רבים על חומר זה כחומר מחזיר התמיינות: Clin Oncol (R Coll Radiol). 2004 Dec;16(8):569-74. Related Articles, Links A phase II study using retinoids as redifferentiation agents to increase iodine uptake in metastatic thyroid cancer. Short SC, Suovuori A, Cook G, Vivian G, Harmer C. The Royal Marsden Hospital Thyroid Unit, London AND Sutton, UK. [email protected] AIMS: Radio-iodine is effective in treating metastatic differentiated thyroid cancers. In 20% of cases, however, these tumours fail to take up radio-iodine, AND treatment options are then limited. Failure of iodine uptake might be reversible using redifferentiating agents. Retinoids redifferentiate a variety of cell types AND increase iodine uptake in thyroid tumour cells in vitro. The aim of this study was to assess whether oral isotretinoin could increase radio-iodine uptake in patients with iodine-uptake-negative metastatic thyroid cancer. METHODS: Patients who had iodine-uptake-negative metastatic papillary OR follicular thyroid cancers were selected from the thyroid database at The Royal Marsden Hospital AND enrolled to an open-label, non-randomised phase II trial. Sites of metastatic disease were assessed using computed tomography OR magnetic resonance imaging, AND absence of iodine uptake was confirmed using a diagnostic radio-iodine scan before study entry. In eligible patients, isotretinoin was prescribed at 1.5 mg/kg/day orally for 8 weeks. Response was assessed within 2 weeks of completing treatment with repeat radio-iodine scan. All patients were reviewed every 2 weeks during treatment for assessment of toxicity. RESULTS: Sixteen patients were treated with isotretinoin between January 2001 AND July 2002: nine with metastatic papillary thyroid cancer, five with metastatic follicular cancer AND two with Hurthle cell carcinoma. Median age was 57 years. All patients tolerated 8 weeks of oral isotretinoin. Mucocutaneous side-effects AND minor changes in biochemical OR lipid profiles were documented in most patients. In one patient, radio-iodine uptake increased after retinoid administration; however, this was not large enough to permit a significant dose of iodine to be given to sites of metastatic disease. In the other 15 patients, no radio-iodine uptake was documented. CONCLUSION: Treatment with isotretinoin does not reliably increase radio-iodine uptake in patients with metastatic thyroid cancer. This treatment alone does not enable radio-iodine to be used for further treatment. ד"ר יוסף ברנר