He, and G.F. Weber. 2003. Growth factor signaling induces metastasis genes in transformed cells: molecular connection between Akt kinase and osteopontin in breast cancer. Mol Cell Biol. 23:6507-19.
New therapies, using selegiline (deprenyl) and antioxidants (tocopherol or Vitamin E) focus on halting the progression of the disease by potentially salvaging surviving SNpc cells (Ahlskog, 1990). A more aggressive approach in the treatment of PD has surfaced in recent years. Researchers are experimenting with the prospects of transplanting tissue directly into the afflicted areas of the central nervous system (CNS) of PD patients. In both animal models of PD and humans, marginally successful transplants have been performed using adrenal chromaffin cells and fetal neurons. Genetically-altered, dopamine-producing tissues are currently being proposed as an alternative in transplant therapy of PD.
One of the recent developments in the research behind oncogenesis and its relationship to cancer is the theory of “oncogenic addiction”. This theory explains the phenomena of “a tumor cell seemingly exhibiting dependence on a single oncogenic pathway or protein for its sustained proliferation and/or survival” (Sharma & Settleman 2007). These findings suggest that there may be a way to “switch off the crucial pathway of dependence”, which in theory should negatively affect or inhibit the cancer, “while sparing normal cells that are not similarly addicted” (Sharma & Settleman 2007). This has been established with the ability to inactivate “counterparts of oncogenic proteins in normal tissues” and see that there is toleration without “obvious consequences” (Sharma & Settleman 2007). This is the concept of “addiction” in cancer, and the dependence on particular genes to activate prolifer... ... middle of paper ... ...need to be developed to begin this study, we can infer from past research the steps in which determination of these relationships could be done.
Cancer can be cured with gene therapy by many methods. The tumor suppressor genes can be replaced, you can use gene-marking methods to find cancerous cells, and remove them, an d cells can be stopped from overexpressing genes Gene therapy works by genetically altering cells of the body, but not reproductive cells, (somatic gene therapy), or by altering the reproductive cells (germ-line gene therapy). Both of these methods are used to alter genetically diseased cells to treat genetic diseases. Gene therapy is a developing field in genetics that is being used to find ways to cure cancer and other diseases that has been progressing over the past 50 years. Works Cited Culver, Kenneth W. Gene Therapy: a Primer for Physicians.
Summary: Background and objective. Tumor heterogeneity is shown to be related to clinical outcome in cancer patients. The concept of a small subset of cancer stem cells being responsible for tumor relapse and metastasis comes out as a promising strategy for targeted cancer therapy. However, cancer stem cells are not easy to identify and isolate. The aim of this study was to determine the putative colon cancer stem cell subsets in human colon cancer cell lines HCT116 and HT29, which differ in their aggressiveness and differentiation capacity.
30. Singh D, Joshi DD, Hameed M, Qian J, Gascon P, Maloof PB, et al. Increased expression of preprotachykinin-I and neurokinin receptors in human breast cancer cells: implications for bone marrow metastasis. Proc Natl Acad Sci U S A. 2000;97(1):388-93.
According to NCI dictionary of cancer terms1, cancer cell lines are cancer cells that keep dividing and growing over time, under certain conditions in a laboratory. Cancer cell lines are used in research to study the biology of cancer and to test cancer treatments. As there are ethical issues in using animal models to study cancer, cell lines have been used as an alternative model. There are many pros and cons in using cell lines as a model for cancer study. A large number of cancer cell lines are available and are easily accessible for scientific research.
A large percent of cancers with active p53 have been noted to have defects in the p53-mediated apoptotic pathway or the degradation of p53 by p53 degradation pathways has been noted. Another large percent of cancers exist in which there is mutated, non-active p53. The overexpression of ARF or the interruption of the MDM2:p53 interaction are a couple of therapeutic strategies for alleviating p53 degradation in cancer cells with active p53. Other chemotherapies exist that seek to correct the defect in the p53-mediated apoptotic pathway in the cancer cells with active p53. One strategy of therapy for cancer cells lacking active p53/containing mutated p53, is t... ... middle of paper ... ...properties of NPM1 are possible reasons why NPM1 also influences cell growth and transformation during tumor development.
INTRODUCTION: There are new approaches and agents against certain types of cancer that are urgently needed. Some of the new agents use highly advanced technology utilizing nanoencapsulation that will improve the therapeutic index of the natural drugs. Nanoparticles for cancer therapeutics are rapidly evolving and are being introduced in an attempt to overcome several limitations of conventional small-molecule chemotherapeutics. Though chemotherapy is successful to some extent in certain cancers, it has several limitations (14). I will be discussing three natural products (Currcumin, Thymoquinone and Genistein) from plants that have anti-cancer effects.
Scintigraphic evaluation of neuroendocrine tumors. Applied Radiology, 30 (6), 11-17. Krenning E.P., De Jong, M, Kooij, P.M., et al. (1999). Radiolabelled somatostatin analogue for peptide receptor scintigraphy and radionuclide therapy.