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Cancer Differentiation

VanMeter AJ, Rodriguez AS, Bowman ED et al (2008) Laser capture microdissection and protein microarray analysis of human non-smaU cell lung cancer differential epidermal growth factor receptor (EGPR) phosphorylation events associated with mutated EGFR compared with wild type. Mol Cell Proteomics 7 1902-1924... [Pg.212]

Lung Cancer Differentiation Implications for Diagnosis and Treatment, edited by S. D. Bemal and P. J. Hesketh... [Pg.596]

Schalken, J. A., Hessels, D., and Verhaegh, G. (2003) New targets for therapy in prostate cancer differential display code 3 (DD3(PCA3)), a highly prostate cancer-specific gene. Urology 62, 34-43. [Pg.14]

Fig. 10.31. Metastases from colon cancer. Sagittal CT shows a well-delineated mixed cystic and solid ovarian mass (arrow), which abuts the uterus fundus and elevates small bowel loops. No ascites was found in the pelvis or abdomen. In this patient with stage T4 colon cancer, differentiation of metastasis from ovarian cancer is not possible by imaging... Fig. 10.31. Metastases from colon cancer. Sagittal CT shows a well-delineated mixed cystic and solid ovarian mass (arrow), which abuts the uterus fundus and elevates small bowel loops. No ascites was found in the pelvis or abdomen. In this patient with stage T4 colon cancer, differentiation of metastasis from ovarian cancer is not possible by imaging...
Cintapalli KN, Chopra S, Ghiatas AA et al (1999) Diverticulitis versus colon cancer differentiation with helical CT findings. Radiology 210 429-435... [Pg.376]

Cancer. Cancer is a cellular malignancy characterized by loss of normal controls resulting in unregulated growth, lack of differentiation, and the abihty to invade local tissues and metastasize. Most cancers are potentially curable, if detected at an early enough stage. The ideal antineoplastic agent would destroy cancer cells without adverse effects or toxicities to normal cells. No such dmg exists. [Pg.41]

Modem cancer therapy has been primarily dependent upon surgery, radiotherapy, chemotherapy, and hormonal therapy (72) (see Chemotherapeutics,anticancer Hormones Radiopharmaceuticals). Chemotherapeutic agents maybe able to retard the rate of growth, but are unable to eradicate the entire population of neoplastic cells without significant destmction of normal host tissue. This serious side effect limits general use. More recentiy, the immunotherapeutic approach to cancer has involved modification and exploitation of the cellular and molecular mechanisms in host defense, regulation of tissue proliferation, tissue differentiation, and tissue survival. The results have been more than encouraging. [Pg.41]

In order to discuss the biological mechanisms involved in the aetiology of genital tract malformations, testicular cancer and lowered sperm counts, some knowledge of the processes involved in the differentiation and development of the male reproductive tract and determination of normal testicular function is required. An early embryo has the potential to develop either a male or a female... [Pg.88]

Cellular therapies in transplantation and cancer are based on specific cells separated or sorted from human blood, bone marrow, or cord blood by means of their specific cell surface markers or cell differentiation antigens, e.g., CD3, CD4, CD8, CD 14, CD 19, and CD34. For example, the CD34+ stem cells, especially those derived from human embryos, have the capacity to differentiate in culture to generate different somatic cells, e.g., liver cells, heart cells, neurons, etc. This exploding field of research is now termed regenerative medicine. [Pg.265]

The CaR regulates numerous biological processes, including the expression of various genes (e.g., PTH) the secretion of hormones (PTH and calcitonin), cytokines (MCP-1), and calcium (e.g., into breast milk) the activities of channels (potassium channels) and transporters (aquaporin-2) cellular shape, motility (of macrophages), and migration cellular adhesion (of hematopoietic stem cells) and cellular proliferation (of colonocytes), differentiation (of keratinocytes), and apoptosis (of H-500 ley dig cancer cells) [3]. [Pg.303]

Reports of ChE abnormalities in tumours, e.g., meningioma, glioma, acoustic neurinomas and lung cancers, megakaryocytopoietic disorders and leukemias, ovarian tumours and neuroblastomas, suggest cell proliferation and differentiation activities. [Pg.358]

ET-1 also stimulates anti-apoptotic signal cascades in fibroblasts, vascular smooth muscles and endothelial cells (via phosphatidylinositol-3-kinase and Akt/pro-tein kinase B). In prostate and ovarian cancer, upregulation of endothelin synthesis and ETA receptors has been associated with a progression of the disease. The inhibiton of ETA receptors results in a reduced tumour growth. In malignant melanoma, ETB receptors are associated with tumour progression. Endothelins can also stimulate apoptosis in stretch-activated vessels via the ETB receptor, which contrasts the above-mentioned effects. The molecular basis for these differential anti- and pro-apoptotic reactions mediated by endothelins remains elusive. [Pg.474]


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