Studies on Herbal Compounds With Broad-Spectrum Anti-Cancer Activity through Generation of Reactive Oxygen Species

together with invasion of the surrounding tissue and the spread of malignant cells (Karin M et al., 2005) by the ability to implant into distant sites through metastasis. In a living organism, the multiplication of cells is regulated. Within a young animal, the cell multiplication actually exceeds cell death, as a result animal increases in size. Very occasionally, the complicated mechanisms that regulate cell multiplication fail and a cell begins to grow and divide although the body has no need for further cells of its type. The indefinite clonal expansion of the cell ultimately gives rise to a tumor. Tumor in medical language simply means swelling or lump, neoplastic, inflammatory or other. In common language, however, it is synonymous with 'neoplasm', either benign or malignant. The benign tumor does not spread to its surrounding tissues. On the other hand malignant tumor possesses a specific characteristic feature known as metastasis which means spread of tumor cells from their site of origin and establishment of areas of secondary growth (Fig 1). The term ‘cancer’ refers to specifically malignant forms of tumor

Thyrostimulin Regulates Osteoblastic Bone Formation During Early Skeletal Development

The ancestral glycoprotein hormone thyrostimulin is a heterodimer of unique glycoprotein hormone subunit alpha (GPA)2 and glycoprotein hormone subunit beta (GPB)5 subunits with high affinity for the TSH receptor. Transgenic overexpression of GPB5 in mice results in cranial abnormalities, but the role of thyrostimulin in bone remains unknown. We hypothesized that thyrostimulin exerts paracrine actions in bone and determined: 1) GPA2 and GPB5 expression in osteoblasts and osteoclasts, 2) the skeletal consequences of thyrostimulin deficiency in GPB5 knockout (KO) mice, and 3) osteoblast and osteoclast responses to thyrostimulin treatment. Gpa2 and Gpb5 expression was identified in the newborn skeleton but declined rapidly thereafter. GPA2 and GPB5 mRNAs were also expressed in primary osteoblasts and osteoclasts at varying concentrations. Juvenile thyrostimulin-deficient mice had increased bone volume and mineralization as a result of increased osteoblastic bone formation. However, thyrostimulin failed to induce a canonical cAMP response or activate the noncanonical Akt, ERK, or mitogen-activated protein kinase (P38) signaling pathways in primary calvarial or bone marrow stromal cell-derived osteoblasts. Furthermore, thyrostimulin did not directly inhibit osteoblast proliferation, differentiation or mineralization in vitro. These studies identify thyrostimulin as a negative but indirect regulator of osteoblastic bone formation during skeletal developmen