Oxidative Phosphorylation Promotes Primary Melanoma Invasion

Notch signaling promotes growth and invasion in uveal melanoma.

PURPOSE To determine whether uveal melanoma, the most common primary intraocular malignancy in adults, requires Notch activity for growth and metastasis. EXPERIMENTAL DESIGN Expression of Notch pathway members was characterized in primary tumor samples and in cell lines, along with the effects of Notch inhibition or activation on tumor growth and invasion. RESULTS Notch receptors, ligands, ...

Bradykinin promotes the chemotactic invasion of primary brain tumors.

Primary brain tumors, gliomas, diffusely invade the brain by active cell migration either intraparenchymal, along white matter tracts or along blood vessels. The close relationship of glioma with the vasculature assures a continuous supply of oxygen and nutrients essential for cell growth, and exposes cells to a variety growth factors, chemokines, cytokines, and kinins. Signals that attract gli...

Primary duodenal malignant melanoma: A case report

Background: Melanoma is a neoplasm derived commonly from melanocytic cells of skin. Although coetaneous presentation of malignant melanoma is easily recognizable, the presentation of melanoma in other organs is so confusing. In particular, when it metastasizes to other organs, many bizarre figures and unusual organs may be involved. In this report, we present a case of primary duodenal malignan...

Lymphatic Invasion is Independently Prognostic of Metastasis in Primary Cutaneous Melanoma Running Title: Lymphatic Invasion and Melanoma Prognosis

O-13: Phosphorylation of 4E-BP1 Promotes Translation at The Oocyte Spindle

Background: Fully grown mammalian oocyte utilizes transcripts synthetized and stored during earlier development. In the mouse oocyte there are three forms of cap-dependent translational repressors: 4E-BP1, 4E-BP2, and 4E-BP3. The dominant form, 4E-BP1, inhibits cap-dependent translation by binding to the eIF4E translation initiation factor. Hyperphosphorylation of 4E-BP1 disrupts this inhibitor...