Constraints on radiative decay of the 17-keV neutrino from COBE Measurements

It is shown that, for a nontrivial radiative decay channel of the 17-keV neutrino, the photons would distort the microwave background radiation through ionization of the universe. The constraint on the branching ratio of such decays from COBE measurements is found to be more stringent than that from other considerations. The limit on the branching ratio in terms of the Compton $y$ parameter is $B_\gamma < 1.5 \times 10^{-7} ({\tau_\nu \over 10^{11} sec})^{0.45} ({y \over 10^{-3}})^{1.11} h^{-1}$ for an $\Omega=1, \Omega_b=0.1$ universe.Comment: 7 pages. (figures will be sent on request) (To appear in Phys. Rev. D.

Loss of p19Arf Facilitates the Angiogenic Switch and Tumor Initiation in a Multi-Stage Cancer Model via p53-Dependent and Independent Mechanisms

The Arf tumor suppressor acts as a sensor of oncogenic signals, countering aberrant proliferation in large part via activation of the p53 transcriptional program, though a number of p53-independent functions have been described. Mounting evidence suggests that, in addition to promoting tumorigenesis via disruptions in the homeostatic balance between cell proliferation and apoptosis of overt cancer cells, genetic alterations leading to tumor suppressor loss of function or oncogene gain of function can also incite tumor development via effects on the tumor microenvironment. In a transgenic mouse model of multi-stage pancreatic neuroendocrine carcinogenesis (PNET) driven by inhibition of the canonical p53 and Rb tumor suppressors with SV40 large T-antigen (Tag), stochastic progression to tumors is limited in part by a requirement for initiation of an angiogenic switch. Despite inhibition of p53 by Tag in this mouse PNET model, concomitant disruption of Arf via genetic knockout resulted in a significantly accelerated pathway to tumor formation that was surprisingly not driven by alterations in tumor cell proliferation or apoptosis, but rather via earlier activation of the angiogenic switch. In the setting of a constitutional p53 gene knockout, loss of Arf also accelerated tumor development, albeit to a lesser degree. These findings demonstrate that Arf loss of function can promote tumorigenesis via facilitating angiogenesis, at least in part, through p53-independent mechanisms