Additional J/ΨJ/\Psi Suppression from High Density Effects

At high energies the saturation effects associated to the high parton density should modify the behavior of the observables in proton-nucleus and nucleus-nucleus scattering. In this paper we investigate the saturation effects in the nuclear $J/\Psi$ production and estimate the modifications in the energy dependence of the cross section as well as in the length of the nuclear medium. In particular, we calculate the ratio of $J/\Psi$ to Drell-Yan cross sections and show that it is strongly modified if the high density effects are included. Moreover, our results are compared with the data from the NA50 Collaboration and predictions for the RHIC and LHC kinematic regions are presented. We predict an additional $J/\Psi$ suppression associated to the high density effects.Comment: 13 pages, 5 figures, version to be published in Eur. Phys. J.

Off-Forward Parton Distributions

Recently, there have been some interesting developments involving off-forward parton distributions of the nucleon, deeply virtual Compton scattering, and hard diffractive vector-meson production. These developments are triggered by the realization that the off-forward distributions contain information about the internal spin structure of the nucleon and that diffractive electroproduction of vector mesons depends on these unconventional distributions. This paper gives a brief overview of the recent developments

The oncogene AAMDC links PI3K-AKT-mTOR signaling with metabolic reprograming in estrogen receptor-positive breast cancer

Adipogenesis associated Mth938 domain containing (AAMDC) represents an uncharacterized oncogene amplified in aggressive estrogen receptor-positive breast cancers. We uncover that AAMDC regulates the expression of several metabolic enzymes involved in the one-carbon folate and methionine cycles, and lipid metabolism. We show that AAMDC controls PI3K-AKT-mTOR signaling, regulating the translation of ATF4 and MYC and modulating the transcriptional activity of AAMDC-dependent promoters. High AAMDC expression is associated with sensitization to dactolisib and everolimus, and these PI3K-mTOR inhibitors exhibit synergistic interactions with anti-estrogens in IntClust2 models. Ectopic AAMDC expression is sufficient to activate AKT signaling, resulting in estrogen-independent tumor growth. Thus, AAMDC-overexpressing tumors may be sensitive to PI3K-mTORC1 blockers in combination with anti-estrogens. Lastly, we provide evidence that AAMDC can interact with the RabGTPase-activating protein RabGAP1L, and that AAMDC, RabGAP1L, and Rab7a colocalize in endolysosomes. The discovery of the RabGAP1L-AAMDC assembly platform provides insights for the design of selective blockers to target malignancies having the AAMDC amplification