Theoretical description of deformed proton emitters: nonadiabatic coupled-channel method

The newly developed nonadiabatic method based on the coupled-channel Schroedinger equation with Gamow states is used to study the phenomenon of proton radioactivity. The new method, adopting the weak coupling regime of the particle-plus-rotor model, allows for the inclusion of excitations in the daughter nucleus. This can lead to rather different predictions for lifetimes and branching ratios as compared to the standard adiabatic approximation corresponding to the strong coupling scheme. Calculations are performed for several experimentally seen, non-spherical nuclei beyond the proton dripline. By comparing theory and experiment, we are able to characterize the angular momentum content of the observed narrow resonance.Comment: 12 pages including 10 figure

RAS/MAPK activation is associated with reduced Tumor-infiltrating lymphocytes in Triple-Negative Breast Cancer: Therapeutic Cooperation Between MEK and PD-1/PD-L1 Immune Checkpoint Inhibitors

PURPOSE: Tumor-infiltrating lymphocytes (TIL) in the residual disease (RD) of triple-negative breast cancers (TNBC) after neoadjuvant chemotherapy (NAC) are associated with improved survival, but insight into tumor cell-autonomous molecular pathways affecting these features are lacking. EXPERIMENTAL DESIGN: We analyzed TILs in the RD of clinically and molecularly characterized TNBCs after NAC and explored therapeutic strategies targeting combinations of MEK inhibitors with PD-1/PD-L1-targeted immunotherapy in mouse models of breast cancer. RESULTS: Presence of TILs in the RD was significantly associated with improved prognosis. Genetic or transcriptomic alterations in Ras-MAPK signaling were significantly correlated with lower TILs. MEK inhibition upregulated cell surface MHC expression and PD-L1 in TNBC cells both in vivo and in vitro. Moreover, combined MEK and PD-L1/PD-1 inhibition enhanced antitumor immune responses in mouse models of breast cancer. CONCLUSIONS: These data suggest the possibility that Ras-MAPK pathway activation promotes immune-evasion in TNBC, and support clinical trials combining MEK- and PD-L1-targeted therapies. Furthermore, Ras/MAPK activation and MHC expression may be predictive biomarkers of response to immune checkpoint inhibitors