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Q: Ira, you point to Dewayne Dedmon as a playoff-rotation player for the Heat to address the rebounding. But last year he was with the Heat when they were crushed on the glass by the Bucks in the playoffs. -- Wes. A: But the Heat last year also were trying to get by with Trevor Ariza as the starting power forward and with less collective rebounding. This season, Kyle Lowry provides help on the glass and there is more of a group mentality. But I do agree that there could become some potential matchups where Dewayne Dedmon is asked to step aside in terms of smaller ball. If the Cavaliers, for example, are without Jarrett Allen, or even when Allen would leave the game in such a matchup, there arguably could be better options than having Dewayne going out to the corners to defend Kevin Love or having to deal with the athleticism of Evan Mobley. So that could open it more to Caleb Martin, which could in turn open it up more for an additional wing (Victor Oladipo?). Advertisement [ Submit your "Ask Ira" question here! ] Q: How do you not play someone who just scored 40 points? Doesn’t Erik Spoelstra need to figure this out, and soon? -- Bob, Davie. A: But, again, as mentioned in this space yesterday, Victor Oladipo’s 40-point performance in Sunday’s regular-season finale in Orlando came against an opponent with the second-worst record in the NBA that largely was playing its second-team players. Then also consider that on closing night, Victor’s 40 stood as just the night’s fifth-highest scoring total, a night when Obi Toppin scored 42 for the Knicks, Jalen Green 41 for the Rockets and Malik Monk 41 for the Lakers, with none of those three to appear in the playoffs. Yes, Vic’s performance was heartening. But he assuredly is not starting. And the Heat’s wing priorities in the playoffs are going to be Jimmy Butler, Kyle Lowry and Tyler Herro. So it’s not as if Vic will get to play as a volume shooter or volume scorer. And to this point, when Vic has been cast in a limited ro

Background & aims: Immune checkpoint inhibitors have limited efficacy in many tumors. We investigated mechanisms of tumor resistance to inhibitors of programmed cell death-1 (PDCD1, also called PD-1) in mice with gastric cancer, and the role of its ligand, PD-L1. Methods: Gastrin-deficient mice were given N-methyl-N-nitrosourea (MNU) in drinking water along with Helicobacter felis to induce gastric tumor formation; we also performed studies with H/K-ATPase-hIL1B mice, which develop spontaneous gastric tumors at the antral-corpus junction and have parietal cells that constitutively secrete interleukin 1B. Mice were given injections of an antibody against PD-1 or an isotype control before tumors developed, or anti-PD-1 and 5-fluorouracil and oxaliplatin, or an antibody against lymphocyte antigen 6 complex locus G (also called Gr-1), which depletes myeloid-derived suppressor cells [MDSCs]), after tumors developed. We generated knock-in mice that express PD-L1 specifically in the gastric epithelium or myeloid lineage. Results: When given to gastrin-deficient mice before tumors grew, anti-PD-1 significantly reduced tumor size and increased tumor infiltration by T cells. However, anti-PD-1 alone did not have significant effects on established tumors in these mice. Neither early nor late anti-PD-1 administration reduced tumor growth in the presence of MDSCs in H/K-ATPase-hIL-1β mice. The combination of 5-fluorouracil and oxaliplatin reduced MDSCs, increased numbers of intra-tumor CD8 + T cells, and increased the response of tumors to anti-PD-1; however, this resulted in increased tumor expression of PD-L1. Expression of PD-L1 by tumor or immune cells increased gastric tumorigenesis in mice given MNU. Mice with gastric epithelial cells that expressed PD-L1 did not develop spontaneous tumors, but they developed more and larger tumors after administration of MNU and H felis, with accumulation of MDSCs. Conclusions: In mouse models of gastric cancer, 5-fluorouracil and oxalipl

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