The Rhetorics of Health and Medicine: Inventional Possibilities for Scholarship and Engaged Practice

This essay argues that rhetoricians of health of medicine should continue to carve out an expansive focus on the exigencies, functions, and impacts of health-related discourse; attend to the movement, surrounding networks, and ecologies of this discourse; and work with other scholars/researchers, both inside and outside disciplinary rhetorical studies, toward a variety of goals

Overlapping Agencies: The Collision of Cancer, Consumers, and Corporations in Richard Powers’s Gain

Richard Powers\u27s 1998 novel Gain establishes a complicated relationship between its two main characters, a corporation called Clare International and suburban mom named Laura Bodey. Readers, assuming the malignity of such corporations, mistake the hints Laura encounters that Clare is responsible for her ovarian cancer for facts. Such readings overlook the science of ovarian cancer as well as how Powers depicts Laura\u27s relation to her disease. I analyze Laura\u27s understudied half of the novel, framing it as a cancer narrative that reworks conventions of that genre. In placing her cancer in broad social and environmental contexts, Powers eschews the individualist strain that characterizes many illness narratives. In so doing, the novel demands engagement with consumer agency and bodily frailty in the face of corporate dominance

Large-scale sequencing identifies multiple genes and rare variants associated with Crohn’s disease susceptibility

peer reviewe

31st Annual Meeting and Associated Programs of the Society for Immunotherapy of Cancer (SITC 2016) : part two

Background The immunological escape of tumors represents one of the main ob- stacles to the treatment of malignancies. The blockade of PD-1 or CTLA-4 receptors represented a milestone in the history of immunotherapy. However, immune checkpoint inhibitors seem to be effective in specific cohorts of patients. It has been proposed that their efficacy relies on the presence of an immunological response. Thus, we hypothesized that disruption of the PD-L1/PD-1 axis would synergize with our oncolytic vaccine platform PeptiCRAd. Methods We used murine B16OVA in vivo tumor models and flow cytometry analysis to investigate the immunological background. Results First, we found that high-burden B16OVA tumors were refractory to combination immunotherapy. However, with a more aggressive schedule, tumors with a lower burden were more susceptible to the combination of PeptiCRAd and PD-L1 blockade. The therapy signifi- cantly increased the median survival of mice (Fig. 7). Interestingly, the reduced growth of contralaterally injected B16F10 cells sug- gested the presence of a long lasting immunological memory also against non-targeted antigens. Concerning the functional state of tumor infiltrating lymphocytes (TILs), we found that all the immune therapies would enhance the percentage of activated (PD-1pos TIM- 3neg) T lymphocytes and reduce the amount of exhausted (PD-1pos TIM-3pos) cells compared to placebo. As expected, we found that PeptiCRAd monotherapy could increase the number of antigen spe- cific CD8+ T cells compared to other treatments. However, only the combination with PD-L1 blockade could significantly increase the ra- tio between activated and exhausted pentamer positive cells (p= 0.0058), suggesting that by disrupting the PD-1/PD-L1 axis we could decrease the amount of dysfunctional antigen specific T cells. We ob- served that the anatomical location deeply influenced the state of CD4+ and CD8+ T lymphocytes. In fact, TIM-3 expression was in- creased by 2 fold on TILs compared to splenic and lymphoid T cells. In the CD8+ compartment, the expression of PD-1 on the surface seemed to be restricted to the tumor micro-environment, while CD4 + T cells had a high expression of PD-1 also in lymphoid organs. Interestingly, we found that the levels of PD-1 were significantly higher on CD8+ T cells than on CD4+ T cells into the tumor micro- environment (p < 0.0001). Conclusions In conclusion, we demonstrated that the efficacy of immune check- point inhibitors might be strongly enhanced by their combination with cancer vaccines. PeptiCRAd was able to increase the number of antigen-specific T cells and PD-L1 blockade prevented their exhaus- tion, resulting in long-lasting immunological memory and increased median survival