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Canadian and American population-based research concerning sexual and/or gender minority populations provides evidence of persistent breast and gynecologic cancer-related health disparities and knowledge divides. The Cancer's Margins research investigates the complex intersections of sexual and/or gender marginality and incommensurabilities and improvisation in engagements with biographical and biomedical cancer knowledge. The study examines how sexuality and gender are intersectionally constitutive of complex biopolitical mappings of cancer health knowledge that shape knowledge access and its mobilization in health and treatment decision-making. Interviews were conducted with a diverse group (n=81) of sexual and/or gender minority breast or gynecologic cancer patients. The LGBQ//T2 cancer patient narratives we have analyzed document in fine grain detail how it is that sexual and/or gender minority cancer patients punctuate the otherwise lockstep assemblage of their cancer treatment decision-making with a persistent engagement in creative attempts to resist, thwart and otherwise manage the possibility of discrimination and likewise, the probability of institutional erasure in care settings. Our findings illustrate the demands that cancer places on LGBQ//T2 patients to choreograph access to, and mobilization of knowledge and care, across significantly distinct and sometimes incommensurable systems of knowledge.

Previous studies have shown that dibutyltin (DBT) interferes with the function of human natural killer (NK) cells, diminishing their capacity to destroy tumor cells, in vitro. DBT is a widespread environmental contaminant and has been found in human blood. As NK cells are our primary immune defense against tumor cells, it is important to understand the mechanism by which DBT interferes with their function. The current study examines the effects of DBT exposures on key enzymes in the signaling pathway that regulates NK responsiveness to tumor cells. These include several protein tyrosine kinases (PTKs), mitogen-activated protein kinases (MAPKs), and mitogen-activated protein kinase kinases (MAP2Ks). The results showed that in vitro exposures of NK cells to DBT had no effect on PTKs. However, exposures to DBT for as little as 10 min were able to increase the phosphorylation (activation) of the MAPKs. The DBT-induced activations of these MAPKs appear to be due to DBT-induced activations of the immediate upstream activators of the MAPKs, MAP2Ks. The results suggest that DBT-interference with the MAPK signaling pathway is a consequence of DBT exposures, which could account for DBT-induced decreases in NK function.