Reports Of Conferences, Institutes, And Seminars

This quarter\u27s column offers coverage of multiple sessions from the 2016 Electronic Resources & Libraries (ER&L) Conference, held April 3–6, 2016, in Austin, Texas. Topics in serials acquisitions dominate the column, including reports on altmetrics, cost per use, demand-driven acquisitions, and scholarly communications and the use of subscriptions agents; ERMS, access, and knowledgebases are also featured

Reports Of Conferences, Institutes, And Seminars

This quarter\u27s column features a report from Electronic Resources & Libraries, held February 22–25, 2015, in Austin, TX, and several reports from the Association of College and Research Libraries, held in Portland, OR, March 25–28, 2015, including one from the ScholCommCamp unconference. Topics discussed include e-resources workflows, discovery, accessibility, open access, collection development decision making, and linked data

IL-2– and IL-15–induced activation of the rapamycin-sensitive mTORC1 pathway in malignant CD4+ T lymphocytes

We examined functional status, activation mechanisms, and biologic role of the mTORC1 signaling pathway in malignant CD4+ T cells derived from the cutaneous T-cell lymphoma (CTCL). Whereas the spontaneously growing CTCL-derived cell lines displayed persistent activation of the TORC1 as well as the PI3K/Akt and MEK/ERK pathways, the IL-2–dependent cell lines activated the pathways in response to IL-2 and IL-15 but not IL-21. Activation of mTORC1 and MEK/ERK was nutrient dependent. The mTORC1, PI3K/Akt, and MEK/ERK pathways could also be activated by IL-2 in the primary leukemic, mitogen-preactivated CTCL cells. mTORC1 activation was also detected in the CTCL tissues in the lymphoma stage–dependent manner with the highest percentage of positive cells present in the cases with a large cell transformation. Rapamycin inhibited mTORC1 signaling and suppressed CTCL cell proliferation but showed little effect on their apoptotic rate when used as a single agent. Activation of the mTORC1, PI3K/Akt, and MEK/ERK pathways was strictly dependent on the Jak3 and Jak1 kinases. Finally, mTORC1 activation was transduced preferentially through the PI3K/Akt pathway. These findings document the selective γc-signaling cytokine-mediated activation of the mTORC1 pathway in the CTCL cells and suggest that the pathway represents a therapeutic target in CTCL and, possibly, other T-cell lymphomas