[ASCO- and ESMO-update 2017 - highlights of the 53. meeting of the American Society of Clinical Oncology/ASCO 2017 and European Society for Medical Oncology/ESMO congress 2017]. / ASCO- und ESMO-Update 2017 ­ Neuigkeiten vom 53. Meeting der American Society of Clinical Oncology/ASCO 2017 und European Society for Medical Oncology/ESMO-Congress 2017.

At ASCO 2017, and subsequently the ESMO congress 2017, a number of studies were presented which, in part, may change the present standard of therapy in gastrointestinal oncology. The German FLOT4 trial established perioperative Docetaxel, Oxaliplatin and 5-Fluorouracil (5-FU) as the new treatment standard for resectable adenocarcinoma of the gastroesophageal junction and the stomach. In hepatocellular carcinoma (HCC), two large studies did not show a survival benefit for selective internal therapy (SIRT), so an increasing use of SIRT in HCC is not recommended. On the other hand, the multityrosinekinase inhibitor Lenvatinib seems to be a promising alternative to sorafenib in first line treatment of metastatic HCC. In early colon cancer-following the data from the large IDEA initiative-three months of capecitabine and oxaliplatin is recommended for low-risk stage III cancers (T1 - 3, N1), while in high-risk stage III cancers (T4 or N2) patients should still receive six months of oxaliplatin and a fluoropyrimidine. Aside from regular exercise, one study found that regular intake of tree nuts (at least 2 servings per week), may decrease the risk of recurrence. In first line metastatic colorectal cancer (mCRC), SIRT should not be applied, whereas in BRAF mutant cancers, the combination of irinotecan, cetuximab and vemurafenib seems to be a promising second line treatment option. In biliary tract cancer, after curative resection, six months of capecitabine is considered the new treatment standard. Finally, in pancreatic cancer, targeting the tumor stroma with pegylated hyaluronidase (PEGPH20) may be a new treatment option that needs to be proven in phase 3 studies.

Severe cytokine release syndrome after the first dose of Brentuximab Vedotin in a patient with relapsed systemic anaplastic large cell lymphoma (sALCL): a case report and review of literature.

Brentuximab Vedotin is an antibody - drug conjugate targeting CD30. We report a case of severe cytokine release syndrome (CRS) after administration of the first dose of Brentuximab Vedotin in a 64-yr-old patient with relapsed systemic anaplastic large cell lymphoma (sALCL). To our knowledge, this is the first case of CRS to Brentuximab Vedotin described in the literature. However, CRS to Brentuximab Vedotin might be underestimated, as the drug has not been tested in large phase III trials yet.

CD8+ CD122+ PD-1- effector cells promote the development of diabetes in NOD mice.

It is well established that CD4 and CD8 T cells are required for the initiation of autoimmune diabetes in NOD mice. However, different subsets of CD4 or CD8 cells may play different roles in the initiation of insulitis. In this study, we evaluated the role of the previously described CD8(+) CD122(+) in this process. We found that prediabetic NOD mice have an almost 50% reduction of CD8(+) CD122(+) T cells in their secondary lymphoid organs compared with BL/6 or Balb/c mouse strains. This reduction is explained by the lack of the regulatory CD8(+) CD122(+) PD-1(+) cell population in the NOD mice, as we found that all CD8(+) CD122(+) T cells from prediabetic NOD mice lack PD-1 expression and regulatory function. Depletion of CD8(+) CD122(+) PD-1(-) cells through injection of anti-CD122 mAb in prediabetic female NOD mice reduced the infiltration of mononuclear cells into the Langerhans islets and delayed the onset and decreased the incidence of overt diabetes. In addition, we found that transfer of highly purified and activated CD8(+) CD122(+) PD-1(-) cells, together with diabetogenic splenocytes from NOD donors to NOD SCID recipients, accelerates the diabetes development in these mice. Together, these results demonstrate that CD8(+) CD122(+) PD-1(-) T cells from NOD mice are effector cells that are involved in the pathogenesis of autoimmune diabetes.