Jeg ser fra andre tråder at enkelte etterspør hva BGBIO skal presentere framover. Jeg har tidligere lagt ut detaljert om dette, men det ser ut til at noen troll klarer å lage så mye støy på mine tråder at man kan miste fokus. Jeg prøver igjen:

1) AACR fra 14. april:
BGBIO skal altså presentere (den 17. april) på den store konferansen American Association for Cancer Research (AACR). BGBIO skal presentere «BGB324, a selective small-molecule inhibitor of receptor tyrosine kinase AXL, targets tumor immune suppression and enhances immune checkpoint inhibitor efficacy».
Kommentar: BGBIO skal lese av «interim data» på flere kliniske forsøk i første halvdel av 2018. Noen av de resultatene kan komme på AACR, men det mest sannsynlige er at de blir presentert på konferansen ASCO, som er i sommer 1.-5. juni, og andre konferanser derfra.

Abstract
The AXL receptor tyrosine kinase is associated with poor overall survival in a wide spectrum of cancers. AXL signaling is important for tumor cell plasticity related to epithelial-to-mesenchymal transition (EMT), immune escape and intrinsic resistance to cytotoxic lymphocytes. AXL is expressed on several cells associated with the tumor immune microenvironment, including natural killer (NK) cells, dendritic cells and a subset of tumor-associated myeloid cells. AXL signaling enhances secretion of immune-suppressive cytokines from innate immune cells that limit antitumor immunity. Hence AXL resides uniquely at the nexus between tumor and microenvironmental antitumor immune suppression mechanisms. BGB324, a selective clinical-stage small-molecule Axl kinase inhibitor, is currently being evaluated in combination with pembrolizumab in three phase II clinical trials in patients with TNBC (NCT03184558), NSCLC (NCT03184571) and melanoma (NCT02872259). We show that BGB324 targets immune suppression mechanisms in the tumor microenvironment that improve immunotherapy in different murine tumor models. BGB324 treatment reduces myeloid-derived suppressor cells and tumor-associated macrophages, and lowers CCL11, IL-7, IL-1β, and IL-6 in murine pancreatic cancer models. This altered immune landscape is associated with increased tumor infiltration of NK and CD8+ T cells and enhanced therapy responses. Further, BGB324 targets tumor intrinsic immune resistance and enhances human CD8+ T cell and NK-cell mediated NSCLC tumor cell lysis. We are currently using high-dimensional mass cytometry analysis (CyTOF) to map adaptive Axl-dependent immune suppression during immune checkpoint blockade. Collectively these results highlight a prominent function for AXL in resistance to immune therapy and support continued clinical translation of combining BGB324 with immune checkpoint inhibitors to improve cancer treatment.

Kommentar: Presentasjonen er blant de utvalgte som er høystatus plassert som Session Type: Working Groups/Council Recommendation.
Link: http://www.abstractsonline.com/pp8/#!/4562/sessions/bergenbio/1

Vi kan her bl.a. notere oss følgende meget interessante statement: "Collectively these results highlight a prominent function for AXL in resistance to immune therapy and support continued clinical translation of combining BGB324 with immune checkpoint inhibitors to improve cancer treatment".


2) ASCO fra 1. juni:
BGBIO skal også presentere på den svært viktige ASCO-konferansen som starter 1.juni, og som foreløpig ser ut til å bli årets "slugger" fra BGBIO.
Dette får vi komme mer detaljert tilbake til når det nærmer seg.