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Koeppke, J.

Publications and source records attributed to Koeppke, J..

2 recordsLinked to original sources

Lineage origin and microenvironment shape neuroblastoma transcriptional state and plasticity

Neuroblastoma, a neural-crest-derived malignancy of the peripheral nervous system, is a devastating pediatric disease characterized by high intra- and intertumoral heterogeneity. While several tumor expression programs correlate with patient outcome, the developmental and contextual determinants of their emergence remain incompletely understood. Here, we systematically dissected neuroblastoma transcriptional heterogeneity and measured how tumor expression programs are associated with lineage history and developmental context. To achieve this, we combined single-cell transcriptomics with high-throughput lineage tracing and tumor cell transplantation in zebrafish models of MYCN-driven neuroblastoma. We identified developmental cell-state-associated programs that align with sympathoadrenal development, as well as general cellular-process programs. Clonal analysis showed that developmental programs are preferentially clone-associated, whereas cellular-process programs are more context-responsive. Transplantation into an embryonic environment reshaped the activation of several initially clone-associated programs, consistent with developmentally determined state reconfiguration and/or selection of state-competent cells. Together, our results show that lineage history and developmental context jointly shape tumor-state architecture in vivo.

cancer biology↗

Amplicon structure creates collateral therapeutic vulnerability in cancer

Although DNA amplifications in cancers frequently harbor passenger genes alongside oncogenes, the functional consequence of such co-amplifications and their impact for therapy remains ill-defined. We discovered that passenger co-amplifications can create amplicon structure-specific collateral vulnerabilities. We present the DEAD-box helicase 1 (DDX1) gene as a bona fide passenger co-amplified with MYCN in cancers. Survival of cancer cells with DDX1 co-amplifications strongly depends on the mammalian target of rapamycin complex 1 (mTORC1). Mechanistically, aberrant DDX1 expression inhibits the tricarboxylic acid cycle through a previously unrecognized interaction with dihydrolipoamide S-succinyltransferase, a component of the alpha-ketoglutarate dehydrogenase complex. Cells expressing aberrant DDX1 levels compensate for the metabolic shift by enhancing mTORC1 activity. Consequently, pharmacological mTORC1 inhibition triggered cell death specifically in cells harboring the DDX1 co-amplification. This work highlights a significant contribution of passenger gene alterations to the therapeutic susceptibility of cancers. Graphical abstract O_FIG O_LINKSMALLFIG WIDTH=200 HEIGHT=130 SRC="FIGDIR/small/506647v2_ufig1.gif" ALT="Figure 1"> View larger version (34K): org.highwire.dtl.DTLVardef@58b27dorg.highwire.dtl.DTLVardef@12e2fccorg.highwire.dtl.DTLVardef@1440f33org.highwire.dtl.DTLVardef@141e933_HPS_FORMAT_FIGEXP M_FIG C_FIG

cancer biology↗