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Biology subjects

Werner-Klein, M.

Publications and source records attributed to Werner-Klein, M..

3 recordsLinked to original sources

Ex vivo drug testing in metastatic biopsies reveals patient-specific vulnerabilities to cancer targeting and immune activating drugs

Biomarker-guided therapies in oncology often fail to induce considerable responses in patients with advanced cancer. As a complementary approach, direct drug testing on individual patient samples is highly attractive yet is currently hampered by the lack of assays that combine (i) fast reporting, (ii) the ability to inform about immune-mediated responses, (iii) robust quantification, and (iv) scalability for parallel assessment of multiple drugs. Here, we introduce our patient-derived ex vivo drug response assay (PEDRA) that fulfills all these requirements. Using malignant pleural effusions (MPEs) from five non-small cell lung cancer (NSCLC) patients with detailed clinical treatment histories, we tested 52 guideline-recommended therapies and eight investigational antibody-drug conjugates (ADCs). In all patients, PEDRA identified treatment options that outperformed the therapies the patients had received. The results reflected clinical observations as well as expectations derived from mutational profiling and disease courses. To extend the applicability of PEDRA beyond MPEs to other metastatic lesions, we generated a protocol starting from core needle biopsies. Owing to its reproducible and quantitative nature, PEDRA may provide a valuable diagnostic tool to guide time-sensitive clinical therapy decisions. Additionally, PEDRA has great potential for preclinical testing of investigational drugs, thereby reducing the need for animal experiments.

cancer biology↗

Metastasis founder cells activate immunosuppression early in human melanoma metastatic colonization

The earliest steps of lethal metastasis in patients are incompletely understood. To dissect them, we prospectively searched for the earliest detectable disseminated cancer cells (DCC) in sentinel lymph node biopsies of 492 stage I-III patients. By visually-controlled, micromanipulator-assisted isolation and single cell transcriptome analysis of these extremely rare DCC, we identified MCSP+ melanoma cells as strong candidates for metastasis founder cells (MFC) in lymph nodes. Based on a median follow-up time of 6 years, their detection was the strongest predictor of systemic metastasis and death upon multivariable analysis. During transition from single cells to metastasis-initiating clusters, melanoma DCC were exposed to CD8 T cell attack, activated the extracellular vesicular exosomal pathway, and expressed the immunomodulatory proteins CD155 and CD276, but rarely PD-L1. CD155 and CD276-positive extracellular vesicles from patient-derived DCC models exhibited an immunosuppressive activity on CD8 T cells. Our data indicate that either direct targeting of MFC employing MCSP or their immune escape mechanisms might be key for cure of early-stage melanoma.

cancer biology↗

Interleukin-6 trans-signaling is a candidate mechanism to drive progression of human DCCs during periods of clinical latency

Although thousands of breast cancer cells disseminate and home to bone marrow until primary surgery, usually less than a handful will succeed in establishing manifest metastases months to years later. To identify signals that support survival or outgrowth in patients, we profiled rare bone marrow-derived disseminated cancer cells (DCCs) long before manifestation of metastasis and identified IL6/PI3K-signaling as candidate pathway for DCC activation. Surprisingly, and similar to mammary epithelial cells, DCCs lacked membranous IL6 receptor expression and mechanistic dissection revealed IL6 trans-signaling to regulate a stem-like state of mammary epithelial cells via gp130. Responsiveness to IL6 trans-signals was found to be niche-dependent as bone marrow stromal and endosteal cells down-regulated gp130 in premalignant mammary epithelial cells as opposed to vascular niche cells. PIK3CA activation rendered cells independent from IL6 trans-signaling. Consistent with a bottleneck function of microenvironmental DCC control, we found PIK3CA mutations highly associated with late-stage metastatic cells while being extremely rare in early DCCs. Our data suggest that the initial steps of metastasis formation are often not cancer cell-autonomous, but also depend on microenvironmental signals.

cancer biology↗