American Association for Cancer Research
00085472can160608-sup-162938_1_supp_0_hb8hmf.pptx (62.06 kB)

Supplementary Table 3- Tumor incidence of CD24 negative & CD24 positive cell populations from Inflammation Triggers Zeb1-Dependent Escape from Tumor Latency

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posted on 2023-03-31, 00:26 authored by Jasmine M. De Cock, Tsukasa Shibue, Anushka Dongre, Zuzana Keckesova, Ferenc Reinhardt, Robert A. Weinberg

Summary of tumor incidences at limiting dilutions for CD24negative and CD24positive cell populations





The emergence of metastatic disease in cancer patients many years or decades after initial successful treatment of primary tumors is well documented but poorly understood at the molecular level. Recent studies have begun exploring the cell-intrinsic programs, causing disseminated tumor cells to enter latency and the cellular signals in the surrounding nonpermissive tissue microenvironment that maintain the latent state. However, relatively little is known about the mechanisms that enable disseminated tumor cells to escape cancer dormancy or tumor latency. We describe here an in vivo model of solitary metastatic latency in the lung parenchyma. The induction of a localized inflammation in the lungs, initiated by lipopolysaccharide treatment, triggers the awakening of these cells, which develop into macroscopic metastases. The escape from latency is dependent on the expression of Zeb1, a key regulator of the epithelial-to-mesenchymal transition (EMT). Furthermore, activation of the EMT program on its own, as orchestrated by Zeb1, is sufficient to incite metastatic outgrowth by causing carcinoma cells to enter stably into a metastasis-initiating cell state. Cancer Res; 76(23); 6778–84. ©2016 AACR.