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Krüppel-like factors in cancer

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TLDR
The roles and regulation of the 17 known KLFs in various cancer-relevant processes are discussed, with some KLFs having different roles in normal cells and cancer, during cancer development and progression and in different cancer types.
Abstract
Kruppel-like factors (KLFs) are a family of DNA-binding transcriptional regulators with diverse and essential functions in a multitude of cellular processes, including proliferation, differentiation, migration, inflammation and pluripotency. In this Review, we discuss the roles and regulation of the 17 known KLFs in various cancer-relevant processes. Importantly, the functions of KLFs are context dependent, with some KLFs having different roles in normal cells and cancer, during cancer development and progression and in different cancer types. We also identify key questions for the field that are likely to lead to important new translational research and discoveries in cancer biology.

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Krüppel-like factors in cancer progression: three fingers on the steering wheel.

TL;DR: Current knowledge on Krüppel-like transcription in the epithelial-mesenchymal transition (EMT), invasion and metastasis, with a focus on epithelial cancer biology and the extensive interface with pluripotency is discussed.
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Pericytes in the Premetastatic Niche

TL;DR: Strikingly, genetic inactivation of KLF4 in pericytes inhibits pulmonary pericyte expansion and decreases metastasis in the lung.
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Early Transcriptional Responses during Heat Stress in the Coral Acropora hyacinthus.

TL;DR: A model for early transcriptional regulation of protein degradation and cell adhesion response that may ultimately lead to the bleaching and stress response is proposed.
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Single-cell profiling identifies pre-existing CD19-negative subclones in a B-ALL patient with CD19-negative relapse after CAR-T therapy.

TL;DR: In this article, leukemic cells of a relapsing B-ALL patient were investigated at two-time points: before (T1) and after (T2) anti-CD19 CAR-T treatment.
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CWP232228 targets liver cancer stem cells through Wnt/β‑catenin signaling: a novel therapeutic approach for liver cancer treatment

TL;DR: It is shown that liver CSCs with elevated Wnt/β-catenin signaling possess much greater self-renewal and clonogenic potential, and the small molecule inhibitor CWP232228 acts as a candidate therapeutic agent for liver cancer by preferentially targeting liver C SCs.
References
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Journal ArticleDOI

Epithelial-Mesenchymal Transitions in Development and Disease

TL;DR: The mesenchymal state is associated with the capacity of cells to migrate to distant organs and maintain stemness, allowing their subsequent differentiation into multiple cell types during development and the initiation of metastasis.
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Wnt/beta-catenin signaling in development and disease.

TL;DR: A remarkable interdisciplinary effort has unraveled the WNT (Wingless and INT-1) signal transduction cascade over the last two decades, finding that Germline mutations in the Wnt pathway cause several hereditary diseases, and somatic mutations are associated with cancer of the intestine and a variety of other tissues.
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Lessons from Hereditary Colorectal Cancer

TL;DR: The authors are grateful to the members of their laboratories for their contributions to the reviewed studies and to F. Giardiello and S. Hamilton for photographs of colorectal lesions.
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Phylogeny.fr: robust phylogenetic analysis for the non-specialist

TL;DR: The Phylogeny.fr platform transparently chains programs to automatically perform phylogenetic analyses and can also meet the needs of specialists; the first ones will find up-to-date tools chained in a phylogeny pipeline to analyze their data in a simple and robust way, while the specialists will be able to easily build and run sophisticated analyses.
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Macrophage plasticity and interaction with lymphocyte subsets: cancer as a paradigm

TL;DR: A better understanding of the molecular basis of myelomonocytic cell plasticity will open new vistas in immunopathology and therapeutic intervention and provide a paradigm for macrophage plasticity and function.
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