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Keywords {🔍}

cancer, cell, google, scholar, doi, pubmed, cells, pmc, article, free, plasticity, faculty, opinions, recommendation, drug, resistance, tumour, models, emt, melanoma, dtps, state, control, epigenetic, level, treatment, populations, stem, nature, inhibition, showed, shown, expression, immune, adaptive, factor, transition, figure, landscape, system, biol, biological, phenotypic, signalling, breast, population, view, nat, biology, study,

Topics {✒️}

double-negative feedback loop increased tcf/lef-dependent transcription glucocorticoid-inducible factor tsc22d3 stress-induced glucocorticoid surge epithelial-hybrid-mesenchymal fate determination brain-derived neurotrophic factor promote oxidative-stress tolerance pmc beta search fusion gene pml-rarα error-prone dna polymerases van den boorn-konijnenberg mapki-induced melanoma regression inter-cellular communications build cyclin-dependent kinase inhibitors immunotherapy-induced epigenetic remodelling melanocyte-inducing transcription factor gain fat-lose metastasis chimeric protein pml-rarα phenotype-structured differential equations yap/taz/tead-axl pathway axl antibody–drug conjugate axl antibody-drug conjugate recurrent tumor cell-intrinsic transient drug-induced tolerance oncogenic-driven mutations favoured continuum phenotype-structured models proto-oncogene b-raf treatment-induced tumor dormancy anti-interleukin-6 monoclonal antibody yap-mediated transcriptional reprogramming braf-driven melanoma progression pi3k/akt signalling pathway time-scheduled drug delivery braf wild-type melanoma castration-resistant prostate cancer early-stage lung cancers influence anti-tumour immunity drug-induced cell plasticity fatty acid saturation brafv600e-mutated melanoma 4 cell-autonomous adaptive resistance distinct homogeneous subpopulations heterotypic tumor cell-cancer rb1-deficient prostate cancer promoter-mediated transcriptional noise lactate-producing cancer cells tgfβ-mediated signalling response called drug-tolerant persisters androgen-dependent prostate cancer cell–inflamed tumour microenvironment

Questions {❓}

• Is EMT always totally reversible?
• Israel L: Tumour progression: Random mutations or an integrated survival response to cellular stress conserved from unicellular organisms?
• Müller WEG: Review: How was metazoan threshold crossed?
• Open questions that arise are the following: Is plasticity a feature of cancer cell populations with binary phenotypic switch or with continuous changes (or both)?
• Soto AM, Sonnenschein C: The somatic mutation theory of cancer: Growing problems with the paradigm?
• The non-standard points of view mentioned above all lead to fundamental questions: What is an organism?
• This quasi-phenomenological view of a multicellular organism, which ignores the genetic/epigenetic design (metaphorically illustrated by the Waddington epigenetic landscape relative to a single genome), has the merit of proposing an essential role for the immune system in answer to the question ‘What exactly is an organism?
• To make things clear, cancer being a disease of multicellular organisms (a cancerous bacterium simply does not make sense), the question of ‘what exactly is an organism?
• Vincent M: Cancer: A de-repression of a default survival program common to all cells?
• What is plasticity in cancer?
• You JS, Jones PA: Cancer Genetics and Epigenetics: Two Sides of the Same Coin?

Social Networks {👍}(6)

• https://twitter.com/ncbi
• https://www.facebook.com/ncbi.nlm
• https://www.linkedin.com/company/ncbinlm
• https://twitter.com/nlm_nih
• https://www.facebook.com/nationallibraryofmedicine
• https://www.youtube.com/user/NLMNIH

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