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Shauntae McDaniel, Kristen Rumer, S. Biroc, R. Metz, Meenakshi Singh, W. Porter, P. Schedin (2006)
Remodeling of the mammary microenvironment after lactation promotes breast tumor cell metastasis.The American journal of pathology, 168 2
Tony Gutschner, S. Diederichs (2012)
The hallmarks of cancerRNA Biology, 9
C. Sonnenschein, A. Soto (2013)
The society of cells cancer and control of cell proliferation
Sandra Mitchell (2002)
Integrative PluralismBiology and Philosophy, 17
(2015)
The association between health-related quality of life and survival in patients with head and neck cancer: a systematic reviewBDJ, 218
M. Maffini, A. Soto, Janine Calabro, A. Ucci, C. Sonnenschein (2004)
The stroma as a crucial target in rat mammary gland carcinogenesisJournal of Cell Science, 117
(1972)
Transplantation studies of the role of the stroma in epidermal carcinogenesis, tissue interactions in carcinogenesis
J. Marcum (2009)
Cancer: complexity, causation, and systems biology, 9
SD Mitchell (2004)
Why integrative pluralism?E:CO, 6
I. Lakatos (1976)
Falsification and the Methodology of Scientific Research Programmes
BA Chabner, TG Roberts (2005)
Timeline: chemotherapy and the war on cancerNat Rev Cancer, 5
A. Soto, C. Sonnenschein (2013)
Paradoxes in Carcinogenesis: There Is Light at the End of That Tunnel!Disruptive science and technology, 1 3
H. Rajagopalan, M. Nowak, B. Vogelstein, C. Lengauer (2003)
The significance of unstable chromosomes in colorectal cancerNature Reviews Cancer, 3
A. Soto, C. Sonnenschein (2006)
Emergentism by default: A view from the benchSynthese, 151
S. Rosenfeld (2013)
Are the Somatic Mutation and Tissue Organization Field Theories of Carcinogenesis Incompatible?Cancer Informatics, 12
C. Sonnenschein, A. Soto, A. Rangarajan, Prakash Kulkarni (2014)
Competing views on cancerJournal of Biosciences, 39
S. Baker (2011)
TOFT better explains experimental results in cancer research than SMT (Comment on DOI 10.1002/bies.201100025 and DOI 10.1002/bies.201100022)BioEssays, 33
W. Barclay, R. Woodruff, M. Hall, S. Cramer (2005)
A system for studying epithelial-stromal interactions reveals distinct inductive abilities of stromal cells from benign prostatic hyperplasia and prostate cancer.Endocrinology, 146 1
C. Sonnenschein, A. Soto (2011)
Response to “In defense of the somatic mutation theory of cancer” DOI: 10.1002/bies.201100022BioEssays, 33
D. Vaux (2011)
In defense of the somatic mutation theory of cancerBioEssays, 33
C. Nelson, M. Bissell (2005)
Modeling dynamic reciprocity: engineering three-dimensional culture models of breast architecture, function, and neoplastic transformation.Seminars in cancer biology, 15 5
S. Daniel (2011)
On somatic mutations and tissue fields in cancerBioEssays, 33
B. Chabner, T. Roberts (2005)
Chemotherapy and the war on cancerNature Reviews Cancer, 5
J. Coffman (2005)
On reductionism, organicism, somatic mutations and cancerBioEssays, 27
S. Baker (2014)
Recognizing paradigm instability in theories of carcinogenesis.British journal of medicine and medical research, 4
P. Stephens, C. Greenman, B. Fu, Fengtang Yang, G. Bignell, L. Mudie, E. Pleasance, K. Lau, D. Beare, L. Stebbings, Stuart Mclaren, Meng‐Lay Lin, D. Mcbride, I. Varela, S. Nik-Zainal, Catherine Leroy, Mingming Jia, A. Menzies, A. Butler, J. Teague, M. Quail, J. Burton, H. Swerdlow, N. Carter, L. Morsberger, C. Iacobuzio-Donahue, G. Follows, A. Green, A. Flanagan, A. Flanagan, M. Stratton, P. Futreal, P. Campbell, Peter Campbell (2011)
Massive Genomic Rearrangement Acquired in a Single Catastrophic Event during Cancer DevelopmentCell, 144
A. Soto, C. Sonnenschein (2004)
The somatic mutation theory of cancer: growing problems with the paradigm?BioEssays : news and reviews in molecular, cellular and developmental biology, 26 10
C. Sonnenschein, A. Soto (2008)
Theories of carcinogenesis: an emerging perspective.Seminars in cancer biology, 18 5
A. Soto, C. Sonnenschein (2011)
The tissue organization field theory of cancer: A testable replacement for the somatic mutation theoryBioEssays, 33
(2011)
Insights & Perspectives Response to ‘‘In defense of the somatic mutation theory of cancer’’
T. Kuhn, David Hawkins (1963)
The Structure of Scientific RevolutionsAmerican Journal of Physics, 31
C. Hudis (2007)
Trastuzumab--mechanism of action and use in clinical practice.The New England journal of medicine, 357 1
D. Satgé (2011)
On somatic mutations and tissue fields in cancer: additional observations challenge the SMT.BioEssays : news and reviews in molecular, cellular and developmental biology, 33 12
K. Strebhardt, A. Ullrich (2008)
Paul Ehrlich's magic bullet concept: 100 years of progressNature Reviews Cancer, 8
D. Smithers (1962)
CANCER AN ATTACK ON CYTOLOGISMThe Lancet, 279
C. Sonnenschein, A. Soto (2000)
Somatic mutation theory of carcinogenesis: Why it should be dropped and replacedMolecular Carcinogenesis, 29
C Tomasetti, B Vogelstein (2015)
Cancer etiology. variation in cancer risk among tissues can be explained by the number of stem cell divisionsScience, 347
J. Kupiec, P. Sonigo (2000)
Ni Dieu Ni Gène Pour Une Autre Théorie de L'Hérédité
M. Barcellos-Hoff, Shraddha Ravani (2000)
Irradiated mammary gland stroma promotes the expression of tumorigenic potential by unirradiated epithelial cells.Cancer research, 60 5
A. Soto, C. Sonnenschein (2005)
Emergentism as a default: Cancer as a problem of tissue organizationJournal of Biosciences, 30
C. Lengauer, K. Kinzler, B. Vogelstein (1998)
Genetic instabilities in human cancersNature, 396
S. Baker (2013)
Paradox-Driven Cancer Research, 1
The building of a global model of carcinogenesis is one of modern biology’s greatest challenges. The traditional somatic mutation theory (SMT) is now supplemented by a new approach, called the Tissue Organization Field Theory (TOFT). According to TOFT, the original source of cancer is loss of tissue organization rather than genetic mutations. In this paper, we study the argumentative strategy used by the advocates of TOFT to impose their view. In particular, we criticize their claim of incompatibility used to justify the necessity to definitively reject SMT. First, we note that since it is difficult to build a non-ambiguous experimental demonstration of the superiority of TOFT, its partisans add epistemological and metaphysical arguments to the debate. This argumentative strategy allows them to defend the necessity of a paradigm shift, with TOFT superseding SMT. To do so, they introduce a notion of incompatibility, which they actually use as the Kuhnian notion of incommensurability. To justify this so-called incompatibility between the two theories of cancer, they move the debate to a metaphysical ground by assimilating the controversy to a fundamental opposition between reductionism and organicism. We show here that this argumentative strategy is specious, because it does not demonstrate clearly that TOFT is an organicist theory. Since it shares with SMT its vocabulary, its ontology and its methodology, it appears that a claim of incompatibility based on this metaphysical plan is not fully justified in the present state of the debate. We conclude that it is more cogent to argue that the two theories are compatible, both biologically and metaphysically. We propose to consider that TOFT and SMT describe two distinct and compatible causal pathways to carcinogenesis. This view is coherent with the existence of integrative approaches, and suggests that they have a higher epistemic value than the two theories taken separately.
Acta Biotheoretica – Springer Journals
Published: Apr 8, 2015
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