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The Oncofetal Paradigm Revisited

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The Oncofetal Paradigm Revisited : MSF and HA as Contextual Drivers of Cancer Progression. / Schor, Seth L.; Schor, Ana M.; Ellis, Ian R.; Jones, Sarah J.; Florence, Margaret; Cox, Jacqueline; Woolston, Anne-Marie.

Hyaluronan in cancer biology. San Diego, CA. : Academic Press, 2009. p. 283-306.

Research output: Chapter in Book/Report/Conference proceedingChapter (peer-reviewed)

Harvard

Schor, SL, Schor, AM, Ellis, IR, Jones, SJ, Florence, M, Cox, J & Woolston, A-M 2009, 'The Oncofetal Paradigm Revisited: MSF and HA as Contextual Drivers of Cancer Progression'. in Hyaluronan in cancer biology. Academic Press, San Diego, CA., pp. 283-306.

APA

Schor, S. L., Schor, A. M., Ellis, I. R., Jones, S. J., Florence, M., Cox, J., & Woolston, A-M. (2009). The Oncofetal Paradigm Revisited: MSF and HA as Contextual Drivers of Cancer Progression. In Hyaluronan in cancer biology. (pp. 283-306). San Diego, CA.: Academic Press. doi: 10.1016/B978-012374178-3.10015-8

Vancouver

Schor SL, Schor AM, Ellis IR, Jones SJ, Florence M, Cox J et al. The Oncofetal Paradigm Revisited: MSF and HA as Contextual Drivers of Cancer Progression. In Hyaluronan in cancer biology. San Diego, CA.: Academic Press. 2009. p. 283-306.

Author

Schor, Seth L.; Schor, Ana M.; Ellis, Ian R.; Jones, Sarah J.; Florence, Margaret; Cox, Jacqueline; Woolston, Anne-Marie / The Oncofetal Paradigm Revisited : MSF and HA as Contextual Drivers of Cancer Progression.

Hyaluronan in cancer biology. San Diego, CA. : Academic Press, 2009. p. 283-306.

Research output: Chapter in Book/Report/Conference proceedingChapter (peer-reviewed)

Bibtex - Download

@inbook{71dce02480974d8b8afcb3f91c8711db,
title = "The Oncofetal Paradigm Revisited",
publisher = "Academic Press",
author = "Schor, {Seth L.} and Schor, {Ana M.} and Ellis, {Ian R.} and Jones, {Sarah J.} and Margaret Florence and Jacqueline Cox and Anne-Marie Woolston",
year = "2009",
isbn = "9780123741783",
pages = "283-306",
booktitle = "Hyaluronan in cancer biology",

}

RIS (suitable for import to EndNote) - Download

TY - CHAP

T1 - The Oncofetal Paradigm Revisited

T2 - Hyaluronan in cancer biology

A1 - Schor,Seth L.

A1 - Schor,Ana M.

A1 - Ellis,Ian R.

A1 - Jones,Sarah J.

A1 - Florence,Margaret

A1 - Cox,Jacqueline

A1 - Woolston,Anne-Marie

AU - Schor,Seth L.

AU - Schor,Ana M.

AU - Ellis,Ian R.

AU - Jones,Sarah J.

AU - Florence,Margaret

AU - Cox,Jacqueline

AU - Woolston,Anne-Marie

PB - Academic Press

CY - San Diego, CA.

PY - 2009

Y1 - 2009

N2 - Migration stimulating factor (MSF) is an oncofetal protein which is constitutively produced by both epithelial and stromal cells during fetal development, not expressed by the majority of their normal adult counterparts, but re-expressed during pathological processes such as cancer and wound healing. MSF exhibits a number of potent bioactivities, including the stimulation of cell migration, hyaluronan (HA) synthesis and angiogenesis. HA appears to mediate the effects of MSF on the migration of certain target cell types and may also contribute to the observed effects of MSF on angiogenesis. MSF expression and its precise effects on target cells are both subject to contextual (tissue-level) control mechanisms involving the complex interplay of soluble factors, such as TGFß1, and macromolecular constituents of the extracellular matrix, such as HA. Using MSF as an exemplar, we have suggested an “extended” oncofetal model of cancer pathogenesis in which epigenetic mechanisms make important contributions to the local and systemic re-expression of oncofetal molecules during disease progression. Critically, we propose that such oncofetal effectors may act as severity factors accelerating the disease process. Should this prove to be the case, the ability to switch-off inappropriate MSF expression may provide a platform for the development of novel adjuvant therapies designed to lower the risk of disease recurrence and mortality.

AB - Migration stimulating factor (MSF) is an oncofetal protein which is constitutively produced by both epithelial and stromal cells during fetal development, not expressed by the majority of their normal adult counterparts, but re-expressed during pathological processes such as cancer and wound healing. MSF exhibits a number of potent bioactivities, including the stimulation of cell migration, hyaluronan (HA) synthesis and angiogenesis. HA appears to mediate the effects of MSF on the migration of certain target cell types and may also contribute to the observed effects of MSF on angiogenesis. MSF expression and its precise effects on target cells are both subject to contextual (tissue-level) control mechanisms involving the complex interplay of soluble factors, such as TGFß1, and macromolecular constituents of the extracellular matrix, such as HA. Using MSF as an exemplar, we have suggested an “extended” oncofetal model of cancer pathogenesis in which epigenetic mechanisms make important contributions to the local and systemic re-expression of oncofetal molecules during disease progression. Critically, we propose that such oncofetal effectors may act as severity factors accelerating the disease process. Should this prove to be the case, the ability to switch-off inappropriate MSF expression may provide a platform for the development of novel adjuvant therapies designed to lower the risk of disease recurrence and mortality.

U2 - 10.1016/B978-012374178-3.10015-8

DO - 10.1016/B978-012374178-3.10015-8

M1 - Chapter (peer-reviewed)

SN - 9780123741783

BT - Hyaluronan in cancer biology

SP - 283

EP - 306

ER -

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