The Oncofetal Paradigm Revisited: MSF and HA as Contextual Drivers of Cancer Progression

Seth L. Schor, Ana M. Schor, Ian R. Ellis, Sarah J. Jones, Margaret Florence, Jacqueline Cox, Anne-Marie Woolston

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

    1 Citation (Scopus)

    Abstract

    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.
    Original languageEnglish
    Title of host publicationHyaluronan in cancer biology
    Place of PublicationSan Diego, CA.
    PublisherAcademic Press
    Pages283-306
    Number of pages24
    ISBN (Print)9780123741783
    DOIs
    Publication statusPublished - 2009

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    Hyaluronic Acid
    Neoplasms
    Angiogenesis Inducing Agents
    Pathologic Processes
    Stromal Cells
    Fetal Development
    Epigenomics
    Wound Healing
    Cell Movement
    Extracellular Matrix
    Disease Progression
    Epithelial Cells
    Recurrence
    Mortality
    Therapeutics

    Cite this

    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. https://doi.org/10.1016/B978-012374178-3.10015-8
    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. pp. 283-306
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    abstract = "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 TGF{\ss}1, 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.",
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    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. https://doi.org/10.1016/B978-012374178-3.10015-8

    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)

    TY - CHAP

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    AU - Schor, Ana M.

    AU - Ellis, Ian R.

    AU - Jones, Sarah J.

    AU - Florence, Margaret

    AU - Cox, Jacqueline

    AU - Woolston, Anne-Marie

    PY - 2009

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    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.

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    M3 - Chapter (peer-reviewed)

    SN - 9780123741783

    SP - 283

    EP - 306

    BT - Hyaluronan in cancer biology

    PB - Academic Press

    CY - San Diego, CA.

    ER -

    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 https://doi.org/10.1016/B978-012374178-3.10015-8