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Research ArticleContinuing Education

Thyroid Follicular Epithelial Cell–Derived Cancer: New Approaches and Treatment Strategies

Julie Bolin
Journal of Nuclear Medicine Technology September 2021, 49 (3) 199-208; DOI: https://doi.org/10.2967/jnmt.120.257105
Julie Bolin
Nuclear Medicine Technology Program, GateWay Community College, Phoenix, Arizona
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  • FIGURE 1.
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    FIGURE 1.

    Cellular differentiation and diagnostic/prognostic implications.

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    FIGURE 2.

    Key molecular signaling pathways involved in thyroid cancer initiation and progression. (Left) MAPK pathway, which is activated by mutations in RET, RAS, and BRAF. (Right) Pathways involved in tumor progression, including PI3K/AKT, p53 tumor suppressor, and TERT. Blue boxes represent molecular targets for therapies approved by Food and Drug Administration. ERK = extracellular-signal–regulated kinase; MEK = mitogen/extracellular-signal–regulated kinase; mTOR = mammalian target of rapamycin; PTEN = phosphatase and tensin homolog mutation; p53 = Tp53 or tumor protein; RAF = rapidly accelerated fibrosarcoma; RAS = rat sarcoma point mutations; RET = rearrangement during transfection; TERT = telomerase reverse transcriptase. (Reprinted with permission of (6).)

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    FIGURE 3.

    Thyroid hormone synthesis negative-feedback loop. Arrow with plus sign indicates stimulation. Arrow with minus sign indicates inhibition. T3 = triiodothyronine; T4 = tetraiodothyronine; TRH = TSH-releasing hormone.

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    TABLE 1

    Genetic Abbreviations

    NameAbbreviation
    Mitogen-activated protein kinaseMAPK
    Rearrangement during transfection/papillary thyroid cancer mutationsRET/PTC
    Rat sarcoma point mutationsRAS
    B-rapidly accelerated fibrosarcomaBRAF
    Telomerase reverse transcriptase promoterTERT
    Tumor proteinTp53
    Phosphatase and tensin homolog deleted from chromosome 10PTEN
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    TABLE 2

    Genetic Mutations and Associated Prognostic Significance

    Genetic mutationCancers displaying genetic mutationPrognostic significance
    BRAFPTC (BRAF V660E), PDTC, ATCNo clear consensus on prognostic significance; linked to extrathyroidal invasion, lymph node metastasis, vascular invasion, advanced tumor stage in primary tumor, and multifocality; linked to cellular dedifferentiation; linked to loss of iodine avidity; upregulates platelet-derived growth factor; upregulates vascular endothelial growth factor
    PTENDifferentiated thyroid cancers, PDTCUncontrolled cell growth and proliferation
    RASPTC, PTC-FV, FTC, PDTC, ATCRAS mutations alone likely associated with limited aggressiveness
    RET/PTC rearrangementsPTC (adult and pediatric), PTC-FV, FTCNot fully established; RET/PTC1 does not correlate with clinical pathologic features; RET/PTC3 is associated greater primary tumor size, cellular variations, and more advanced stage at diagnosis
    TERT90% of human cancers, differentiated thyroid cancers, PDTC, ATCRestores telomerase complex activity (prevents apoptosis); promotes epithelial mesenchymal transition, which promotes metastasis and cellular dedifferentiation
    Tp53PTC, FTC, PDTC, ATCExtrathyroidal extension; distant metastasis; potentially promotes cellular dedifferentiation
    • BRAF = B-rapidly accelerated fibrosarcoma mutation; PTEN = phosphatase and tensin homolog mutation; RAS = rat sarcoma point mutation; PTC-FV = follicular variant of papillary thyroid cancer; RET/PTC = rearrangement during transfection/papillary thyroid cancer (RET/PTC) mutation; TERT = telomerase reverse transcriptase mutation.

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    TABLE 3

    Targets in Molecular Therapy

    AbbreviationDefinition
    FGFFibroblast growth factor
    FLT-3Type III receptor tyrosine kinase
    KITType of receptor tyrosine kinase and type of tumor marker
    MEKMitogen/extracellular signal-regulated kinase
    mTORMammalian target of rapamycin
    PDGFαPlatelet-derived growth factor α
    PDGFRβPlatelet-derived growth factor receptor β
    PPARγPeroxisome proliferator-activated receptor γ
    RETRearrangement during transfection
    RET/PTCRearrangement during transfection/papillary thyroid cancer
    VEGFRVascular endothelial growth factor receptor
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Journal of Nuclear Medicine Technology: 49 (3)
Journal of Nuclear Medicine Technology
Vol. 49, Issue 3
September 1, 2021
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Thyroid Follicular Epithelial Cell–Derived Cancer: New Approaches and Treatment Strategies
Julie Bolin
Journal of Nuclear Medicine Technology Sep 2021, 49 (3) 199-208; DOI: 10.2967/jnmt.120.257105

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Thyroid Follicular Epithelial Cell–Derived Cancer: New Approaches and Treatment Strategies
Julie Bolin
Journal of Nuclear Medicine Technology Sep 2021, 49 (3) 199-208; DOI: 10.2967/jnmt.120.257105
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  • Article
    • Abstract
    • THE BASICS
    • PRESERVATION OF CELL TYPE
    • OVERVIEW OF FOLLICULAR EPITHELIAL CELL–DERIVED THYROID CANCERS
    • GENETIC CHANGES INVOLVED IN THYROID CARCINOGENESIS
    • NON-MAPK GENETIC MUTATIONS
    • ASSESSMENT AND TREATMENT
    • CONCLUSION
    • DISCLOSURE
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Keywords

  • anaplastic thyroid carcinoma
  • follicular thyroid carcinoma
  • papillary thyroid carcinoma
  • mitogen activated protein kinase
  • ATC
  • FTC
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