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Establishment and Characterization of Patient-Derived Xenograft Models of Anaplastic Thyroid Carcinoma and Head and Neck Squamous Cell Carcinoma
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Targeted therapy: a new hope for thyroid carcinomas.

Francesco Perri1, Luciano Pezzullo2, Maria Grazia Chiofalo2

  • 1Division of Head and Neck Medical Oncology, Istituto Nazionale Tumori di Napoli "Fondazione G. Pascale-IRCCS", Naples, Italy.

Critical Reviews in Oncology/Hematology
|December 4, 2014
PubMed
Summary

Targeted therapies offer new hope for advanced thyroid cancers, including anaplastic and medullary types. Understanding molecular pathways like MAP-Kinase is key to developing effective treatments for these rare but aggressive malignancies.

Keywords:
AnaplasticFollicularMedullaryPapillaryPathwayRadioiodine therapyTargeted therapyThyroid carcinoma

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Area of Science:

  • Oncology
  • Molecular Biology
  • Genetics

Background:

  • Thyroid carcinomas are rare, heterogeneous malignancies, with differentiated types (papillary, follicular) generally having good prognoses.
  • However, approximately 10% of differentiated carcinomas, and all anaplastic and medullary types, can become resistant to standard therapies like radioiodine.
  • Recurrence and resistance necessitate novel therapeutic strategies for advanced thyroid cancers.

Purpose of the Study:

  • To explore the potential of targeted therapy for thyroid carcinomas based on recent advances in molecular biology.
  • To identify key molecular pathways and genetic alterations implicated in thyroid cancer development and progression.
  • To review current and emerging targeted agents for treating advanced or resistant thyroid cancers.

Main Methods:

  • Review of scientific literature focusing on molecular mechanisms of thyroid tumorigenesis.
  • Analysis of dysregulated signaling pathways, including MAP-Kinase, RET/PTC, B-RAF, mTOR, and VEGFR.
  • Examination of clinical data for targeted therapies and angiogenesis inhibitors in thyroid cancer treatment.

Main Results:

  • The MAP-Kinase pathway is frequently dysregulated in thyroid carcinomas.
  • Specific mutations like RET/PTC and B-RAF are common in papillary, medullary, and anaplastic subtypes.
  • Disruptions in mTOR and VEGFR pathways are observed in advanced thyroid cancers, highlighting potential therapeutic targets.
  • Several targeted agents, including angiogenesis inhibitors and RET/PTC pathway blockers (e.g., vandetanib, cabozanitinib, sorafenib), are in clinical use or trials.

Conclusions:

  • Targeted therapies represent a promising new avenue for managing advanced and resistant thyroid carcinomas.
  • A deeper understanding of thyroid cancer biology, particularly its molecular underpinnings, is crucial for designing effective, personalized treatment strategies.
  • Continued research into molecular pathways and targeted agents holds potential for improving outcomes in patients with rare and aggressive thyroid cancers.