Refractory thyroid cancers include medullary and differentiated cancers with locally advanced disease that is not amenable to surgery or with distant metastases, differentiated thyroid carcinomas being refractory to radio-iodine treatment and all anaplastic carcinomas. These carcinomas are rare, with an estimated incidence in France of 350 new cases per year. Their management may benefit from the TUTHYREF network. Kinase inhibitors inhibit kinases of the VEGF receptors, and this inhibits angiogenesis, and some of these agents also inhibit other kinases of the MAPkinase pathway. These inhibitors are effective in differentiated and medullary thyroid cancers, and induce a partial response or a long-term stabilisation in more than half of patients. Their toxicity is significant and these treatments should be given only to selected patients with locally advanced or metastatic disease, with progression or with clinical symptoms.
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http://dx.doi.org/10.1016/j.lpm.2011.09.011 | DOI Listing |
Endocr Relat Cancer
January 2025
A Nikitski, Department of Pathology, University of Pittsburgh, Pittsburgh, 15261, United States.
Approximately 10-20% of thyroid cancers are driven by gene fusions, which activate oncogenic signaling through aberrant overexpression, ligand-independent dimerization, or loss of inhibitory motifs. We identified 13 thyroid tumors with thyroglobulin (TG) gene fusions and aimed to assess their histopathology and the fusions' oncogenic and tumorigenic properties. Of 11 cases with surgical pathology, 82% were carcinomas and 18% noninvasive follicular thyroid neoplasms with papillary-like nuclear features (NIFTP).
View Article and Find Full Text PDFMicrosurgery
February 2025
Plastic and Reconstructive Surgery, Department of Precision Medicine in Medical, Surgical and Critical Care (Me.Pre.C.C.), University of Palermo, Palermo, Italy.
Background: Scalp reconstruction is a challenging field for plastic surgeons. In case of large or complex defects, microsurgical-free flaps are usually required. Reconstructive failure can result in high morbidity and in some cases be life-threatening.
View Article and Find Full Text PDFArch Endocrinol Metab
January 2025
Universidade de São Paulo Instituto de Ciências Biomédicas Departamento de Biologia Celular e do Desenvolvimento São PauloSP Brasil Departamento de Biologia Celular e do Desenvolvimento, Instituto de Ciências Biomédicas, Universidade de São Paulo, São Paulo, SP, Brasil.
Modulating the expression of a coding or noncoding gene is a key tool in scientific research. This strategy has evolved methodologically due to advances in cloning approaches, modeling/algorithms in short hairpin RNA (shRNA) design for knockdown efficiency, and biochemical modifications in RNA synthesis, among other developments. Overall, these modifications have improved the ways to either reduce or induce the expression of a given gene with efficiency and facility for implementation in the lab.
View Article and Find Full Text PDFSci Rep
January 2025
Department of Thyroid and Neck Tumor, Tianjin Medical University Cancer Institute and Hospital, National Clinical Research Center for Cancer, Tianjin's Clinical Research Center for Cancer, Key Laboratory of Cancer Prevention and Therapy, Tianjin, 300060, China.
Programmed cell death (PCD) is a vital biological process that is essential for regulating cell progression and tumor microenvironment. This study aimed to explore the relationship between PCD-related genes expression and prognosis in thyroid cancer (THCA), especially IL20RA, as a potential prognostic marker for THCA. Data from The Cancer Genome Atlas (TCGA) database was utilized to develop a PCD-related risk prediction model based on LASSO regression along with univariate Cox regression.
View Article and Find Full Text PDFEur Thyroid J
January 2025
J Knauf, Center for Immunotherapy and Precision Immuno-Oncology, Cleveland Clinic, Cleveland, United States.
The development of mouse models for thyroid cancer has significantly advanced over the years, enhancing our understanding of thyroid tumorigenesis, molecular pathways, and treatment responses. The earliest mouse models of thyroid cancer relied on hormone, radiation, or chemical carcinogenesis to induce tumors. However, as our understanding of the genetic alterations driving thyroid cancer has expanded, more sophisticated genetic engineering techniques have been employed to create models with thyroid-specific expression of these driver mutations.
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