Rationale:Malignant struma ovarii is extremely rare in the clinic. The diagnosis and modalities of treatment are still controversial. Here we describe a case of extensive peritoneal implant metastasis originating from malignant struma ovarii discovered 14 years after ovariectomy and chemotherapy.Patient concerns:A 48-year-old female was admitted to our clinic due to hematochezia with a past history of left malignant struma ovarii. Enhanced computed tomography (CT) examination suggested multiple metastasis nodules in the abdomen and pelvic cavity.Diagnoses:Laparoscopy biopsy results of intraperitoneal nodules showed a metastasis of papillary thyroid carcinoma. While pathological examination after total thyroidectomy showed no definite malignant tumor component in the thyroid tissue. Finally, combined with the patient's past history of malignant struma ovarii, peritoneal implantation metastasis derived from the malignant struma ovarii was diagnosed.Interventions:The patient was treated by total thyroidectomy and iodine 131 (131I) therapy. Post-therapy iodine scan and the single-photon emission computed tomography/computed tomography (SPECT/CT) fusion image showed iodine uptake in the distal descending colon, sigmoid colon, rectal lesions, and a larger lesion in the liver.Outcome:After treatment, although the thyroid globulin remained at a high level 3 months after treatment, the patient's hematochezia was relieved.Lessons:Therefore, thyroidectomy followed by adjuvant 131I treatment should be recommended in patients with malignant struma ovarii as metastatic risk is difficult to predict based on histopathologic examination.

PurposeThe incidence rate of thyroid cancer, the most common endocrine malignancy, has increased rapidly over the past 10 years. However, the fundamental molecular mechanisms underlying the malignant progression of thyroid cancer are unclear.Materials and methodsFirstly, quantitative real-time PCR analysis and Western blot analysis were used to investigate the expression of Cbp/p300 interacting transactivator with Glu/Asp rich carboxy-terminal domain 1 (CITED1) in papillary thyroid carcinoma (PTC) cell lines. Then, we investigated the effects of CITED1 knockdown on cell proliferation, apoptosis, and invasion in in vitro and in vivo models of PTC.ResultsCITED1 was upregulated in PTC cell lines, and CITED1 knockdown significantly suppressed the proliferation, migration, and invasion of K1 cells resulting in a G0/G1 phase block. Furthermore, the silencing of CITED1 significantly promoted cell apoptosis. In the in vivo study, the growth speed and weight of the transplanted tumor were significantly suppressed in nude mice infected with short hairpin RNA targeting CITED1 (CITE1-shRNA) cells. Furthermore, we found that CITED1-shRNA activated Wnt/β-catenin signaling in PTC.ConclusionTaken together, our findings suggest that CITED1 knockdown facilitates apoptosis and inhibits proliferation and invasion in K1 cells via the Wnt/β-catenin signaling pathway.

Radioiodine refractory differentiated thyroid cancer (RR-DTC) is the main factor adversely affecting the overall survival rate of patients with thyroid cancer. The aim of the present study was to investigate the underlying molecular mechanism of pathogenesis of RR-DTC and to explore novel therapeutic targets for clinical treatment. A proteomic analysis was performed using the tumor tissues of patients with RR-DTC. A total of 6 metastatic lymph nodes were collected during lymph node dissection, 3 from patients with RR-DTC and 3 from patients with papillary thyroid cancer. The expression of chitinase-3-like 1 (CHI3L1) and sodium-iodine symporter (NIS) in the tumor tissue was detected by immunohistochemistry (IHC). Western blotting was used to detect the expression of CHI3L1, phosphorylated (p)-MEK and p-ERK1/2 in PTC-K1 cells transfected with CHI3L1 overexpression vector. The proteomic analysis identified 665 differentially expressed proteins (DEPs), including 327 upregulated and 338 downregulated proteins in the RR-DTC group, which were enriched in 59 signaling pathways by Kyoto Encyclopedia of Genes and Genomes database analysis. In particular, CHI3L1 was demonstrated to be significantly upregulated in RR-DTC as evidenced by quantitative proteomic analysis and IHC. Western blotting suggested that the overexpression of CHI3L1 activated the MEK/ERK1/2 signaling pathway, which may lead to NIS dysfunction. In conclusion, the present study suggests that CHI3L1 is a potential molecular target for the radiotherapy of patients with RR-DTC.

Purpose To study the differentially expressed protein between thyroid cancer and radioactive iodine refractory differentiated thyroid cancer (RR-DTC), which presents highly aggressive and unfavorable prognosis. Meanwhile, to search for a potential radiotherapeutic target for patients suffer from RR-DTC. Methods Totally 6 metastatic lymph nodes of RR-DTC and DTC were collected during lymph node dissection for proteomics studies. Immunohistochemical staining was performed to verify the expression of Chitinase-3-like 1 (CHI3L1) in RR-DTC and DTC tissues. Western blotting was used to detect the expression of sodium-iodine symporter (NIS), MEK, and ERK1/2 in CHI3L1 over-expression stable transfectants, control stable transfectants, and PTC-K1 cells. Results CHI3L1 was demonstrated to be significantly up-regulated in RR-DTC by immunohistochemical staining. Besides, CHI3L1 over expression would inhibit expression of sodium-iodine symporter, a key protein for iodine accumulation, by activating MEK/ERK1/2 signal pathway. Conclusion CHI3L1 might be a potential molecular target for RR-DTC due to its over expression in RR-DTC and membrane location.