Thyroid Gland Papillary Carcinoma

Up-regulated LINC00667 may serve as a biomarker for PTC. Knockdown of LINC00667 may inhibit the progression of PTC by regulating miR-34c-5p.

P=N/A, N=876, Recruiting, Sun Yat-Sen Memorial Hospital of Sun Yat-Sen University | Not yet recruiting --> Recruiting

This study comprehensively mapped PRGs in PTC, established a validated risk model, and provided insights into immune-microenvironment interactions and therapeutic targets, advancing precision oncology for PTC.

Rescue experiments and immunofluorescence confirmed UBE2T promotes oncogenesis by destabilizing SOCS2, thereby relieving its inhibition of STAT3 phosphorylation. These findings establish UBE2T as a novel regulator of PTC progression through SOCS2/JAK-STAT3 axis manipulation, providing potential therapeutic targets to mitigate metastasis and recurrence in aggressive thyroid carcinomas.

BRAF inhibitors yielded only transient responses, and outcomes were poor. These cases underscore the diagnostic and therapeutic value of multigene testing in SCC, highlighting the need to integrate detailed clinical history into precision oncology strategies.

Our findings highlight the NR2F2-BGN axis as a critical regulator of PTC progression. Targeting this axis offers a promising therapeutic strategy for PTC treatment and immune microenvironment modulation.

Both the de novo synthesis and exogenous uptake of FAs are important for PTC cell proliferation. The combined inhibition of LPL and FASN inhibitors shows promise for PTC treatment.

The presence of infiltrative tumor margin, plump pink cells, and myxoid desmoplasia, may serve as active markers associated with the normalized BRAF V600E mutation. These findings suggest that the mutation acts as a driver in both early and late stages of PTC development. Furthermore, a direct relationship between tumor size and clonality underscores the role of BRAF V600E mutation in tumor progression and morphological evolution.

miR-155 appears to be a promising minimally invasive biomarker for thyroid malignancy, while miR-429 cannot reliably distinguish malignant from non-malignant lesions; further studies are needed to validate these findings.

In such a situation, the possibility of coexistence of MTC and PTC should be highly suspected. A standardized surgical treatment plan should be selected, and during the pathological examination, standardized sampling and meticulous reading of the slides should be emphasized, combined with immunohistochemical detection, to reduce the risk of missed diagnosis, provide accurate pathological diagnosis, and thereby offer reliable basis for the formulation of postoperative treatment strategies and prognosis assessment.

ABO blood group and Rhesus factor do not appear to be independent biomarkers in papillary thyroid cancer. Our study presents findings that do not support a relationship between ABO blood group, Rhesus factor, and PTC. However, further studies with larger patient cohorts are needed to reach more definitive conclusions.

Although a rare cause of hypercalcemia, familial hypocalciuric hypercalcemia (FHH) is an inherited condition most often due to a missense mutation in the calcium-sensing receptor (CASR) gene, giving rise to increased calcium levels with elevated parathyroid hormone (PTH) levels and hypocalciuria. Many clinical features of FHH show a high degree of overlap with the much more common disorder of primary hyperparathyroidism (PHPT), making the correct diagnosis a challenge since surgery should be avoided in FHH. In the current case, although PHPT was initially suspected based on urine biochemistry and imaging, FHH-1 and metastatic micropapillary thyroid cancer were diagnosed following thyroid surgery. Moreover, an underlying novel missense CASR mutation shared with the patient's biological father was uncovered. This case highlights the challenge of making the correct hypercalcemic diagnosis without genetic tools. The concurrence with thyroid cancer has been reported once before, albeit not with this novel CASR mutation.