Thyroid Gland Carcinoma

This multi-omics analysis supports a causal link between SLE and TC in European populations and identifies the SLEscore as a potential prognostic biomarker, offering new opportunities for precision risk assessment and targeted management in SLE-associated TC.

This integrative multi-cohort study uncovered common transcriptional and immune signatures underlying SjD, MALT lymphoma, and thyroid cancer. The identification of shared hub genes, particularly PLA2G7 and TGFB1I1, provides novel insight into the immune-driven transition from chronic inflammation to malignancy and offers promising biomarkers for cross-disease diagnosis and immunotherapeutic stratification. Key Points • Key genes (PLA2G7 and TGFB1I1) affecting the occurrence of Sjögren's syndrome, mucosa-associated lymphoid tissue lymphoma, and thyroid cancer are identified for the first time. • Bioinformatics methods were employed to simultaneously study three diseases for the first time.

It underscores the importance of extensive sampling and a multidisciplinary approach for effective management. Given the lack of standardized treatment guidelines, personalised care and close follow-up are essential, with consideration of aggressive treatment based on risk assessment.

P=N/A, N=50, Completed, University of Michigan Rogel Cancer Center | Active, not recruiting --> Completed

Co-existent PTC, immunopositivity for thyroid-differentiation markers, and the genetic profile confirm a squamoglandular metaplasia of follicular cells as the origin. The absence of MAML2 fusion questions its WHO categorization as a "salivary gland-type carcinoma." Detailed molecular profiling, while contributing to a better understanding of the pathogenesis of this enigmatic neoplasm, also helped decipher potentially actionable genetic variants.

Using high-throughput screening, we established that combining p38 inhibitors with the BRAF inhibitor dabrafenib showed strong synergy in vitro, including in cells resistant to dabrafenib and trametinib that had acquired a secondary TP53 mutation. Overall, our findings suggest an oncogenic link between the MAPK and p38/MAPK14 pathways and that combining p38 pathway inhibitors with dabrafenib-targeted therapy could improve treatment outcomes for aggressive thyroid cancers. However, more specific and effective p38 inhibitors are required to fully harness this potential.

BRAF-mut PTC is associated with a pro-inflammatory TME milieu compared to BRAF-wt PTC. However, in this limited data set, treatment choice was not associated with differences in OS in BRAF-mut PTC.

Unexplained splenomegaly warrants consideration of primary splenic lymphoma in the differential diagnosis, even without lymphadenopathy or classic B symptoms, particularly when detected during abdominal imaging for hepatosplenic evaluation.Histopathologic and molecular confirmation is essential, as indolent subtypes (e.g. SMZL) and aggressive subtypes (e.g. DLBCL) may present identically but require fundamentally different treatment approaches.PET/CT-guided diagnostic strategy optimises outcomes by enabling accurate staging, identifying the most metabolically active site for biopsy, and informing the need for splenectomy versus direct systemic therapy.

The presented data highlighted the molecular heterogeneity of MTCs and the need for personalized treatment strategies. For this reason, the obtained profiles could offer novel perspectives into the molecular landscape of this neoplasm within the scientific community.

CircPTPRM can encode circPTPRM-187aa polypeptide. circPTPRM-187aa, regulates the expression of IQGAP1 protein, and up-regulates RAC1 and CDC42 proteins in TGF-β signaling pathway, enhancing the PTC cells proliferation, migration, and invasion.

Our bioinformatic analysis reveals a correlation between elevated Wnt target gene expression and E-cadherin loss in a Wnt-driven model of thyroid cancer. Our results have relevance for tumorigenesis, as cadherin loss is commonly associated with poor prognosis and increased metastatic potential.

Prevalence of secondary RET mutations after SRIs was low, underscoring greater role for off-target resistance. Recurrent acquired alterations involving tumor suppressor genes or upstream regulators of MAPK and PI3K pathways were identified, most commonly MET amplification. Continued efforts to characterize SRI resistance biology are critical to guide development of novel therapeutic strategies.