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At least 19 recordsLinked to original sources
PubMed2026

Myeloid landscape of BRAF-mutant papillary thyroid cancer and thyroiditis.

Papillary thyroid cancer (PTC) is less aggressive when associated with lymphocytic thyroiditis (LT), even in the presence of oncogenic BRAF, including smaller tumours, less lymph node involvement and reduced extrathyroidal extension. To investigate possible immune mechanisms underlying this association, we compared the tumour microenvironment of PTC-BRAF with LT and that without LT using single-cell RNA sequencing (scRNA-seq). Single-cell libraries were generated from fresh and fixed tumour samples with post-dissociation viability >70% using the 10x Genomics Chromium Platform and sequenced on an Illumina NovaSeq 6000. We analysed scRNA-seq data from 11 PTC-BRAF tumours: four with LT (one publicly available sample) and seven without LT. Downstream analyses included quality control, batch correction, dimensionality reduction, and differential gene expression analysis. We found that neutrophils were the predominant myeloid cell type in PTCs without LT. Thyrocytes without LT showed significant expression of the neutrophil recruitment chemokine ECRG4. In the absence of LT, neutrophils expressed oncogenic genes with poor clinical outcomes. In contrast, thyrocytes from tumours with LT showed increased expression of MHC-II antigen presentation, consistent with effective immune surveillance. Thyrocytes and macrophages in the presence of LT showed enrichment of interferon gamma response pathways. Our data suggest that LT in thyroid cancer is associated with enhanced antigen presentation and fewer features of pro-tumourigenic innate immune activity. These results identify previously under-recognised innate immune cell population and associated transcriptomic features, which suggest new mechanisms to target immune treatments in PTC refractory to other therapies.

Humans↗
PubMed1979

Serum thyroglobulin concentrations and whole-body radioiodine scan in follow-up of differentiated thyroid cancer after thyroid ablation.

Measurement of serum thyroglobulin (Tg) concentrations and whole-body radioiodine scan were performed simultaneously during follow-up of 32 patients with differentiated thyroid cancer who had undergone thyroid ablation by operation and radioiodine. Almost all patients in whom serum Tg was undetectable had normal scans. Concentrations exceeding 50 ng/ml were invariably associated with residual or metastatic tumour uptake in the scan. Out of 21 observations of detectable values below 50 ng/ml, 14 were in patients whose scans showed subclinical or sub-radiological tumour uptake and seven in patients with normal scans. The sensitivity of serum Tg as a tumour marker compared favourably to that of the whole-body scan. A scan is unnecessary when serum Tg is undetectable, but in patients with detectable serum Tg concentrations, particularly if these are below 50 ng/ml, a scan is important to assess and localise tumour uptake of iodine before advising treatmet with iodine-131.

Adenocarcinoma↗
PubMed1978

Calcitonin heterogeneity in lung cancer and medullary thyroid cancer.

An investigation was made of the increased serum calcitonin in patients with medullary thyroid cancer and bronchogenic carcinoma in order to determine whether these conditions can be differentiated immunochemically. Exdogenous fractions of immunoreactive calcitonin were separated by gel filtration and radioimmunoassayed with calcitonin antibodies having different region specificities. The pattern of serum heterogeneity of patients with medullary thyroid cancer was characterized by the presence of at least seven different fractions of immunoreactive calcitonin, ranging from fraction I (greater than or equal to 30 000 molecular weight (MW) to fraction V (approximately 2500 MW). In contrast, most patients with bronchogenic cancer had a predominance of high MW fractions (i.e. fractions I and IIA). Following in vitro incubation of the serum, the typical MW pattern of bronchogenic cancer serum could be converted to the more diffuse pattern seen in the serum of medullary thyroid cancer. We were able to differentiate, pre-operatively, the hypercalcitonaemia serum of medullary thyroid cancer patients from that of bronchogenic cancer patients by determination of the ratio of calcitonin as radioimmunoassayed with midportion versus carboxyl terminal antibody.

Calcitonin↗
PubMed2026

Targeting ncRNA control networks with engineered exosomes to overcome therapy resistance in thyroid cancer.

Papillary thyroid cancer (PTC) is the most prevalent endocrine malignancy, accounting for over 90% of thyroid cancers. While differentiated thyroid cancers (DTCs) typically have favorable outcomes, a significant subset progresses to radioactive iodine-refractory (RAIR) disease, characterized by impaired iodine uptake and a 10-year survival rate below 10%. Genetic alterations and dysregulated signaling pathways underlie this transition. Non-coding RNAs (ncRNAs), including microRNAs (miRNAs), circular RNAs (circRNAs), and long non-coding RNAs (lncRNAs), play critical regulatory roles in tumor biology and may be transported via exosomes, facilitating intercellular communication and contributing to RAIR-PTC. This systematic review, conducted according to PRISMA 2020 guidelines, evaluated the role of exosomal ncRNAs in RAIR-PTC. A comprehensive search of PubMed, PubMed Central, and Google Scholar identified studies published within the past 15 years in English. Following stringent quality appraisal, studies with a non-bias score above 40% were included. Of 961 identified publications, 96 high-quality studies met inclusion criteria. Evidence indicates that therapy resistance in RAIR-PTC is driven by convergent ncRNA regulatory networks that suppress sodium-iodide symporter (NIS) expression and activate oncogenic pathways, most notably MAPK, PI3K/AKT/mTOR, and Wnt/β-catenin signaling. Multiple ncRNAs converge on key regulatory nodes, forming redundant circuits that sustain dedifferentiation, metabolic adaptation, and impaired iodide transport. Several consistently dysregulated ncRNAs directly or indirectly regulate NIS expression and trafficking, highlighting actionable targets. Exosomes emerge as biologically compatible, programmable delivery vehicles capable of transporting therapeutic ncRNA payloads independent of endogenous packaging mechanisms. These findings support a precision therapeutic paradigm in which engineered exosomes reprogram ncRNA networks to restore iodine-handling pathways and overcome therapy resistance in RAIR-PTC.

Humans↗
PubMed2026

A per- and polyfluoroalkyl substances-based gene signature links prognosis to immune landscapes in thyroid cancer.

BACKGROUND: Thyroid cancer (THCA) is the most common endocrine malignancy with a rising global incidence and significant heterogeneity. Although per- and polyfluoroalkyl substances (PFAS) exposure is linked to thyroid dysfunction, the prognostic value of per- and polyfluoroalkyl substances-related genes (PFASRGs) and their role in the tumor immune microenvironment (TME) remain poorly understood. This study aims to systematically screen key PFASRGs and evaluate their prognostic value as biomarkers for THCA. METHODS: Utilizing The Cancer Genome Atlas (TCGA)-THCA transcriptomic data and PFASRGs, we constructed a prognostic model through differential expression analysis, univariate and multivariate Cox regression analyses, and the least absolute shrinkage and selection operator (LASSO). The model's robustness was validated using receiver operating characteristic (ROC) curves, Kaplan-Meier analysis, and clinical nomograms. Furthermore, the TME, immunotherapy response, and drug sensitivities were systematically evaluated. Distinct molecular landscapes were characterized by stratifying the cohort via unsupervised consensus clustering analysis. RESULTS: The eight-gene prognostic model demonstrated robust performance, with area under the curve (AUC) values exceeding 0.85 across all validation cohorts. High-risk patients exhibited significantly shorter overall survival and an "inflamed" TME characterized by high immune scores and checkpoint expression. In contrast, the therapeutic efficacy of anti-programmed death-ligand 1 (PD-L1) agents was more pronounced in the low-risk category, as evidenced by a superior objective response. Furthermore, distinct molecular subtypes and risk-specific sensitivities to targeted agents, such as sorafenib and sunitinib, were identified, highlighting the model's clinical utility for personalized treatment. CONCLUSIONS: We established a novel THCA prognostic framework based on eight PFASRGs. This model exhibits superior performance in risk stratification, effectively distinguishing cohorts with divergent clinical trajectories, unique immune microenvironment features, and varied therapeutic responses. Our findings provide a powerful predictive tool for refining prognostic evaluation and facilitating the implementation of personalized management strategies for THCA patients.

Per- and polyfluoroalkyl substances-related genes ↗
PubMed2026

Exploring shared biomarkers and their mechanisms in thyroid cancer and systemic lupus erythematosus via bioinformatics analysis.

BACKGROUND: Systemic lupus erythematosus (SLE), an autoimmune disorder, is linked to a heightened risk of multiple malignancies, including thyroid cancer. Thyroid cancer is the most prevalent malignancy of the endocrine system, and its autoimmune-related pathological features render it an optimal subject for investigating the mechanisms of their comorbidity. The molecular mechanisms underlying this comorbidity are still ambiguous. The accurate diagnosis and treatment of thyroid cancer urgently necessitate innovative molecular targets that extend beyond conventional pathological characteristics. This study seeks to employ integrated bioinformatics approaches to elucidate potential shared molecular mechanisms and immunological features between thyroid cancer and systemic lupus erythematosus (SLE), aiming to enhance understanding of their comorbidity and identify novel intervention targets. METHODS: This study initially acquired gene expression data for TC and SLE from the GEO database and subsequently screened and identified differentially expressed genes (DEGs) shared by both diseases. Subsequently, we conducted Gene Ontology (GO), Kyoto Encyclopedia of Genes and Genomes (KEGG), and Reactome functional enrichment analyses on these 46 shared differentially expressed genes (DEGs) and further assessed the activation status of pertinent pathways using Gene Set Enrichment Analysis (GSEA). Subsequently, we employed CIBERSORTx to examine immune infiltration patterns and developed protein-protein interaction networks utilising the STRING database. We identified hub genes utilising the MCODE and cytoHubba plugins and visualised the findings with Cytoscape software. We additionally assessed the diagnostic efficacy of these core hub genes in an independent dataset utilising ROC curves and investigated their prognostic relevance in thyroid cancer through Kaplan-Meier survival analysis and multivariate Cox proportional hazards regression. Ultimately, we employed the Network Analyst platform to forecast transcription factor-gene and miRNA-gene regulatory networks and identified potential targeted therapeutic compounds utilising the DSigDB database. RESULTS: This study identified 46 differentially expressed genes (DEGs) commonly linked to thyroid cancer and systemic lupus erythematosus (SLE), which were significantly enriched in signalling pathways associated with immune-inflammatory activation, type I interferon responses, and complement pathway activation. Moreover, GSEA findings validated that immune-inflammatory and autoimmune-related pathways are markedly activated in both conditions. Twelve hub genes were discerned through protein-protein interaction networks. Analysis of immune infiltration indicated that thyroid cancer and systemic lupus erythematosus exhibit a shared characteristic of innate immune dysregulation, marked by the infiltration of myeloid cells (neutrophils, M0/M2 macrophages). Receiver operating characteristic (ROC) curve analysis identified six significant core hub genes with substantial diagnostic value: C1QB, LCN2, C1QC, LTF, VSIG4, and C3AR1. Univariate survival analysis indicated that elevated expression of C1QC and C3AR1 significantly enhances overall survival in thyroid cancer patients; however, multivariate COX regression analysis revealed that their independent prognostic significance necessitates further validation. This study predicted the interaction networks of transcription factors and miRNAs regulating key genes, with LCN2 demonstrating the highest connectivity to miRNAs, and identified candidate therapeutic compounds linked to it. CONCLUSION: This study employed bioinformatics analysis to identify critical shared hub genes and molecular pathways connecting thyroid cancer and systemic lupus erythematosus, offering novel insights into their shared pathogenesis and the advancement of targeted biomarkers and therapeutic strategies.

Bioinformatics analysis↗
PubMed2026

Protective TGFβ2/SMAD3 axis identified by TWAS in papillary thyroid cancer.

Papillary thyroid carcinoma (PTC) is the most common endocrine malignancy. Although generally indolent, a subset shows aggressive behaviour. Furthermore, the genetic heterogeneity of PTC is not fully explained by known driver mutations, underscoring the need to identify additional susceptibility genes and regulatory mechanisms. To identify additional susceptibility genes and regulatory mechanisms, we integrated transcriptome-wide association studies (TWAS) with summary-data-based Mendelian randomisation (SMR), joint/conditional testing (JCT), and colocalisation analyses across multiple independent cohorts, followed by heterogeneity in dependent instruments (HEIDI) test. Gene prioritisation analyses consistently highlighted TGFB2 and SMAD3 as candidate susceptibility genes for PTC, with SMR supporting putative protective effects. Besides, GEPIA confirmed the positive correlation between TGFB2 and SMAD3 expression in TCGA-THCA. Functional experiments in TPC-1 cells showed that TGFβ2 treatment inhibited cell proliferation and migration, induced apoptosis, and resulted in G0/G1 cell-cycle arrest, accompanied by increased SMAD3 phosphorylation, suggesting activation of canonical TGFβ signalling. Collectively, these findings bridge population-based genetic inference with mechanistic validation and suggest convergent evidence supporting a tumour-suppressive role of the TGFβ2/SMAD3 axis in PTC.

Humans↗
PubMed1978

Thyroid cancer in childhood.

Thyroid cancer in childhood is a relatively rare condition. Often it shows biological characteristics different from those seen in adults. Based upon 10 cases in our clinic and 57 cases collected from the Japanese literatures, clinical features, pathology, treatment and prognosis of thyroid cancer in childhood are discussed. Pathogenesis is most likely to be related to hormonal changes during adolescence and previous radiation of the neck region. Cervical lymph nodes swelling was the chief complaint in 84.6 per cent of the cases. On the other hand, pulmonary metastases were recognized in the early stages in 33.5 per cent of the cases. Radical excision of the tumor with modified radical neck dissection is the treatment most frequently employed even in the presence of lung metastases. However, hypoparathyroidism and recurrent nerve injuries should be avoided at all cost in view of long life expectancy and the difficulty in treating them satisfactorily. Prognosis could be as good for children as it is for adults except in cases with early lung metastases.

Adenocarcinoma↗
PubMed2026

Anti-tumour effects of combined lenvatinib and EGFR Inhibition in advanced differentiated thyroid cancer cells.

PURPOSE: Differentiated thyroid cancer (DTC) typically has a favourable prognosis, while advanced forms of these tumours exhibit aggressive behaviour, leading to decreased survival. Lenvatinib has demonstrated effectiveness in managing advanced DTC. However, its long-term efficacy is compromised by resistance mechanisms, which remain unexplored, limiting its clinical utility. METHODS: In vitro studies were conducted using three advanced DTC cell lines of the papillary subtype: K1 (BRAF p.V600E), BCPAP (BRAF p.V600E) and TPC-1 (RET/PTC1). IC50 for Lenvatinib and Gefitinib were defined, and their effects on cell viability, colony formation, gene expression, and pathway activation were assessed individually and in combination. Comparative genomic hybridisation was performed to uncover intrinsic resistance mechanisms. RESULTS: Lenvatinib IC50 was higher in K1 and BCPAP than in TPC-1, indicating greater TPC-1 susceptibility, as confirmed by viability assays. Gefitinib showed similar IC50 values across all cell lines. The Lenvatinib plus Gefitinib combination (Combo) significantly reduced K1 and BCPAP viability when comparing with monotherapies, with no significant effects in TPC-1. Clonogenic assays mirrored these results and revealed higher recovery in K1 and BCPAP after Combo withdrawal. Combo treatment increased EGFR expression and induced ERK1/2 and AKT phosphorylation’s dysregulation in all cell lines. CONCLUSIONS: This study showed that RET/PTC1 cells are more responsive to Lenvatinib than BRAF-mutated cells, and that EGFR targeting with Gefitinib enhanced Lenvatinib’s inhibitory effect in BRAF-mutated cells. Dysregulation of EGFR and Lenvatinib target gene’s expression, as well as of MAPK and PI3K signalling may indicate short-term adaptive resistance. These findings provide insight into Lenvatinib resistance mechanisms in thyroid cancer and highlight the need for further research to overcome refractoriness.

Humans↗
PubMed1979

Changing incidence of thyroid cancer.

The incidence of thyroid cancer was examined temporally and geographically by age and sex from data provided by tumor registries in the United States and abroad. The temporal trends in Connecticut showed an increase in annual incidence after 1945, with an especially sudden increase in incidence in females. The increase occurred predominantly in older males and younger females. The increase in young females was confirmed by cohort analysis. The rates rose with age in both sexes, but recently females have developed a secondary peak in the fourth decade of life. The same phenomenon was observed in other U.S. data but not as clearly in data from ten foreign registries. These observations are consistent with the hypothesis that X-radiation therapy for benign conditions of the head and neck in childhood was a factor in the increased incidence of thyroid cancer in U.S. females, but some other etiologic or modifying factor should be sought to explain the increased incidence in U.S. males.

Adult↗
PubMed1977

Serum thyroglobulin and recurrent thyroid cancer.

Many thyroid malignancies are sufficiently differentiated to produce thyroglobulin both in situ and in perpipheral blood. Since patients who have undergone total thyroidectomy for malegnancy should not have normally circulating thyroglobulin, their serum thyroglobulin may provide a simple and specific tumour marker for recurrent disease. Of 30 such athyroid patients who were studied, all of the 20 patients who were disease-free ten years after thyroidectomy had minimal (less than15 ng/ml) serum-thyroglobulin levels while all of 10 patients with recurrences had raised levels (greater than 90 ng/ml). Controls ranged from 0 to 60 ng/ml. This assay should prove valuable in following patients who have undergone total thyroidectomy for recurrent thyroid malignancy.

Adolescent↗
PubMed1978

Anaplastic transformation of medullary thyroid cancer.

The paper presents a detailed microscopic study of a case of medullary thyroid carcinoma with the loss of amyloid production and of argyrophilic cellular granules combined with the prevalence of giant multinucleated cells in a part of the primary tumor and namely in metastatic deposits. These changes are believed to give evidence of anaplastic dedifferentiation. Similar cases to that reported are reviewed with the conclusion that not only differentiated thyroid cancers but medullary thyroid cancers as well are capable of anaplastic transformation. However rare the medullary thyroid cancers are, they should be diagnosed and radically treated so as to prevent their fatal anaplastic transformation.

Aged↗
PubMed1979

Comparison of the distribution of diagnostic and thyroablative I-131 in the evaluation of differentiated thyroid cancers.

In 206 patients with differentiated thyroid cancer, the distribution of iodine-131 were compared after diagnostic (200-500 microCi) and thyroblative (approximately 100 mCi) doses. In the diagnostic scans, only normal thyroid tissue could be seen, whereas in one-fourth of the patients the therapeutic scans showed tumor tissue as well, usually in lymphnode metastases. In 16% of patients, the therapeutic scan was the only way to demonstrate the presence of tumor tissue, since no further uptake was achievable. In patients in whom all tumor was believed to have been removed by surgery alone, a "preventive" I-131 ablation was used, and in 16 of these 97 patients tumor was revealed in the therapeutic scan. In ten more, tumor was found in subsequent followup scans, its functioning having been induced by destruction of postsurgical remnants of normal thyroid. Some possible explanations for the differences in scans are proposed, and the importance of therapeutic scans for correct staging of thyroid cancer is stressed.

Adult↗
PubMed1979

The epidemiology of thyroid cancer in Los Angeles county.

More than 300 new cases of thyroid cancer are diagnosed in Los Angeles County every year. The age-adjusted annual incidence rates of this disease for all races combined are 2.4 for males and 6.1 for females. Rates for women are more than twice rates for men in each major ethnic group. Blacks of both sexes have the lowest rates; Japanese, Chinese, other Asians and Spanish-surnamed whites all have rates that are as high as or higher than rates among non-Spanish-surnamed whites. Other demographic patterns include the excess of thyroid cancer among Jewish residents of Los Angeles. There have been an increase in thyroid cancer incidence and a decline in mortality for this disease in the United States over the past several decades. Several possible explanations can be made for these trends. Also, the risk factors for thyroid cancer deserve review.

Adenocarcinoma↗
PubMed1977

[Causes of death in thyroid cancer patients].

To determine the necessary extent of surgery in thyroid cancer 128 autopsy reports of patients with thyroid cancer were studied. It was found that in a group of those died from cancer the specific weight of death issues due to papillary cancer, most frequently observed, was small (8.5%), consequently these patients would show a recovery postoperatively. Patients with one lobe involved die following its resection but, as a rule, not because of the process spreading to the second lobe. The prognosis for patients with thyroid cancer largely depends on the histological type of tumor rather than the extent of surgery. All this supports the idea that in appropriate cases it is feasible to continue oneself to the resection of the lateral thyroid lobe for this kind of tumor.

Autopsy↗