Development Of Thyroid Cancer Research Articles

2225P FOX1 (rs965513), NKX2-1 (rs944289) and BRAF (V600E) gene mutations and their role in development of papillary thyroid cancer

2225P FOX1 (rs965513), NKX2-1 (rs944289) and BRAF (V600E) gene mutations and their role in development of papillary thyroid cancer

The impact of metformin on the development and course of anaplastic thyroid cancer in comparison to other histologic types of thyroid cancer

The impact of metformin on the development and course of anaplastic thyroid cancer in comparison to other histologic types of thyroid cancer

Identification of transcriptional level variations in microRNA-221 and microRNA-222 as alternate players in the thyroid cancer tumor microenvironment

Thyroid cancer (TC) is caused by genetic factors and or their cross talk with lifestyle and environment. An important role of miRNA involvement has been identified in different human diseases alongside the cancer. The growing cloud of miRNA discoveries narrates miRNA-221 and miRNA-222 as key elements of ready arsenal in the cancer micro-niches. The aim of present study was to identify the variations of miRNA-221 and miRNA-222 expression in TC tissues and their likely association with TC. miRNA-221 and miRNA-222 were investigated for their expressional alterations in TC tissue samples and healthy thyroid tissue. Expression of miRNA-221 and -222 was analyzed through real time PCR. The relative gene expression of both the miRNA was quantified and statistically evaluated. miRNA-221 and miRNA-222 were found to be highly over expressed when compared with samples of multinodular goiter (MNG) and normal controls. Interestingly, it was also noted that miRNA-221 and miRNA-222 expression is working in a cluster in thyroid cancer patients. So, it can be concluded that the expressional alterations of miRNA-221 and -222 are playing their potential role in the development of thyroid cancer.

The Role of Blood Microbiome in the Development of Thyroid Cancer in Breast Cancer Survivors.

Patients diagnosed with breast cancer are likely to be diagnosed with thyroid cancer as a second primary cancer. Similarly, patients with thyroid cancer are likely to develop breast cancer. In this study, we found an association between these two types of cancers in the microbiomes of patients with breast cancer. Blood samples were collected from 96 patients with breast cancer, their bacterial extracellular vesicles were isolated, and their microbiomes were analyzed. After microbiome analysis, researchers performed thyroid function tests, estrogen levels, and thyroid ultrasound results of these patients, and the relationships among these parameters were analyzed. Based on the thyroid ultrasonography results, differences in the microbiome were confirmed in the normal, cyst, nodule, and thyroid lobectomy groups. We investigated the microbiome differences between normal thyroid and thyroid cancer. In particular, the abundance of the genus Bacillus is related to estrogen levels, which could affect thyroid abnormalities and increase thyroid-stimulating hormone levels. This study explains the causes of thyroid cancer in patients with breast cancer using microbiomes and serological tests for thyroid hormones and estrogen. These can be used as basic data for preventing thyroid cancer in patients with breast cancer.

SBP1 promotes tumorigenesis of thyroid cancer through TXN/NIS pathway

BackgroundAs the tissue with the highest selenium content in the body, the occurrence and development of thyroid cancer are closely related to selenium and selenoproteins. Selenium-binding protein 1 (SBP1) has been repeatedly implicated in several cancers, but its role and molecular mechanisms in thyroid cancer remains largely undefined.MethodsThe expression of SBP1, sodium/iodide symporter (NIS) and thioredoxin (TXN) were analyzed in clinical samples and cell lines. Cell counting kit-8 (CCK-8) and tube formation assays were used to analyze the cell viability and tube formation of cells. Immunofluorescence was used to determine the expression of the NIS. Co-immunoprecipitation (Co-IP) assay was carried out to verify the interaction of SBP1 with TXN. The mouse xenograft experiment was performed to investigate the growth of thyroid cancer cells with SBP1 knockdown in vivo.ResultsSBP1 was significantly increased in human thyroid cancer tissues and cells, especially in anaplastic thyroid cancer. Overexpression of SBP1 promoted FTC-133 cell proliferation, and the culture supernatant of SBP1-overexpression FTC-133 cells promoted tube formation of human retinal microvascular endothelial cells. Knockdown of SBP1, however, inhibited cell proliferation and tube formation. Furthermore, overexpression of SBP1 inhibited cellular differentiation of differentiated thyroid cancer cell line FTC-133, as indicated by decreased expression of thyroid stimulating hormone receptors, thyroglobulin and NIS. Knockdown of SBP1, however, promoted differentiation of BHT101 cells, an anaplastic thyroid cancer cell line. Notably, TXN, a negative regulator of NIS, was found to be significantly upregulated in human thyroid cancer tissues, and it was positively regulated by SBP1. Co-IP assay implied a direct interaction of SBP1 with TXN. Additionally, TXN overexpression reversed the effect of SBP1 knockdown on BHT101 cell viability, tube formation and cell differentiation. An in vivo study found that knockdown of SBP1 promoted the expression of thyroid stimulating hormone receptors, thyroglobulin and NIS, as well as inhibited the growth and progression of thyroid cancer tumors.ConclusionSBP1 promoted tumorigenesis and dedifferentiation of thyroid cancer through positively regulating TXN.

Activation of mitogen-activated protein kinase signaling and development of papillary thyroid carcinoma in thyroid-stimulating hormone receptor D633H knockin mice.

Nonautoimmune hyperthyroidism (NAH) is rare and occurs due to a constitutively activating thyroid stimulating hormone receptor (TSHR) mutation. In contrast to other thyroid nodules, no further evaluation for malignancy is recommended for hot thyroid nodules. In the first model for NAH in mice nearly all homozygous mice had developed papillary thyroid cancer by 12 months of age. To further evaluate these mice, whole exome sequencing and phosphoproteome analysis were employed in a further generation of mice to identify any other mutations potentially responsible and to identify the pathways involved in thyroid carcinoma development. Only three genes (Nrg1, Rrs1, Rasal2) were mutated in all mice examined, none of which were known primary drivers of papillary thyroid cancer development. Wild-type and homozygous TSHR D633H knockin mice showed distinct phosphoproteome profiles with an enrichment of altered phosphosites found in ERK/mitogen-activated protein kinase (MAPK) signaling. Most importantly, phosphosites with known downstream effects included BRAF p.S766, which forms an inhibitory site: a decrease of phosphorylation at this site suggests an increase in MEK/ERK pathway activation. The decreased phosphorylation at BRAF p.S766 would suggest decreased AMP-activated protein kinase (AMPK) signaling, which is supported by the decreased phosphorylation of STIM1 p.S257, a downstream AMPK target. The modified phosphoproteome profile of the homozygous mice in combination with human literature suggests a potential signaling pathway from constitutive TSHR signaling and cAMP activation to the activation of ERK/MAPK signaling. This is the first time that a specific mechanism has been identified for a possible involvement of TSH signaling in thyroid carcinoma development.

PIWI interacting RNA-13643 contributes to papillary thyroid cancer development through acting as a novel oncogene by facilitating PRMT1 mediated GLI1 methylation

Recently, aberrant expression of PIWI-interacting RNAs (piRNAs) has been discovered in a variety of cancer cells. However, the roles of PIWI proteins and piRNAs in papillary thyroid carcinoma (PTC) are still elusive. RT-qPCR and Northern blotting were used to evaluate piR-13643 levels in PTC and para-carcinoma tissues, as well as in PTC cell lines. piR-13643 mimic and piR-13643 inhibitor were transfected into K-1 and B-CPAP cells. CCK-8, Transwell, annexin V-FITC/PI, flow cytometry and Western blot assays were performed to measure cell proliferation, invasion, apoptosis, cell cycle and E-cadherin and Vimentin proteins, respectively. Total RNA from B-CPAP cells was pulled down with PIWIL1, PIWIL2, or PIWIL3 specific antibodies or IgG as a control, respectively, followed by detection of piR-13643 expression with RT-qPCR. Immunoblotting of PRMT1 was detected in piR-13643 / PIWIL1 complex immune-precipitates by Co-IP assay. Subsequently, PRMT1 protein expression was detected by stably transfection of Flag tagged GLI1 (Flag-GLI1) into B-CPAP cells. Methylation assay with PRMT1 and wild-type or R597 lysine (R597K)-mutant GLI1. Then rescue experiments were applied to explore effects of piR-13643 and GLI1 on the malignant behavior of PTC cells. B-CPAP cells transfected with piR-13643 inhibitor were subcutaneously injected into nude mice to evaluate the effect of piR-13643 knockdown on the xenograft tumor growth of PTC. piR-13643 was elevated in PTC patient specimens and cell lines. piR-13643 overexpression facilitated cell proliferation, invasion and Vimentin level, and restrained apoptosis and E-cadherin expression, whereas piR-13643 knockdown showed the opposite results. Mechanically, piR-13643 could bind to PIWIL1 to form the PIWIL1/piR-13643 complex, and PRMT1 enhanced GLI1 transcription by methylating GLI1 at R597. Further, PIWIL1/piR-13643 promoted PRMT1-mediated GLI1 methylation. GLI1 knockdown countered the effects of piR-13643 mimic on cell malignant behaviors. piR-13643 knockdown preeminently prevented the xenograft tumor growth of PTC in vivo. This study confirmed that piR-13643 facilitates PTC malignant behaviors in vitro and in vivo by promoting PRMT1-mediated GLI1 methylation via forming a complex with PIWIL1, which may provide a novel insight for PTC treatment.

Myc-Associated Zinc Finger Protein Promotes Metastasis of Papillary Thyroid Cancer.

Myc-associated zinc finger protein (MAZ) plays a role in cancer progression and metastasis. However, the role and underlying molecular mechanism of MAZ in thyroid cancer have not yet been fully elucidated. This study aimed to explore the clinical significance of MAZ in thyroid cancer tissues, and clarify its mechanism in the occurrence and development of thyroid cancer. The expression level of MAZ protein in thyroid cancer tissues was detected by bioinformatics analysis and immunohistochemistry (IHC). The relationship between the expression level of MAZ and clinicopathological characteristics of thyroid cancer patients was analyzed by multivariate logistic regression analysis. Quantitative reverse-transcription polymerase chain reaction (RT-qPCR) was used to detect the mRNA expression level of MAZ in thyroid cancer cell lines. After MAZ knockdown cell lines were constructed, wound healing and Transwell assays were used to detect the migratory and invasive abilities of cancer cells. The results of IHC showed that the expression level of MAZ protein in thyroid cancer tissues was higher than that in normal adjacent thyroid tissues (p < 0.05), which was consistent with the high expression level of MAZ in thyroid cancer tissues found in The Cancer Genome Atlas (TCGA) database. The results of multivariate logistic regression analysis indicated that the expression level of MAZ was correlated with tumor diameter and tumor capsule of thyroid cancer patients. Moreover, patients with the high MAZ expression level had shorter overall and disease-free survival compared with thyroid cancer patients with the low MAZ expression level (p < 0.05). Further cell function assays indicated that downregulation of MAZ expression level could inhibit the migration and invasion of thyroid cancer cell lines. Moreover, the expression level of epithelial-mesenchymal transition (EMT)-related factor fibronectin 1 (FN1) was obtained from the RNA-seq of MAZ knockdown in thyroid cancer cells. RT-qPCR confirmed that the expression level of FN1 was elevated in MAZ knockdown cell lines (p < 0.05). Bioinformatics analysis indicated that the expression level of FN1 was upregulated in thyroid cancer tissues and had a negative relationship with the expression level of MAZ, as evidenced by correlation analysis. A high expression level of MAZ in thyroid cancer tissues was associated with a poor prognosis of patients. MAZ could affect the progression of thyroid cancer by inducing the EMT process.

CircAGTPBP1 promotes the progression of papillary thyroid cancer through the notch pathway via the miR-34a-5p/notch1 axis

The dysregulation of circular RNAs (circRNAs) has been implicated in the development and progression of papillary thyroid cancer (PTC). In this study, we analyzed the dysregulated circRNA profile using PTC tissues and matched adjacent normal tissues by RNA-seq. We conducted invitro and invivo experiments to investigate the biological functions of circAGTPBP1 in PTC progression. We found that circAGTPBP1 was upregulated in PTC tissues and cell lines, and its expression was positively correlated with tumor size, lymph node metastasis, and clinical stage. Using RNA-seq and bioinformatic analysis, we identified miR-34a-5p and NOTCH1 as downstream targets of circAGTPBP1. Functionally, circAGTPBP1 knockdown significantly inhibited the migration, invasion, and metastasis of PTC cell lines invitro, while the miR-34a-5p inhibitor reversed these effects. Additionally, circAGTPBP1 knockdown inhibited tumor growth invivo. Our findings suggest that circAGTPBP1 may act as a tumor promoter and could be a potential therapeutic target for PTC.

MEX3A induces the development of thyroid cancer via targeting CREB1.

Thyroid cancer is a prevalent form of endocrine cancer, and its global incidence has been steadily increasing. MEX3A is a protein that is known to be highly expressed in various human malignant tumors, including thyroid cancer, and it has been linked to patient prognosis. However, the molecular mechanisms underlying MEX3A's tumorigenic capabilities in thyroid cancer are not fully understood. In this study, we aimed to investigate the role of MEX3A in thyroid cancer. We confirmed that MEX3A was overexpressed in both thyroid cancer tissues and cell lines. Additionally, we found a positive correlation between high levels of MEX3A and the AJCC stage. To further understand the functional significance of MEX3A in thyroid cancer, we depleted MEX3A expression in B-CPAP and TPC-1 cells. Interestingly, we observed a significant reduction in thyroid cancer cell proliferation and migration, as well as ameliorated cell apoptosis and arrested tumor growth upon MEX3A depletion. These findings strongly suggested that MEX3A played a critical role in the development of thyroid cancer. Furthermore, our study uncovered an important interaction between MEX3A and CREB1 (cAMP response element-binding protein 1). The interaction between MEX3A and CREB1 appeared to contribute to the tumor-promoting effects of MEX3A in thyroid cancer by directly targeting CREB1. Silencing CREB1 was observed to alleviate the malignant phenotypes promoted by MEX3A in thyroid cancer cells. Together, this study highlighted the importance of the MEX3A-CREB1 interaction in thyroid cancer development and suggested the therapeutic potential of targeting MEX3A for the treatment of this disease.

ПРОГНОЗ РАДИАЦИОННЫХ РИСКОВ РАКА ЩИТОВИДНОЙ ЖЕЛЕЗЫ СРЕДИ НАСЕЛЕНИЯ РАЙОНОВ БРЯНСКОЙ ОБЛАСТИ, ЗАГРЯЗНЕННЫХ ВСЛЕДСТВИЕ АВАРИИ НА ЧЕРНОБЫЛЬСКОЙ АЭС, С УЧЕТОМ НЕОПРЕДЕЛЕННОСТЕЙ ОЦЕНОК МОДЕЛЕЙ РИСКА

Purpose: Forecasting the lifetime attributable radiation risk of incidence with malignant neoplasm (MN) of the thyroid gland and identifying groups of increased radiation risk (HR) for the population of the Bryansk region currently (at the beginning of 2023) living in six areas most contaminated with radionuclides after the accident at Chernobyl NPP, based on a conservative approach, taking into account dose uncertainty factors and parameters of mathematical risk models. Material and methods: The mathematical model of the radiation risk of thyroid cancer is the model recommended by the International Commission on Radiological Protection (ICRP). The uncertainty assessment of radiation risks was carried out by simulation modeling, i.e. by multiple calculation of random realizations of the risk using the normal or log-normal distribution of all parameters involved in the calculation of this risk. Based on a set of random realizations, 95 % confidence limits of risks were estimated. The Unified Federal Database of the National Radiation and Epidemiological Register (NRER) containing reconstructed absorbed doses in the thyroid gland in the population was used as the initial data for the calculation. Results: At the beginning of 2023, the group of 37–40-year-old women is characterized by the maximum radiation risks of thyroid cancer. According to conservative estimates (according to the upper 95 % confidence limits of radiation risk assessments), up to 19.9 % of people from this group may experience the development of radiation-induced thyroid cancer in the future, and for 37-year-old women this proportion can be up to 30.0 %. The greatest risk is predicted for people living in the Krasnogorsk district of the Bryansk region. Radiation-induced thyroid cancer can develop in 40.1 % of individuals from this group. Radiation risks of thyroid cancer in men are up to 10 times lower than in women. For 74.5 % of the population of the entire studied cohort, it is predicted that the maximum individual risk of 5.0×10-5, established by NRB-99/2009 for the population under normal operation of ionizing radiation sources, will be exceeded. Conclusions: At present (since 2023 and for life), the population of the most polluted districts of the Bryansk region continues to be at a high risk of developing radiation-induced thyroid cancers. Women at the age of 0–3 years at the time of exposure (in 1986) should be allocated to the maximum risk group. The results of this work can be used in the preparation of recommendations by health authorities to improve medical monitoring of exposed citizens.

Mining Prognostic Biomarkers of Thyroid Cancer Patients Based on the Immune-Related Genes and Development of a Reliable Prognostic Risk Model.

Tumor immunity serves an essential role in the occurrence and development of thyroid cancer (THCA). The aim of this study is to establish an immune-related prognostic model for THCA patients by using immune-related genes (IRGs). Wilcox test was used to screen the differentially expressed immune-related genes (DEIRGs) in THCA and normal tissues, then the DEIRGs related to prognosis were identified using univariate Cox regression analysis. According to The Cancer Genome Atlas (TCGA) cohort, we developed a least absolute shrinkage and selection operator (LASSO) regression prognostic model and performed validation analyses regard to the predictive value of the model in internal (TCGA) and external (International Cancer Genome Consortium) cohorts respectively. Finally, we analyzed the correlation among the prognostic model, clinical variables, and immune cell infiltration. Eighty-two of 2,498 IRGs were differentially expressed between THCA and normal tissues, and 18 of them were related to prognosis. LASSO Cox regression analysis identified seven DEIRGs with the greatest prognostic value to construct the prognostic model. The risk model showed high predictive value for the survival of THCA in two independent cohorts. The risk score according to the risk model was positively associated with poor survival and the infiltration levels of immune cells, it can evaluate the prognosis of THCA patients independent of any other clinicopathologic feature. The prognostic value and genetic alternations of seven risk genes were evaluated separately. Our study established and verified a dependable prognostic model associated with immune for THCA, both the identified IRGs and immune-related risk model were clinically significant, which is conducive to promoting individualized immunotherapy against THCA.

FDX1 inhibits thyroid cancer malignant progression by inducing cuprotosis

Cuprotosis is a recently identified cell death form that caused by intracellular copper accumulation and regulated by FDX1. This work aimed to explore the role of cuprotosis and the pivotal regulatory gene FDX1 in thyroid cancer development. We observed that expression of FDX1 in tumor section was notably lower than that in non-tumor sections in clinical samples. Induction of cuprotosis by elesclomol (ES) significantly repressed the in vitro and in vivo growth of thyroid cancer cells, simultaneously elevated Cu level and expression of FDX1, whereas depletion of FDX1 abolished these effects. Knockdown of FDX1 decreased the lipoylation level of DLAT and DLST in thyroid cancer cells, alleviated cuprotosis-induced cell death, simultaneously upregulated the levels of PA and α-KG. These findings demonstrated that FDX1 promotes the cuprotosis of thyroid cancer cells via regulating the lipoylation of DLAT.

Confounding factors and biases involved in regional differences in the detection rate of thyroid cancer in the second-round Thyroid Ultrasound Examination: the Fukushima Health Management Survey.

In response to concerns about health due to radiation exposure, the Fukushima Prefecture launched the Thyroid Ultrasound Examination program for residents aged 0-18years at the time of the earthquake. Herein, we considered the confounding factors involved in the regional differences in the development of thyroid cancer. In this study, the 242 065 individuals who participated in both first- and second-round surveys were classified into four groups by address according to their air radiation dose. The number of participants diagnosed as malignant or suspicious for malignancy by cytological examination were 17, 38, 10 and 4 with detection rates of 53.8, 27.8, 21.7 and 14.5 per 100 000 participants in Regions 1, 2, 3 and 4, respectively. Sex (P = 0.0400), age at the time of the primary examination (P < 0.0001) and interval between the first- and second-round surveys (P < 0.0001) were significantly different among the four regions, and these were suspected to be confounding factors affecting regional differences in malignant nodule detection rates. In addition, significant regional differences were observed in the participation rate in the confirmatory examination (P = 0.0037) and the fine needle aspiration cytology implementation rate (P = 0.0037), which could be potential biases. No significant regional differences in the detection of malignant nodules were found in the multivariate logistic regression analysis after adjusting for the survey interval alone or for sex, age and survey interval. The confounding factors and biases identified in this study that may have important impacts on thyroid cancer detection rate should be fully considered in future studies.

Exploring the oral-gut microbiota during thyroid cancer: Factors affecting the thyroid functions and cancer development.

Thyroid cancer (TC) is categorized into papillary, follicular, medullary, and anaplastic. The TC is increasing in several countries, including China, the United States, the United Kingdom, Canada, France, Australia, Germany, Japan, Spain, and Italy. Thus, this review comprehensively covers the factors that affect thyroid gland function, TC types, risk factors, and symptoms. Lifestyle factors (such as nutrient consumption and smoking) and pollutants (such as chemicals and heavy metals) increased the thyroid-stimulating hormone (TSH) levels which are directly related to TC prevalence. The conventional and recent TC treatments are also highlighted. The role of the oral and gut microbiota as well as the application of probiotics on TC are also discussed. The variations in the composition of oral and gut microbes influence the thyroid function indirectly through alteration in metabolites (such as short-chain fatty acids) that are eminent for cellular energy metabolism. Maintenance of healthy gut and oral microbiota can help in regulating thyroid function by regulating iodine uptake. Oral or gut microbial dysbiosis can be considered as an early diagnosis factor or TC marker. High TSH during TC can increase the oral microbial diversity while disrupting the high ratio of Firmicutes and Bacteroidetes in the gut. Supplementation of probiotics as an adjuvant in TC treatment is beneficial. However, needs more extensive research to explore the direct effect of probiotics on thyroid function.

Jagged 1 Regulates The Proliferation and Metastasis of Human MDA-T68 Thyroid Cancer Cells.

The current study evaluated the expression profile and explored the therapeutic implications of Jagged 1 in human thyroid cancer. This experimental study was conducted in 60 paired specimens of papillary thyroid and adjacent normal tissues. Gene expression was determined by quantitative real time polymerase chain reaction (qRT-PCR) and western blotting. Transfection of cancer cells was performed by using Lipofectamine 2000. The cell proliferation of PTC cells was estimated by MTT assay. Clonogenic assay was performed for analysis of colony forming potential of cancer cells. The apoptosis of PTC cells was studied by using AO/EB and Annexin V-FITC/PI staining methods. Flow cytometry was done to analyze the cell cycle phase distribution of cancer cells. Migration and invasion PTC cells were determined respectively with the wound-healing and transwell assays. The impact of Jagged 1 silencing was investigated in vivo in a xenografted mice model followed by Immunohistochemistry (IHC) analysis. We found significant (P<0.05) upregulation of Jagged 1 in human thyroid cancer. Silencing of Jagged 1 caused significant (P<0.05) reduction in proliferation and colony formation of MDA-T68 cells. The inhibitory effects of Jagged 1 silencing were found to be due to the induction of apoptosis. We also found enhancement of Bax and repression of Bcl-2 protein levels in MDA-T68 cells. Wound healing assay indicated significant (P<0.05) inhibition of cell migration of MDA-T68 thyroid cancer cells. Additionally, we found that invasion of the thyroid cancer cells was reduced by 55% upon silencing of Jagged 1. Moreover, Jagged 1 silencing was found to cause inhibition of the Notch intracellular domain (NICD) and Notch target gene, Hes-1 expression. Finally, Jagged 1 silencing inhibited the xenografted tumors in vivo. The findings suggest that Jagged 1 regulates the development of thyroid cancer that may act as a therapeutic target for managing thyroid cancer.

Women consuming oral contraceptives containing cyproterone acetate and ethinylestradiol show a higher risk of thyroid cancer than nonusers.

This study explored whether the risk of thyroid cancer in Asian women is associated with consumption of oral contraceptives (Diane-35). We conducted a population-based, retrospective cohort study using the Taiwan National Health Insurance Research Database. From the database, 9865 women aged 18 to 65 years who were prescribed Diane-35 between 2000 and 2012 were included in the Diane-35 group, and 39,460 women who were not prescribed Diane-35 were included in the comparison group and were frequency-matched by age and index year. Both groups were followed until 2013 to calculate the incidence of thyroid cancer. Hazard ratios (HR) and 95% confidence intervals (CI) were estimated using Cox proportional hazard model. The median (standard deviation) follow-up duration was 7.08 (3.63) and 7.04 (3.64) years in the Diane-35 and the comparison group, respectively. The incidence of thyroid cancer was 1.80-fold higher in the Diane-35 group than in the comparison group (2.72 vs 1.51 per 10,000 person-years). The cumulative incidence of thyroid cancer was significantly higher in the Diane-35 group than in the comparison group (log-rank test, P = .03). An elevated hazard ratio of thyroid cancer was observed in the Diane-35 group than in the comparison group (HR: 1.91, 95% CI: 1.10-3.30). In subgroup analysis, patients aged 30 to 39 years showed a higher hazard ratio of developing thyroid cancer after consuming Diane-35 than those in the comparison group (HR: 5.58, 95% CI: 1.84-16.91). The study provides evidence that women aged 30 to 39 years consuming Diane-35 are at increased risk of thyroid cancer. Nevertheless, a larger population with a longer follow-up may be necessary to confirm causality.

Risk and Prognosis of Thyroid Cancer in Patients with Graves’ Disease: An Umbrella Review

Graves’ disease (GD) is an autoimmune disease considered the most common cause of hyperthyroidism. Some studies have investigated its relationship with the risk and prognosis of developing thyroid cancer. Considering that there is no consensus on the relationship between GD and thyroid cancer risk, this umbrella review aimed to summarize the epidemiologic evidence and evaluate its strength and validity on the associations of GD with thyroid cancer risk and its prognosis. This umbrella review was performed using the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) guidelines. We systematically searched PubMed and Scopus from January 2012 to December 2022. The strength of the epidemiological evidence was graded as high, moderate, or weak by the Measurement Tool to Assess Systematic Reviews (AMSTAR-2). “Strong” evidence was found for the risk of thyroid cancer in GD patients with thyroid nodular disease (OR: 5.30; 95% CI 2.43–12) and for the risk of mortality from thyroid cancer in these patients (OR 2.93, 95% CI 1.17–7.37, p = 0.02), particularly in Europe (OR 4.89; 95% CI 1.52–16). The results of this umbrella review should be interpreted with caution; as the evidence comes mostly from retrospective studies, potential concerns are selection and recall bias, and whether the empirically observed association reflects a causal relationship remains an open question.

Retraction: The role of LINC00284 in the development of thyroid cancer via its regulation of the microRNA-30d-5p-mediated ADAM12/Notch axis.

[This retracts the article DOI: 10.3389/fonc.2021.643039.].

Frequency and Type of Thyroid Carcinoma in Patients With Multinodular Goiter.

Background This study aimed to investigate the incidence and subtype of thyroid cancer in multinodular goitre (MNG) patients who underwent total thyroidectomy. Methodology A cross-sectional study was conducted at the Khyber Teaching Hospital, screening 207 MNG patients who received complete thyroidectomies between July and December 2022. The senior consultant diagnosed thyroid cancer based on a complete history, physical examination, and laboratory and radiological studies. Ultrasound-guided fine-needle aspiration cytology was performed by a senior consultant radiologist. Bethesda categories for all lesions were recorded. All patients underwent thyroidectomy, and the diagnosis of thyroid cancer was confirmed on histopathology. Results A total of 207 patients were included in the study, with a mean age of 45.55 ± 8.75 years. Out of 207 patients, 24 (11.59%) were diagnosed with thyroid cancer.Out of 62 male patients, 15 (7.25%) had thyroid cancer. Out of 145 female patients, only nine had cancer (p < 0.001). Nine patients with thyroid cancer had a body mass index (BMI) below 18, compared to only five patients with a BMI of more than 30 kg/m2.The difference in age distribution was not significant in our study (p = 0.102). Conclusion In conclusion, our study sheds light on the frequency and potential risk factors associated with thyroid cancer in patients with multinodular goiter. Our findings reveal that papillary thyroid carcinoma is the most commonly observed form of thyroid cancer in this patient population, with around 12 percent of patients diagnosed with thyroid cancer. Notably, our study highlights that male patients and those with a lower BMI may have a greater risk of developing thyroid cancer in the context of multinodular goiter.The findings of this study have important implications for the care and follow-up of MNG patients who receive total thyroidectomy. Further research is needed to investigate the type and prognosis of thyroid cancer in patients with MNG.