Chromosomal aberrations in thyroid follicular-cell neoplasia: in the search of novel oncogenes and tumour suppressor genes

Zitzelsberger, Horst; Thomas, Gerry; Unger, Kristian

doi:10.1016/j.mce.2009.11.014

Cited by 9 publications

(5 citation statements)

References 92 publications

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“…These studies suggest an increased abundance of Alloprevotella is associated with certain cancers. Additionally, recent studies indicate a strong relationship between the genera Alloprevotella and chromosomal aberrations, which have been shown to be related to the pathogenesis of anaplastic thyroid cancer and impact cancer incidence ( Zitzelsberger et al., 2010 ; Saini et al., 2019 ; Druzhinin et al., 2020 ; Farkas et al., 2021 ). Based on these findings, we conclude that the increased abundance of Alloprevotella in the saliva is associated with thyroid cancer.…”

Section: Discussionmentioning

confidence: 99%

Saliva microbiome changes in thyroid cancer and thyroid nodules patients

Jiao

Zheng

Xia

et al. 2022

Front. Cell. Infect. Microbiol.

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ObjectiveThyroid disease has been reported to associate with gut microbiota, but the effects of thyroid cancer and thyroid nodules on the oral microbiota are still largely unknown. This study aimed to identify the variation in salivary microbiota and their potential association with thyroid cancer and thyroid nodules.MethodsWe used 16S rRNA high-throughput sequencing to examine the salivary microbiota of thyroid cancer patients (n = 14), thyroid nodules patients (n = 9), and healthy controls (n = 15).ResultsThe alpha-diversity indices Chao1 and ACE were found to be relatively higher in patients with thyroid cancer and thyroid nodules compared to healthy controls. The beta diversity in both the thyroid cancer and thyroid nodules groups was divergent from the healthy control group. The genera Alloprevotella, Anaeroglobus, Acinetobacter, unclassified Bacteroidales, and unclassified Cyanobacteriales were significantly enriched in the thyroid cancer group compared with the healthy control group. In contrast, the microbiome of the healthy controls was mainly composed of the genera Haemophilus, Lautropia, Allorhizobium Neorhizobium Pararhizobium Rhizobium, Escherichia Shigella, and unclassified Rhodobacteraceae. The thyroid nodules group was dominated by genre uncultured Candidatus Saccharibacteria bacterium, unclassified Clostridiales bacterium feline oral taxon 148, Treponema, unclassified Prevotellaceae, Mobiluncus, and Acholeplasma. In contrast, the genera unclassified Rhodobacteraceae and Aggregatibacter dominated the healthy control group. The study also found that clinical indicators were correlated with the saliva microbiome.ConclusionThe salivary microbiota variation may be connected with thyroid cancer and thyroid nodules.

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Section: Discussionmentioning

confidence: 99%

Saliva microbiome changes in thyroid cancer and thyroid nodules patients

Jiao

Zheng

Xia

et al. 2022

Front. Cell. Infect. Microbiol.

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“…[24][25][26] Multiple studies using arrayCGH (array comparative genomic hybridization) has shown that besides copy number changes, 8,27 chromosomal gains and losses as well as gene rearrangements involving the RET proto-oncogene are also present in ATC. 28 In an attempt to identify novel markers or therapeutic targets, immunohistochemistry as a tool has been used extensively to evaluate loss or overexpression of various signaling molecules.…”

Section: Genetics Of Atcmentioning

confidence: 99%

Anaplastic thyroid cancer – an overview of genetic variations and treatment modalities

Reddi¹,

Kumar²,

Kulstad³

2015

AGG

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Anaplastic thyroid carcinoma (ATC) is a rare but highly aggressive malignancy that accounts for about 1%-2% of all thyroid cancer diagnoses but is responsible for up to 30%-40% of thyroid cancer deaths. ATCs are poorly differentiated tumors that develop on the background of preexisting, often undiagnosed, papillary thyroid carcinoma or follicular thyroid carcinoma, through progressive accumulation of changes in several oncogenic and tumor suppressor pathways, including p53, RAS, RAF, Wnt-β-catenin and the PTEN-AKT pathways. Consequently, the 1-year survival rate after diagnosis ranges from 5% to 15%. Current therapeutic approaches are aimed at common late oncogenic changes and involve inhibition of MAPK and PI3K cell proliferation pathways or restoration of p53 and PTEN tumor suppressor pathways. Since singlemodality therapy has limited effect on anaplastic thyroid cancer, aggressive multimodal treatments are now the treatment of choice, in spite of which, the mean survival time from diagnosis to death continues to remain at about 6 months. The current review attempts to summarize the genetics involved in the development and progression of ATC and provides some insight into the therapeutic options being evaluated for this aggressive cancer.

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“…CGH array has been extensively used for the identification of genomic imbalances present in cancer [13]. Several data come from studies on thyroid tumors [14][15][16]. In most of them, however, the reference genome used in the CGH array was not that of the same patient.…”

Section: Introductionmentioning

confidence: 99%

Somatic amplifications and deletions in genome of papillary thyroid carcinomas

Passon¹,

Bregant²,

Sponziello

et al. 2015

Endocrine

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Somatic gene copy number variation contributes to tumor progression. Using comparative genomic hybridization (CGH) array, the presence of genomic imbalances was evaluated in a series of 27 papillary thyroid carcinomas (PTCs). To detect only somatic imbalances, for each sample, the reference DNA was from normal thyroid tissue of the same patient. The presence of the BRAF V600E mutation was also evaluated. Both amplifications and deletions showed an uneven distribution along the entire PTC cohort; amplifications were more frequent than deletions (mean values of 17.5 and 7.2, respectively). Number of aberration events was not even among samples, the majority of them occurring only in a small fraction of PTCs. Most frequent amplifications were detected at regions 2q35, 4q26, and 4q34.1, containing FN1, PDE5A, and GALNTL6 genes, respectively. Most frequent deletions occurred at regions 6q25.2, containing OPMR1 and IPCEF1 genes and 7q14.2, containing AOAH and ELMO1 genes. Amplification of FN1 and PDE5A genomic regions was confirmed by quantitative PCR. Frequency of amplifications and deletions was in relationship with clinical features and BRAF mutation status of tumor. In fact, according to the American Joint Committee on Cancer stage and American Thyroid Association (ATA) risk classification, amplifications are more frequent in higher risk samples, while deletions tend to prevail in the lower risk tumors. Analysis of single aberrations according to the ATA risk grouping shows that amplifications containing PDE5A, GALNTL6, DHRS3, and DOCK9 genes are significantly more frequent in the intermediate/high risk group than in the low risk group. Thus, our data would indicate that analysis of somatic genome aberrations by CGH array can be useful to identify additional prognostic variables.

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Chromosomal aberrations in thyroid follicular-cell neoplasia: in the search of novel oncogenes and tumour suppressor genes

Cited by 9 publications

References 92 publications

Saliva microbiome changes in thyroid cancer and thyroid nodules patients

Saliva microbiome changes in thyroid cancer and thyroid nodules patients

Anaplastic thyroid cancer – an overview of genetic variations and treatment modalities

Somatic amplifications and deletions in genome of papillary thyroid carcinomas

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Chromosomal aberrations in thyroid follicular-cell neoplasia: in the search of novel oncogenes and tumour suppressor genes

Cited by 9 publications

References 92 publications

Saliva microbiome changes in thyroid cancer and thyroid nodules patients

Saliva microbiome changes in thyroid cancer and thyroid nodules patients

Anaplastic thyroid cancer &ndash; an overview of genetic variations and treatment modalities

Somatic amplifications and deletions in genome of papillary thyroid carcinomas

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Product

Resources

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Anaplastic thyroid cancer – an overview of genetic variations and treatment modalities