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10th Anniversary of Cells—Advances in Cellular Pathology
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10th Anniversary of Cells—Advances in Cellular Pathology

A special issue of Cells (ISSN 2073-4409). This special issue belongs to the section "Cellular Pathology".

Deadline for manuscript submissions: closed (31 December 2021) | Viewed by 38329

Special Issue Editor

Prof. Dr. Dimitrios Karamichos

E-Mail Website
Guest Editor
North Texas Eye Research Institute (NTERI), University of North Texas Health Science Center, Fort Worth, TX 76107, USA
Interests: corneal wound healing; cornea trauma; keratoconus; bioengineering; bioprinting; diabetic keratopathy
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

The year 2021 marks the 10th anniversary of the publication of Cells. We are delighted and proud to celebrate this important event with a series of Special Issues and events. To date, the journal has published more than 4000 papers, and the journal website attracts more than 50,000 monthly page views. We would like to express our sincerest thanks to our readers, innumerable authors, anonymous peer reviewers, editors, and all the people working in some way for the journal who have made substantial contributions for years. Without your support, we would never have made it this far.

To mark this significant milestone, a Special Issue entitled “10th Anniversary of Cells—Advances in Cellular Pathology” is being launched. This Special Issue will collect research articles and high-quality review papers in the Cellular Pathology research fields. We kindly encourage all research groups working in Cellular Pathology areas to make contributions to this Special Issue.

For the details of the Cells 2021 Best Paper Awards for Anniversary Special Issues please click here.

Prof. Dr. Dimitrios Karamichos
Guest Editor

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Cells is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2700 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Published Papers (11 papers)

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Editorial

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3 pages, 179 KiB  
Editorial
Latest in Cellular Pathology Research
by Dimitrios Karamichos
Cells 2022, 11(24), 4037; https://0-doi-org.brum.beds.ac.uk/10.3390/cells11244037 - 14 Dec 2022
Viewed by 978
Abstract
The year 2021 marked the 10th anniversary of the publication of Cells [...] Full article
(This article belongs to the Special Issue 10th Anniversary of Cells—Advances in Cellular Pathology)

Research

Jump to: Editorial, Review

17 pages, 3596 KiB  
Article
Rhenium Perrhenate (188ReO4) Induced Apoptosis and Reduced Cancerous Phenotype in Liver Cancer Cells
by Samieh Asadian, Abbas Piryaei, Nematollah Gheibi, Bagher Aziz Kalantari, Mohamad Reza Davarpanah, Mehdi Azad, Valentina Kapustina, Mehdi Alikhani, Sahar Moghbeli Nejad, Hani Keshavarz Alikhani, Morteza Mohamadi, Anastasia Shpichka, Peter Timashev, Moustapha Hassan and Massoud Vosough
Cells 2022, 11(2), 305; https://0-doi-org.brum.beds.ac.uk/10.3390/cells11020305 - 17 Jan 2022
Cited by 16 | Viewed by 2690
Abstract
Recurrence in hepatocellular carcinoma (HCC) after conventional treatments is a crucial challenge. Despite the promising progress in advanced targeted therapies, HCC is the fourth leading cause of cancer death worldwide. Radionuclide therapy can potentially be a practical targeted approach to address this concern. [...] Read more.
Recurrence in hepatocellular carcinoma (HCC) after conventional treatments is a crucial challenge. Despite the promising progress in advanced targeted therapies, HCC is the fourth leading cause of cancer death worldwide. Radionuclide therapy can potentially be a practical targeted approach to address this concern. Rhenium-188 (188Re) is a β-emitting radionuclide used in the clinic to induce apoptosis and inhibit cell proliferation. Although adherent cell cultures are efficient and reliable, appropriate cell-cell and cell-extracellular matrix (ECM) contact is still lacking. Thus, we herein aimed to assess 188Re as a potential therapeutic component for HCC in 2D and 3D models. The death rate in treated Huh7 and HepG2 lines was significantly higher than in untreated control groups using viability assay. After treatment with 188ReO4, Annexin/PI data indicated considerable apoptosis induction in HepG2 cells after 48 h but not Huh7 cells. Quantitative RT-PCR and western blotting data also showed increased apoptosis in response to 188ReO4 treatment. In Huh7 cells, exposure to an effective dose of 188ReO4 led to cell cycle arrest in the G2 phase. Moreover, colony formation assay confirmed post-exposure growth suppression in Huh7 and HepG2 cells. Then, the immunostaining displayed proliferation inhibition in the 188ReO4-treated cells on 3D scaffolds of liver ECM. The PI3-AKT signaling pathway was activated in 3D culture but not in 2D culture. In nude mice, Huh7 cells treated with an effective dose of 188ReO4 lost their tumor formation ability compared to the control group. These findings suggest that 188ReO4 can be a potential new therapeutic agent against HCC through induction of apoptosis and cell cycle arrest and inhibition of tumor formation. This approach can be effectively combined with antibodies and peptides for more selective and personalized therapy. Full article
(This article belongs to the Special Issue 10th Anniversary of Cells—Advances in Cellular Pathology)
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13 pages, 10974 KiB  
Article
NOX4 Signaling Mediates Cancer Development and Therapeutic Resistance through HER3 in Ovarian Cancer Cells
by Wen-Jing Liu, Ying-Xue Huang, Wei Wang, Ye Zhang, Bing-Jie Liu, Jian-Ge Qiu, Bing-Hua Jiang and Ling-Zhi Liu
Cells 2021, 10(7), 1647; https://0-doi-org.brum.beds.ac.uk/10.3390/cells10071647 - 30 Jun 2021
Cited by 18 | Viewed by 2699
Abstract
Development of resistance to therapy in ovarian cancer is a major hinderance for therapeutic efficacy; however, new mechanisms of the resistance remain to be elucidated. NADPH oxidase 4 (NOX4) is responsible for higher NADPH activity to increase reactive oxygen species (ROS) production. In [...] Read more.
Development of resistance to therapy in ovarian cancer is a major hinderance for therapeutic efficacy; however, new mechanisms of the resistance remain to be elucidated. NADPH oxidase 4 (NOX4) is responsible for higher NADPH activity to increase reactive oxygen species (ROS) production. In this study, we showed that higher levels of NOX4 were detected in a large portion of human ovarian cancer samples. To understand the molecular mechanism of the NOX4 upregulation, we showed that NOX4 expression was induced by HIF-1α and growth factor such as IGF-1. Furthermore, our results indicated that NOX4 played a pivotal role in chemotherapy and radiotherapy resistance in ovarian cancer cells. We also demonstrated that NOX4 knockdown increased sensitivity of targeted therapy and radiotherapy through decreased expression of HER3 (ERBB3) and NF-κB p65. Taken together, we identified a new HIF-1α/NOX4 signal pathway which induced drug and radiation resistance in ovarian cancer. The finding may provide a new option to overcome the therapeutic resistance of ovarian cancer in the future. Full article
(This article belongs to the Special Issue 10th Anniversary of Cells—Advances in Cellular Pathology)
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14 pages, 4146 KiB  
Article
Extracellularly Released Calreticulin Induced by Endoplasmic Reticulum Stress Impairs Syncytialization of Cytotrophoblast Model BeWo Cells
by Naoyuki Iwahashi, Midori Ikezaki, Kazuchika Nishitsuji, Madoka Yamamoto, Ibu Matsuzaki, Naoki Kato, Naoyuki Takaoka, Mana Taniguchi, Shin-ichi Murata, Kazuhiko Ino and Yoshito Ihara
Cells 2021, 10(6), 1305; https://0-doi-org.brum.beds.ac.uk/10.3390/cells10061305 - 24 May 2021
Cited by 13 | Viewed by 2437
Abstract
The pregnancy-specific syndrome preeclampsia is a major cause of maternal mortality throughout the world. The initial insult resulting in the development of preeclampsia is inadequate trophoblast invasion, which may lead to reduced maternal perfusion of the placenta and placental dysfunction, such as insufficient [...] Read more.
The pregnancy-specific syndrome preeclampsia is a major cause of maternal mortality throughout the world. The initial insult resulting in the development of preeclampsia is inadequate trophoblast invasion, which may lead to reduced maternal perfusion of the placenta and placental dysfunction, such as insufficient trophoblast syncytialization. Endoplasmic reticulum (ER) stress has been implicated in the pathology of preeclampsia and serves as the major risk factor. Our previous studies suggested critical roles of calreticulin (CRT), which is an ER-resident stress response protein, in extravillous trophoblast invasion and cytotrophoblast syncytialization. Here, we studied the mechanism by which ER stress exposes the placenta to the risk of preeclampsia. We found that CRT was upregulated in the serum samples, but not in the placental specimens, from preeclamptic women. By using BeWo cells, an established model of cytotrophoblasts that syncytialize in the presence of forskolin, we demonstrated that thapsigargin-induced ER stress caused extracellular release of CRT from BeWo cells and that the extracellular CRT suppressed forskolin-induced release of β-human chorionic gonadotropin and altered subcellular localization of E-cadherin, which is a key adhesion molecule associated with syncytialization. Our results together provide evidence that induction of ER stress leads to extracellular CRT release, which may contribute to placental dysfunction by suppressing cytotrophoblast syncytialization. Full article
(This article belongs to the Special Issue 10th Anniversary of Cells—Advances in Cellular Pathology)
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12 pages, 2708 KiB  
Article
Extracellular Vesicle Surface Signatures in IPF Patients: A Multiplex Bead-Based Flow Cytometry Approach
by Miriana d’Alessandro, Piera Soccio, Laura Bergantini, Paolo Cameli, Giulia Scioscia, Maria Pia Foschino Barbaro, Donato Lacedonia and Elena Bargagli
Cells 2021, 10(5), 1045; https://0-doi-org.brum.beds.ac.uk/10.3390/cells10051045 - 28 Apr 2021
Cited by 16 | Viewed by 3280
Abstract
Background: Extracellular vesicles (EVs) are secreted by cells from their membrane within circulation and body fluids. Knowledge of the involvement of EVs in pathogenesis of lung diseases is increasing. The present study aimed to evaluate the expression of exosomal surface epitopes in a [...] Read more.
Background: Extracellular vesicles (EVs) are secreted by cells from their membrane within circulation and body fluids. Knowledge of the involvement of EVs in pathogenesis of lung diseases is increasing. The present study aimed to evaluate the expression of exosomal surface epitopes in a cohort of idiopathic pulmonary fibrosis (IPF) patients followed in two Italian Referral Centres for Interstitial Lung Diseases, comparing them with a group of healthy volunteers. Materials and Methods: Ninety IPF patients (median age and interquartile range (IQR) 71 (66–75) years; 69 males) were selected retrospectively. Blood samples were obtained from patients before starting antifibrotic therapy. A MACSPlex Exosome Kit, human, (Miltenyi Biotec, Bergisch-Gladbach, Germany), to detect 37 exosomal surface epitopes, was used. Results: CD19, CD69, CD8, and CD86 were significantly higher in IPF patients than in controls (p = 0.0023, p = 0.0471, p = 0.0082, and p = 0.0143, respectively). CD42a was lower in IPF subjects than in controls (p = 0.0153), while CD209, Cd133/1, MCSP, and ROR1 were higher in IPF patients than in controls (p = 0.0007, p = 0.0050, p = 0.0139, and p = 0.0335, respectively). Kaplan-Meier survival analysis for IPF patients: for median values and a cut-off of 0.48 for CD25, the two subgroups showed a significant difference in survival rate (p = 0.0243, hazard ratio: 0.52 (95%CI 0.29–0.92); the same was true for CD8 (cut-off 1.53, p = 0.0309, hazard ratio: 1.39 (95%CI 0.75–2.53). Conclusion: Our multicenter study showed for the first time the expression of surface epitopes on EVs from IPF patients, providing interesting data on the communication signatures/exosomal profile in serum from IPF patients and new insights into the pathogenesis of the disease and a promising reliability in predicting mid-term survival of IPF patients. Full article
(This article belongs to the Special Issue 10th Anniversary of Cells—Advances in Cellular Pathology)
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17 pages, 5243 KiB  
Article
Protective Effects of Necrostatin-1 in Acute Pancreatitis: Partial Involvement of Receptor Interacting Protein Kinase 1
by Yulin Ouyang, Li Wen, Jane A. Armstrong, Michael Chvanov, Diane Latawiec, Wenhao Cai, Mohammad Awais, Rajarshi Mukherjee, Wei Huang, Peter J. Gough, John Bertin, Alexei V. Tepikin, Robert Sutton and David N. Criddle
Cells 2021, 10(5), 1035; https://doi.org/10.3390/cells10051035 - 27 Apr 2021
Cited by 10 | Viewed by 2912
Abstract
Acute pancreatitis (AP) is a severe and potentially fatal disease caused predominantly by alcohol excess and gallstones, which lacks a specific therapy. The role of Receptor-Interacting Protein Kinase 1 (RIPK1), a key component of programmed necrosis (Necroptosis), is unclear in AP. We assessed [...] Read more.
Acute pancreatitis (AP) is a severe and potentially fatal disease caused predominantly by alcohol excess and gallstones, which lacks a specific therapy. The role of Receptor-Interacting Protein Kinase 1 (RIPK1), a key component of programmed necrosis (Necroptosis), is unclear in AP. We assessed the effects of RIPK1 inhibitor Necrostatin-1 (Nec-1) and RIPK1 modification (RIPK1K45A: kinase dead) in bile acid (TLCS-AP), alcoholic (FAEE-AP) and caerulein hyperstimulation (CER-AP) mouse models. Involvement of collateral Nec-1 target indoleamine 2,3-dioxygenase (IDO) was probed with the inhibitor Epacadostat (EPA). Effects of Nec-1 and RIPK1K45A were also compared on pancreatic acinar cell (PAC) fate in vitro and underlying mechanisms explored. Nec-1 markedly ameliorated histological and biochemical changes in all models. However, these were only partially reduced or unchanged in RIPK1K45A mice. Inhibition of IDO with EPA was protective in TLCS-AP. Both Nec-1 and RIPK1K45A modification inhibited TLCS- and FAEE-induced PAC necrosis in vitro. Nec-1 did not affect TLCS-induced Ca2+ entry in PACs, however, it inhibited an associated ROS elevation. The results demonstrate protective actions of Nec-1 in multiple models. However, RIPK1-dependent necroptosis only partially contributed to beneficial effects, and actions on targets such as IDO are likely to be important. Full article
(This article belongs to the Special Issue 10th Anniversary of Cells—Advances in Cellular Pathology)
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12 pages, 3588 KiB  
Article
Transmembrane and Tetratricopeptide Repeat Containing 4 Is a Novel Diagnostic Marker for Prostate Cancer with High Specificity and Sensitivity
by Rania Makboul, Islam F. Abdelkawi, Dalia M. Badary, Mahmoud R. A. Hussein, Johng S. Rhim, Eman A. Toraih, Mourad Zerfaoui and Zakaria Y. Abd Elmageed
Cells 2021, 10(5), 1029; https://0-doi-org.brum.beds.ac.uk/10.3390/cells10051029 - 27 Apr 2021
Cited by 5 | Viewed by 1858
Abstract
The histopathologic diagnosis of prostate cancer (PCa) from biopsies is a current challenge if double or triple staining is needed. Therefore, there is an urgent need for development of a new reliable biomarker to diagnose PCa patients. We aimed to explore and compare [...] Read more.
The histopathologic diagnosis of prostate cancer (PCa) from biopsies is a current challenge if double or triple staining is needed. Therefore, there is an urgent need for development of a new reliable biomarker to diagnose PCa patients. We aimed to explore and compare the expression of TMTC4 in PCa cells and tissue specimens and evaluate its sensitivity and specificity. The expression of TMTC4 in PCa and normal prostate epithelial cells was determined by real-time PCR and Western blot analyses. Immunohistochemical (IHC) staining of TMTC4 was performed on tissues collected from PCa and benign prostatic hyperplasia (BPH). Our results show a high expression of TMTC4 on mRNA and protein levels in PCa versus BPH1 and normal cells (p < 0.05). IHC results show strong cytoplasmic expressions in PCa cases (p < 0.001) as compared to BPH cases. The overall accuracy as measured by the AUC was 1.0 (p < 0.001). The sensitivity and specificity of the protein were 100% and 96.6%, respectively. Taken together, we report a high TMTC4 expression in PCa cells and tissues and its ability to differentiate between PCa and BPH with high sensitivity and specificity. This finding can be carried over to clinical practice after its confirmation by further studies. Full article
(This article belongs to the Special Issue 10th Anniversary of Cells—Advances in Cellular Pathology)
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Review

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14 pages, 1553 KiB  
Review
Sex Hormones, Growth Hormone, and the Cornea
by Tina B. McKay, Shrestha Priyadarsini and Dimitrios Karamichos
Cells 2022, 11(2), 224; https://0-doi-org.brum.beds.ac.uk/10.3390/cells11020224 - 11 Jan 2022
Cited by 24 | Viewed by 3738
Abstract
The growth and maintenance of nearly every tissue in the body is influenced by systemic hormones during embryonic development through puberty and into adulthood. Of the ~130 different hormones expressed in the human body, steroid hormones and peptide hormones are highly abundant in [...] Read more.
The growth and maintenance of nearly every tissue in the body is influenced by systemic hormones during embryonic development through puberty and into adulthood. Of the ~130 different hormones expressed in the human body, steroid hormones and peptide hormones are highly abundant in circulation and are known to regulate anabolic processes and wound healing in a tissue-dependent manner. Of interest, differential levels of sex hormones have been associated with ocular pathologies, including dry eye disease and keratoconus. In this review, we discuss key studies that have revealed a role for androgens and estrogens in the cornea with focus on ocular surface homeostasis, wound healing, and stromal thickness. We also review studies of human growth hormone and insulin growth factor-1 in influencing ocular growth and epithelial regeneration. While it is unclear if endogenous hormones contribute to differential corneal wound healing in common animal models, the abundance of evidence suggests that systemic hormone levels, as a function of age, should be considered as an experimental variable in studies of corneal health and disease. Full article
(This article belongs to the Special Issue 10th Anniversary of Cells—Advances in Cellular Pathology)
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15 pages, 1891 KiB  
Review
Pterygium—The Good, the Bad, and the Ugly
by Sara I. Van Acker, Bert Van den Bogerd, Michel Haagdorens, Vasiliki Siozopoulou, Sorcha Ní Dhubhghaill, Isabel Pintelon and Carina Koppen
Cells 2021, 10(7), 1567; https://0-doi-org.brum.beds.ac.uk/10.3390/cells10071567 - 22 Jun 2021
Cited by 23 | Viewed by 6541
Abstract
Pterygium is a multifaceted pathology that displays apparent conflicting characteristics: benign (e.g., self-limiting and superficial), bad (e.g., proliferative and potentially recurrent) and ugly (e.g., signs of preneoplastic transformation). The natural successive question is: why are we lacking reports showing that pterygium lesions become [...] Read more.
Pterygium is a multifaceted pathology that displays apparent conflicting characteristics: benign (e.g., self-limiting and superficial), bad (e.g., proliferative and potentially recurrent) and ugly (e.g., signs of preneoplastic transformation). The natural successive question is: why are we lacking reports showing that pterygium lesions become life-threatening through metastasis, especially since pterygium has considerable similarities with UV-related malignancies on the molecular level? In this review, we consider how our pathophysiological understanding of the benign pterygium pathology overlaps with ocular surface squamous neoplasia and skin cancer. The three UV-related disorders share the same initial insult (i.e., UV radiation) and responsive repair mechanisms to the ensuing (in)direct DNA damage. Their downstream apoptotic regulators and other cellular adaptations are remarkably alike. However, a complicating factor in understanding the fine line between the self-limiting nature of pterygium and the malignant transformation in other UV-related diseases is the prominent ambiguity in the pathological evaluation of pterygium biopsies. Features of preneoplastic transformation (i.e., dysplasia) are used to define normal cellular reactions (i.e., atypia and metaplasia) and vice versa. A uniform grading system could help in unraveling the true nature of this ancient disease and potentially help in identifying the earliest intervention point possible regarding the cellular switch that drives a cell’s fate towards cancer. Full article
(This article belongs to the Special Issue 10th Anniversary of Cells—Advances in Cellular Pathology)
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Graphical abstract

42 pages, 2556 KiB  
Review
The Emerging Role of HDACs: Pathology and Therapeutic Targets in Diabetes Mellitus
by Saikat Dewanjee, Jayalakshmi Vallamkondu, Rajkumar Singh Kalra, Pratik Chakraborty, Moumita Gangopadhyay, Ranabir Sahu, Vijaykrishna Medala, Albin John, P. Hemachandra Reddy, Vincenzo De Feo and Ramesh Kandimalla
Cells 2021, 10(6), 1340; https://0-doi-org.brum.beds.ac.uk/10.3390/cells10061340 - 28 May 2021
Cited by 25 | Viewed by 5259
Abstract
Diabetes mellitus (DM) is one of the principal manifestations of metabolic syndrome and its prevalence with modern lifestyle is increasing incessantly. Chronic hyperglycemia can induce several vascular complications that were referred to be the major cause of morbidity and mortality in DM. Although [...] Read more.
Diabetes mellitus (DM) is one of the principal manifestations of metabolic syndrome and its prevalence with modern lifestyle is increasing incessantly. Chronic hyperglycemia can induce several vascular complications that were referred to be the major cause of morbidity and mortality in DM. Although several therapeutic targets have been identified and accessed clinically, the imminent risk of DM and its prevalence are still ascending. Substantial pieces of evidence revealed that histone deacetylase (HDAC) isoforms can regulate various molecular activities in DM via epigenetic and post-translational regulation of several transcription factors. To date, 18 HDAC isoforms have been identified in mammals that were categorized into four different classes. Classes I, II, and IV are regarded as classical HDACs, which operate through a Zn-based mechanism. In contrast, class III HDACs or Sirtuins depend on nicotinamide adenine dinucleotide (NAD+) for their molecular activity. Functionally, most of the HDAC isoforms can regulate β cell fate, insulin release, insulin expression and signaling, and glucose metabolism. Moreover, the roles of HDAC members have been implicated in the regulation of oxidative stress, inflammation, apoptosis, fibrosis, and other pathological events, which substantially contribute to diabetes-related vascular dysfunctions. Therefore, HDACs could serve as the potential therapeutic target in DM towards developing novel intervention strategies. This review sheds light on the emerging role of HDACs/isoforms in diabetic pathophysiology and emphasized the scope of their targeting in DM for constituting novel interventional strategies for metabolic disorders/complications. Full article
(This article belongs to the Special Issue 10th Anniversary of Cells—Advances in Cellular Pathology)
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22 pages, 936 KiB  
Review
The Genomic Landscape of Thyroid Cancer Tumourigenesis and Implications for Immunotherapy
by Amandeep Singh, Jeehoon Ham, Joseph William Po, Navin Niles, Tara Roberts and Cheok Soon Lee
Cells 2021, 10(5), 1082; https://0-doi-org.brum.beds.ac.uk/10.3390/cells10051082 - 01 May 2021
Cited by 26 | Viewed by 4641
Abstract
Thyroid cancer is the most prevalent endocrine malignancy that comprises mostly indolent differentiated cancers (DTCs) and less frequently aggressive poorly differentiated (PDTC) or anaplastic cancers (ATCs) with high mortality. Utilisation of next-generation sequencing (NGS) and advanced sequencing data analysis can aid in understanding [...] Read more.
Thyroid cancer is the most prevalent endocrine malignancy that comprises mostly indolent differentiated cancers (DTCs) and less frequently aggressive poorly differentiated (PDTC) or anaplastic cancers (ATCs) with high mortality. Utilisation of next-generation sequencing (NGS) and advanced sequencing data analysis can aid in understanding the multi-step progression model in the development of thyroid cancers and their metastatic potential at a molecular level, promoting a targeted approach to further research and development of targeted treatment options including immunotherapy, especially for the aggressive variants. Tumour initiation and progression in thyroid cancer occurs through constitutional activation of the mitogen-activated protein kinase (MAPK) pathway through mutations in BRAF, RAS, mutations in the phosphatidylinositol-4,5-bisphosphate 3-kinase (PI3K) pathway and/or receptor tyrosine kinase fusions/translocations, and other genetic aberrations acquired in a stepwise manner. This review provides a summary of the recent genetic aberrations implicated in the development and progression of thyroid cancer and implications for immunotherapy. Full article
(This article belongs to the Special Issue 10th Anniversary of Cells—Advances in Cellular Pathology)
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