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9.9
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Cells
Special Issues
Probing Growth during Health and Disease
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Probing Growth during Health and Disease

A special issue of Cells (ISSN 2073-4409).

Deadline for manuscript submissions: closed (31 October 2023) | Viewed by 20281

Special Issue Editors

Dr. José A. García-Sanz

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Guest Editor
Cancer Genetics & Cancer Stem Cell Laboratory Department of Molecular Biomedicine Centro de Investigaciones Biológicas Margarita Salas-CSIC Ramiro de Maeztu, 9 E-28040 Madrid, Spain
Interests: biology of adult stem cells; cancer stem cells; cancer treatment
Special Issues, Collections and Topics in MDPI journals
Dr. Marisa M. Merino

E-Mail Website
Guest Editor
Institute of Systems, Molecular and Integrative Biology, Department of Molecular & Clinical Cancer Medicine, University of Liverpool, Crown St., Liverpool L69 7ZB, UK
Interests: genetics; gene expression; cell biology; cancer biology; cell death
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Strikingly, nature has been able to reproduce organism patterns, differing several orders of magnitude in size, throughout evolution. This fact has long been discussed, and it is widely agreed that cells within tissues build up successful organisms driven by growth and patterning “forces”. These mechanisms run smoothly, but rebel cells can evade this hierarchy by losing their identity and acquiring uncontrolled proliferative behaviors in diseases such as cancer. In recent decades, key pathways regulating growth and patterning during health and disease have been described, although the mechanisms coordinating growth and patterning remain unclear. Future research efforts will need to bridge individual cell behavior with the tissue scale during development and disease.

This Special Issue is an open multidisciplinary discussion aiming to bring together current knowledge of the mechanisms regulating growth, including research papers, reviews, and communications covering the cell biology aspects of growth in health and disease.

Dr. José A. García-Sanz
Dr. Marisa M. Merino
Guest Editors

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.

Keywords

  • growth
  • tumour
  • development
  • cell competition
  • patterning

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Published Papers (6 papers)

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Research

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15 pages, 1507 KiB  
Article
Enhanced Transcriptional Signature and Expression of Histone-Modifying Enzymes in Salivary Gland Tumors
by Maria Manou, Theodoros Loupis, Dimitrios M. Vrachnos, Nikolaos Katsoulas, Stamatios Theocharis, Dimitrios S. Kanakoglou, Efthimia K. Basdra, Christina Piperi and Athanasios G. Papavassiliou
Cells 2023, 12(20), 2437; https://doi.org/10.3390/cells12202437 - 11 Oct 2023
Cited by 1 | Viewed by 1429
Abstract
Salivary gland tumors (SGTs) are rare and complex neoplasms characterized by heterogenous histology and clinical behavior as well as resistance to systemic therapy. Tumor etiology is currently under elucidation and an interplay of genetic and epigenetic changes has been proposed to contribute to [...] Read more.
Salivary gland tumors (SGTs) are rare and complex neoplasms characterized by heterogenous histology and clinical behavior as well as resistance to systemic therapy. Tumor etiology is currently under elucidation and an interplay of genetic and epigenetic changes has been proposed to contribute to tumor development. In this work, we investigated epigenetic regulators and histone-modifying factors that may alter gene expression and participate in the pathogenesis of SGT neoplasms. We performed a detailed bioinformatic analysis on a publicly available RNA-seq dataset of 94 ACC tissues supplemented with clinical data and respective controls and generated a protein–protein interaction (PPI) network of chromatin and histone modification factors. A significant upregulation of TP53 and histone-modifying enzymes SUV39H1, EZH2, PRMT1, HDAC8, and KDM5B, along with the upregulation of DNA methyltransferase DNMT3A and ubiquitin ligase UHRF1 mRNA levels, as well as a downregulation of lysine acetyltransferase KAT2B levels, were detected in ACC tissues. The protein expression of p53, SUV39H1, EZH2, and HDAC8 was further validated in SGT tissues along with their functional deposition of the repressive histone marks H3K9me3 and H3K27me3, respectively. Overall, this study is the first to detect a network of interacting proteins affecting chromatin structure and histone modifications in salivary gland tumor cells, further providing mechanistic insights in the molecular profile of SGTs that confer to altered gene expression programs. Full article
(This article belongs to the Special Issue Probing Growth during Health and Disease)
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16 pages, 8913 KiB  
Article
Cell Proliferation Indices in Regenerating Alitta virens (Annelida, Errantia)
by Alexandra Y. Shalaeva and Vitaly V. Kozin
Cells 2023, 12(10), 1354; https://doi.org/10.3390/cells12101354 - 10 May 2023
Cited by 2 | Viewed by 1853
Abstract
In recent years, interest in the possible molecular regulators of cell proliferation and differentiation in a wide range of regeneration models has grown significantly, but the cell kinetics of this process remain largely a mystery. Here we try to elucidate the cellular aspects [...] Read more.
In recent years, interest in the possible molecular regulators of cell proliferation and differentiation in a wide range of regeneration models has grown significantly, but the cell kinetics of this process remain largely a mystery. Here we try to elucidate the cellular aspects of regeneration by EdU incorporation in intact and posteriorly amputated annelid Alitta virens using quantitative analysis. We found that the main mechanism of blastema formation in A. virens is local dedifferentiation; mitotically active cells of intact segments do not significantly contribute to the blastemal cellular sources. Amputation-induced proliferation occurred predominantly within the epidermal and intestinal epithelium, as well as wound-adjacent muscle fibers, where clusters of cells at the same stage of the cell cycle were found. The resulting regenerative bud had zones of high proliferative activity and consisted of a heterogeneous population of cells that differed in their anterior–posterior positions and in their cell cycle parameters. The data presented allowed for the quantification of cell proliferation in the context of annelid regeneration for the first time. Regenerative cells showed an unprecedentedly high cycle rate and an exceptionally large growth fraction, making this regeneration model especially valuable for studying coordinated cell cycle entry in vivo in response to injury. Full article
(This article belongs to the Special Issue Probing Growth during Health and Disease)
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13 pages, 2564 KiB  
Article
Down Syndrome Altered Cell Composition in Blood, Brain, and Buccal Swab Samples Profiled by DNA-Methylation-Based Cell-Type Deconvolution
by Ze Zhang, Hannah G. Stolrow, Brock C. Christensen and Lucas A. Salas
Cells 2023, 12(8), 1168; https://doi.org/10.3390/cells12081168 - 15 Apr 2023
Cited by 5 | Viewed by 2357
Abstract
Down syndrome (DS) is a genetic disorder caused by an extra copy of chromosome 21 that presents developmental dysfunction and intellectual disability. To better understand the cellular changes associated with DS, we investigated the cell composition in blood, brain, and buccal swab samples [...] Read more.
Down syndrome (DS) is a genetic disorder caused by an extra copy of chromosome 21 that presents developmental dysfunction and intellectual disability. To better understand the cellular changes associated with DS, we investigated the cell composition in blood, brain, and buccal swab samples from DS patients and controls using DNA methylation-based cell-type deconvolution. We used genome-scale DNA methylation data from Illumina HumanMethylation450k and HumanMethylationEPIC arrays to profile cell composition and trace fetal lineage cells in blood samples (DS N = 46; control N = 1469), brain samples from various regions (DS N = 71; control N = 101), and buccal swab samples (DS N = 10; control N = 10). In early development, the number of cells from the fetal lineage in the blood is drastically lower in DS patients (Δ = 17.5%), indicating an epigenetically dysregulated maturation process for DS patients. Across sample types, we observed significant alterations in relative cell-type proportions for DS subjects compared with the controls. Cell-type proportion alterations were present in samples from early development and adulthood. Our findings provide insight into DS cellular biology and suggest potential cellular interventional targets for DS. Full article
(This article belongs to the Special Issue Probing Growth during Health and Disease)
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Review

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20 pages, 646 KiB  
Review
Organ Abnormalities Caused by Turner Syndrome
by Sang Hoon Yoon, Ga Yeon Kim, Gyu Tae Choi and Jeong Tae Do
Cells 2023, 12(10), 1365; https://doi.org/10.3390/cells12101365 - 11 May 2023
Cited by 6 | Viewed by 6034
Abstract
Turner syndrome (TS), a genetic disorder due to incomplete dosage compensation of X-linked genes, affects multiple organ systems, leading to hypogonadotropic hypogonadism, short stature, cardiovascular and vascular abnormalities, liver disease, renal abnormalities, brain abnormalities, and skeletal problems. Patients with TS experience premature ovarian [...] Read more.
Turner syndrome (TS), a genetic disorder due to incomplete dosage compensation of X-linked genes, affects multiple organ systems, leading to hypogonadotropic hypogonadism, short stature, cardiovascular and vascular abnormalities, liver disease, renal abnormalities, brain abnormalities, and skeletal problems. Patients with TS experience premature ovarian failure with a rapid decline in ovarian function caused by germ cell depletion, and pregnancies carry a high risk of adverse maternal and fetal outcomes. Aortic abnormalities, heart defects, obesity, hypertension, and liver abnormalities, such as steatosis, steatohepatitis, biliary involvement, liver cirrhosis, and nodular regenerative hyperplasia, are commonly observed in patients with TS. The SHOX gene plays a crucial role in short stature and abnormal skeletal phenotype in patients with TS. Abnormal structure formation of the ureter and kidney is also common in patients with TS, and a non-mosaic 45,X karyotype is significantly associated with horseshoe kidneys. TS also affects brain structure and function. In this review, we explore various phenotypic and disease manifestations of TS in different organs, including the reproductive system, cardiovascular system, liver, kidneys, brain, and skeletal system. Full article
(This article belongs to the Special Issue Probing Growth during Health and Disease)
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30 pages, 1350 KiB  
Review
Biology of Cancer-Testis Antigens and Their Therapeutic Implications in Cancer
by Dawn Sijin Nin and Lih-Wen Deng
Cells 2023, 12(6), 926; https://doi.org/10.3390/cells12060926 - 17 Mar 2023
Cited by 17 | Viewed by 5766
Abstract
Tumour-specific antigens have been an area of interest in cancer therapy since their discovery in the middle of the 20th century. In the era of immune-based cancer therapeutics, redirecting our immune cells to target these tumour-specific antigens has become even more relevant. Cancer-testis [...] Read more.
Tumour-specific antigens have been an area of interest in cancer therapy since their discovery in the middle of the 20th century. In the era of immune-based cancer therapeutics, redirecting our immune cells to target these tumour-specific antigens has become even more relevant. Cancer-testis antigens (CTAs) are a class of antigens with an expression specific to the testis and cancer cells. CTAs have also been demonstrated to be expressed in a wide variety of cancers. Due to their frequency and specificity of expression in a multitude of cancers, CTAs have been particularly attractive as cancer-specific therapeutic targets. There is now a rapid expansion of CTAs being identified and many studies have been conducted to correlate CTA expression with cancer and therapy-resistant phenotypes. Furthermore, there is an increasing number of clinical trials involving using some of these CTAs as molecular targets in pharmacological and immune-targeted therapeutics for various cancers. This review will summarise the current knowledge of the biology of known CTAs in tumorigenesis and the regulation of CTA genes. CTAs as molecular targets and the therapeutic implications of these CTA-targeted anticancer strategies will also be discussed. Full article
(This article belongs to the Special Issue Probing Growth during Health and Disease)
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Other

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12 pages, 1629 KiB  
Opinion
Stemming Tumoral Growth: A Matter of Grotesque Organogenesis
by Marisa M. Merino and Jose A. Garcia-Sanz
Cells 2023, 12(6), 872; https://doi.org/10.3390/cells12060872 - 11 Mar 2023
Viewed by 1956
Abstract
The earliest metazoans probably evolved from single-celled organisms which found the colonial system to be a beneficial organization. Over the course of their evolution, these primary colonial organisms increased in size, and division of labour among the cells became a remarkable feature, leading [...] Read more.
The earliest metazoans probably evolved from single-celled organisms which found the colonial system to be a beneficial organization. Over the course of their evolution, these primary colonial organisms increased in size, and division of labour among the cells became a remarkable feature, leading to a higher level of organization: the biological organs. Primitive metazoans were the first organisms in evolution to show organ-type structures, which set the grounds for complex organs to evolve. Throughout evolution, and concomitant with organogenesis, is the appearance of tissue-specific stem cells. Tissue-specific stem cells gave rise to multicellular living systems with distinct organs which perform specific physiological functions. This setting is a constructive role of evolution; however, rebel cells can take over the molecular mechanisms for other purposes: nowadays we know that cancer stem cells, which generate aberrant organ-like structures, are at the top of a hierarchy. Furthermore, cancer stem cells are the root of metastasis, therapy resistance, and relapse. At present, most therapeutic drugs are unable to target cancer stem cells and therefore, treatment becomes a challenging issue. We expect that future research will uncover the mechanistic “forces” driving organ growth, paving the way to the implementation of new strategies to impair human tumorigenesis. Full article
(This article belongs to the Special Issue Probing Growth during Health and Disease)
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