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Molecular Biology of Neuroendocrine Tumors: Pathogenesis, Diagnosis and Treatment
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Molecular Biology of Neuroendocrine Tumors: Pathogenesis, Diagnosis and Treatment

A special issue of Biology (ISSN 2079-7737). This special issue belongs to the section "Cancer Biology".

Deadline for manuscript submissions: 30 April 2024 | Viewed by 6155

Special Issue Editor

Prof. Dr. Michael Lan

E-Mail Website
Guest Editor
Department of Genetics, Louisiana State University Health Sciences Center, New Orleans, LA 70112, USA
Interests: neuroendocrine (NE) differentiation/transformation; NE signal transduction, drug discovery, and cancer therapy; insulin autoimmunity and tolerance in type 1 diabetes

Special Issue Information

Dear Colleagues,

I am pleased to invite you to contribute to a Special Issue of Biology (MDPI) entitled “Molecular Biology of Neuroendocrine Tumors: Pathogenesis, Diagnosis and Treatment”. The aim of this SI is to gather studies conducted on molecular, cellular, clinical, and therapeutic aspects of neuroendocrine tumors (NETs). High-quality original research articles and reviews are welcome. There are more than a dozen NETs derived from various organs with common NE features and the production of unique hormones specific for their target tissues. These NETs consist of carcinoids, islet cell tumors, medullary thyroid carcinoma, pheochromocytoma, NE carcinoma of the skin (merkel cell carcinoma), pulmonary NE tumors (small cell lung carcinoma, large cell NE carcinoma, and lung carcinoid), pituitary tumors, parathyroid carcinoma, gastroentero–pancreatic NE tumors, medulloblastoma, neuroblastoma, retinoblastoma, and genitourinary tract tumors (NE tumor of the cervix/prostate). The process of NET differentiation and transformation is complex and critical, which has a profound impact on the body’s metabolism. It will be informative to provide insights from studying transcription factors in NETs. Research areas of this SI may include (but are not limited to) the following:

  1. Transcription factor regulates NE differentiation and transformation;
  2. Signaling pathways involved in NET development;
  3. Molecular targeting transcription factor and/or signaling pathway for NET therapy;
  4. Diagnostic biomarker for NETs.

I look forward to receiving your contributions.

Best regards,

Prof. Dr. Michael Lan
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. Biology is an international peer-reviewed open access monthly 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

  • transcription factor
  • NE differentiation
  • NE transformation
  • NET signaling pathway
  • neuroblastoma
  • NE lung cancer
  • NETs

Published Papers (4 papers)

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Research

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20 pages, 10744 KiB  
Article
A Study of Alternative TrkA Splicing Identifies TrkAIII as a Novel Potentially Targetable Participant in PitNET Progression
by Maddalena Sbaffone, Marie-Lise Jaffrain-Rea, Lucia Cappabianca, Francesca Carbonara, Francesca Gianno, Tiziana Feola, Marianna Ruggieri, Veronica Zelli, Rita Maccarone, Stefano Guadagni, Marco Clementi, Antonietta Arcella, Vincenzo Esposito, Giulia Carozza, Ilaria Martelli, Antonietta Rosella Farina and Andrew Reay Mackay
Biology 2024, 13(3), 171; https://doi.org/10.3390/biology13030171 - 07 Mar 2024
Viewed by 1048
Abstract
Pituitary neuroendocrine tumors (PitNETs) are generally benign but comprise an aggressive, invasive, therapy-resistant, metastatic subset, underpinning a need for novel therapeutic targets. PitNETs exhibit low mutation rates but are associated with conditions linked to alternative splicing, an alternative oncogene pathway activation mechanism. PitNETs [...] Read more.
Pituitary neuroendocrine tumors (PitNETs) are generally benign but comprise an aggressive, invasive, therapy-resistant, metastatic subset, underpinning a need for novel therapeutic targets. PitNETs exhibit low mutation rates but are associated with conditions linked to alternative splicing, an alternative oncogene pathway activation mechanism. PitNETs express the neurotrophin receptor TrkA, which exhibits oncogenic alternative TrkAIII splicing in other neuroendocrine tumors. We, therefore, assessed whether TrkAIII splicing represents a potential oncogenic participant in PitNETs. TrkAIII splicing was RT-PCR assessed in 53 PitNETs and TrkA isoform(s) expression and activation were assessed by confocal immunofluorescence. TrkAIII splicing was also compared to HIF1α, HIF2α, SF3B1, SRSF2, U2AF1, and JCPyV large T antigen mRNA expression, Xbp1 splicing, and SF3B1 mutation. TrkAIII splicing was detected in all invasive and most non-invasive PitNETs and was significantly elevated in invasive cases. In PitNET lineages, TrkAIII splicing was significantly elevated in invasive PIT1 PitNETs and high in invasive and non-invasive SF1 and TPIT lineages. Immunoreactivity consistent with TrkAIII activation characterized PitNET expressing TrkAIII mRNA, and invasive Pit1 PitNETs exhibited elevated HIF2α expression. TrkAIII splicing did not associate with SF3B1 mutations, altered SF3B1, SRSF2, and U2AF1 or JCPyV large T antigen expression, or Xbp1 splicing. Therefore, TrkAIII splicing is common in PitNETs, is elevated in invasive, especially PIT1 tumors, can result in intracellular TrkAIII activation, and may involve hypoxia. The data support a role for TrkAIII splicing in PitNET pathogenesis and progression and identify TrkAIII as a novel potential target in refractory PitNETs. Full article
(This article belongs to the Special Issue Molecular Biology of Neuroendocrine Tumors: Pathogenesis, Diagnosis and Treatment)
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21 pages, 21797 KiB  
Article
Analysis of High-Risk Neuroblastoma Transcriptome Reveals Gene Co-Expression Signatures and Functional Features
by Mónica Leticia Martínez-Pacheco, Enrique Hernández-Lemus and Carmen Mejía
Biology 2023, 12(9), 1230; https://doi.org/10.3390/biology12091230 - 12 Sep 2023
Viewed by 1331
Abstract
Neuroblastoma represents a neoplastic expansion of neural crest cells in the developing sympathetic nervous system and is childhood’s most common extracranial solid tumor. The heterogeneity of gene expression in different types of cancer is well-documented, and genetic features of neuroblastoma have been described [...] Read more.
Neuroblastoma represents a neoplastic expansion of neural crest cells in the developing sympathetic nervous system and is childhood’s most common extracranial solid tumor. The heterogeneity of gene expression in different types of cancer is well-documented, and genetic features of neuroblastoma have been described by classification, development stage, malignancy, and progression of tumors. Here, we aim to analyze RNA sequencing datasets, publicly available in the GDC data portal, of neuroblastoma tumor samples from various patients and compare them with normal adrenal gland tissue from the GTEx data portal to elucidate the gene expression profile and regulation networks they share. Our results from the differential expression, weighted correlation network, and functional enrichment analyses that we performed with the count data from neuroblastoma and standard normal gland samples indicate that the analysis of transcriptome data from 58 patients diagnosed with high-risk neuroblastoma shares the expression pattern of 104 genes. More importantly, our analyses identify the co-expression relationship and the role of these genes in multiple biological processes and signaling pathways strongly associated with this disease phenotype. Our approach proposes a group of genes and their biological functions to be further investigated as essential molecules and possible therapeutic targets of neuroblastoma regardless of the etiology of individual tumors. Full article
(This article belongs to the Special Issue Molecular Biology of Neuroendocrine Tumors: Pathogenesis, Diagnosis and Treatment)
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Review

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12 pages, 1784 KiB  
Review
Small Molecules Targeting INSM1 for the Treatment of High-Risk Neuroblastoma
by Michael S. Lan and Chiachen Chen
Biology 2023, 12(8), 1134; https://doi.org/10.3390/biology12081134 - 15 Aug 2023
Viewed by 1233
Abstract
Human neuroblastoma (NB) is the most common childhood extracranial tumor arising from the sympathetic nervous system. It is also a clinically heterogeneous disease that ranges from spontaneous regression to high-risk stage 4 disease. The cause of this disease remains elusive. However, the amplification [...] Read more.
Human neuroblastoma (NB) is the most common childhood extracranial tumor arising from the sympathetic nervous system. It is also a clinically heterogeneous disease that ranges from spontaneous regression to high-risk stage 4 disease. The cause of this disease remains elusive. However, the amplification of NMYC oncogene occurred in roughly 30% of NB patients, which strongly correlated with the advanced stage of disease subtype and the worse prognosis status. We discovered that N-Myc oncoprotein binds and activates INSM1, a zinc-finger transcription factor of neuroendocrine tumors. We also found that INSM1 modulates N-Myc stability mediated through PI3K/AKT/GSK3β signaling pathway. Therefore, INSM1 emerges as a critical co-player with N-Myc in facilitating NB tumor cell growth and sustaining the advanced stage of malignancy. Using an INSM1-promoter driven luciferase screening-platform, we have recently identified fifteen small molecules that negatively regulate INSM1 expression. Interestingly, the identified small molecules can be divided into four large groups of compounds such as cell signaling inhibitor, DNA/RNA inhibitor, HDAC inhibitor, and cardiac glycoside. These findings support the presence of a unique mechanism associated with INSM1 and N-Myc interplay, which is critical in regulating NB tumor cell growth. We discuss the feasibility of identifying novel or repurposing small molecules targeting INSM1 as a potential treatment option for high-risk NB. Full article
(This article belongs to the Special Issue Molecular Biology of Neuroendocrine Tumors: Pathogenesis, Diagnosis and Treatment)
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12 pages, 2016 KiB  
Review
Interplay: The Essential Role between INSM1 and N-Myc in Aggressive Neuroblastoma
by Chiachen Chen and Michael S. Lan
Biology 2022, 11(10), 1376; https://doi.org/10.3390/biology11101376 - 20 Sep 2022
Cited by 1 | Viewed by 1912
Abstract
An aggressive form of neuroblastoma (NB), a malignant childhood cancer derived from granule neuron precursors and sympathoadrenal lineage, frequently comprises MYCN amplification/elevated N-Myc expression, which contributes to the development of neural crest-derived embryonal malignancy. N-Myc is an oncogenic driver in NB. Persistent N-Myc [...] Read more.
An aggressive form of neuroblastoma (NB), a malignant childhood cancer derived from granule neuron precursors and sympathoadrenal lineage, frequently comprises MYCN amplification/elevated N-Myc expression, which contributes to the development of neural crest-derived embryonal malignancy. N-Myc is an oncogenic driver in NB. Persistent N-Myc expression during the maturation of SA precursor cells can cause blockage of the apoptosis and induce abnormal proliferation, resulting in NB development. An insulinoma-associated-1 (INSM1) zinc-finger transcription factor has emerged as an NB biomarker that plays a critical role in facilitating tumor cell growth and transformation. INSM1 plays an essential role in sympathoadrenal cell differentiation. N-Myc activates endogenous INSM1 through an E2-box of the INSM1 proximal promoter, whereas INSM1 enhances N-Myc stability via RAC-α-serine/threonine protein kinase (AKT) phosphorylation in NB. The ectopic expression of INSM1 stimulates NB tumor growth in contrast to the knockdown of INSM1 that inhibits NB cell proliferation. The clinical pathological result and bioinformatics analysis show that INSM1 is a strong diagnostic and a prognostic biomarker for the evaluation of NB progression. The INSM1/N-Myc expression shows high clinical relevance in NB. Therefore, targeting the INSM1/N-Myc-associated signaling axis should be a feasible approach to identifying new drugs for the suppression of NB tumor growth. Full article
(This article belongs to the Special Issue Molecular Biology of Neuroendocrine Tumors: Pathogenesis, Diagnosis and Treatment)
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