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Review Article | DOI: https://doi.org/10.31579/2639-4162/311
International Higher School of Medicine, Intergelpo Str, 1F, Bishkek, Kyrgyzstan.
*Corresponding Author: Bon E.I, International Higher School of Medicine, Intergelpo Str, 1F, Bishkek, Kyrgyzstan.
Citation: Bon E.I., Maksimovich N. Ye., Dremza I.K., Velaria Jenish Lakhabhai, (2025), Neuroblastoma - Genetic and Molecular Aspects, J. General Medicine and Clinical Practice, 8(11); DOI:10.31579/2639-4162/311
Copyright: © 2025, Bon E.I. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
Received: 04 November 2025 | Accepted: 18 November 2025 | Published: 25 November 2025
Keywords: neuroblastoma; overexpression of mycn gene; alk gene mutation; chromosomal abnormalities; targeted therapy
Neuroblastoma is a childhood malignant form of cancer that originates from neuroblasts, and affects children under five years of age and rarely occurs in adults. It is a tumor that arises from neural crest cells and mainly affects ssthe adrenal medulla. There is remarkable genetic heterogeneity and chromosomal abnormality that leads to this malignant pediatric tumor.
Purpose: This article is mostly focused on genetic and molecular abnormalities that lead to neuroblastoma. Heterogeneity of MYCN gene and over-expression of MYCN gene as well as translocations or mutation in gene like ALK (anaplastic lymphoma kinase), PHOX2b gene, rearrangements of ATRX and TERT and also chromosomal deletions and gain that are associated with neuroblastoma that are also discussed. Moreover, in this article associated target therapy against specific genes is also discussed.
Neuroblastoma is a type of tumor of the peripheral nervous system that primarily affects children. It arises from immature nerve cells that are known as neuroblasts. In normal conditions neural crest cells migrate from the dorsal neural tube, unfortunately in some cases there are defects in neural crest migration, maturation or differentiation that can lead to development of neuroblastoma [1]. These cells are commonly found on adrenal gland, neck, chest, abdomen or pelvis. So, these areas are commonly affected in neuroblastoma. Neural crest cells maturation, migration and differentiation is regulated by genes [2] thus abnormalities in genes like overexpression of genes lead to tumors. However, neuroblastoma is a type of tumor that highly depends on several driver and suppressor genes. In the genetic view neuroblastoma associated with MYCN gene overexpression, Somatic and germline mutation like ALK [3], and PHOX2B gene [4], mutation of ATRX gene [5], rearrangement of TERT [6] these are predominant in high risk neuroblastoma.
Moreover, chromosomal alterations include deletions of chromosomes 1p,3p,4p and also 11p and gains of 1p,2p and 17q chromosomes associated with high risk neuroblastoma [7]. MYCN genes have groups including N-myc that have additionally 2 sub-groups (C-myc and L-myc ). These MYC proteins are regulators of cell fate and also interact with transcription factors. That transcription factor regulates neural crest cells differentiation, migration and maturation so in MYCN gene overexpression this factor leads to malignant tumors like neuroblastoma and often with poor survival. MYCN gene is one of the prognostic markers, presence of this marker indicates poor prognosis of neuroblastoma [2]. ALK has been classified in a superfamily of tyrosine kinase. The ALK gene is located on the 2p23 chromosome that encodes receptor tyrosine kinase and somatic mutations have been confirmed in the tyrosine kinase domain in that ALK gene is present that is associated with primary type of neuroblastoma. So currently for therapy of ALK positive neuroblastoma molecular inhibitors against ALK can be given [8]
CD44 is a particularly transmembrane adhesive protein involved in tumor metastasis and progression. It regulates cellular growth, motility as well as differentiation. It works as a main receptor for the ligand hyaluronic acid and as other extracellular components [9]. CD44 is found as a good prognosis of neuroblastoma tumor and also it is associated with glial differentiation [9]. Overview of MYCN gene in neuroblastoma The MYCN gene is found at the terminal end of the short arm of chromosome 2. MYCN gene belongs to a very small family, MYCN(N-Myc) gene includes 2 more genes C-Myc and L-Myc. N-Myc is mainly associated for initiating cancer like neuroblastoma. N-Myc works as a cancer stem cell factor in the development of neural crest cells like neuroblasts and C-Myc is a pluripotent stem cell in embryonal development, it promotes development of pluripotent stem cell from ectoderm in embryonal period then it further develops into neural crest cells and MYCN gene then plays main role in differentiation of those neural crest cells. However, in this time overexpression of MYCN gene leads to tumor development [2]. MYCN alone plays multiple roles in development of neuroblastoma, it can activate transcriptions of genes that can be involved in self renewal, angiogenesis, survival and proliferation. It also suppresses the expression of genes that promote cell differentiation, moreover it also activates apoptosis via p53 pathway [10]. Study showed that in neuroblastoma with MYCN gene overexpression p53 protein is a direct target of the MYCN gene and p53 protein is expressed at much higher levels in poor differentiated or undifferentiated types of neuroblastoma [11]. MYCN amplification causes down regulation of TP53 inducible protein 1 and upregulation of SKP2 and CDK4 that show an inability to arrest in G1 phase of cell cycle in responset irradiation and proliferation of cell continues, MYCN gene also directly represses the activity of anti-proliferative proteins [10].
Structure of MYCN gene:
The MYCN gene is made of 464 amino acids and it has so many functional domains. The MYCN gene contains a basic helix-loop-helix-leucine zipper that plays an oncogenic role in cancer, it is responsible for physical interaction and binding to DNA sequence 5′-CACGTG-3′ and that is termed as E-box [12], [13]. This family basic helix-loop-helix-leucine zipper has transcription factors that play a role in cellular proliferation, differentiation, apoptosis and tumorogenesis[11]. Gene transcription of MYCN is regulated by enhancers and promoters, enhancers play an important role in cell type specific gene expression and they are misregulated in neuroblastoma like cancers. CDK1 is a stability regulator protein of MYCN gene, in normal condition CDK1 phosphorylates the MYCN at S62 in G- phase of cell cycle, other stabilizers are AURKA (AA17-43; 61-89), FBXW7(AA61-89) [12].
Mechanism of action:
Molecular mechanisms: The expression of MYCN gene is whether activated or not at DNA, mRNA and proteins is defined by several factors including secondary form of DNA structure, enhances and transcription factors [14]. MYCN gene Through gene amplification can cause proto-oncogene overexpression. This type of process involves formation of
extrachromosomal DNA that leads to increase of gene copy number, it is done by DNA recombination and replication [15].
So abnormal N-Myc is based on gene amplification, enhanced translation and transcription [14].
Metabolic reprogramming:
Part of the MYCN gene c-myc regulates amino acid transporter ASCT2 and c-myc induces metabolic reprogramming in CD44 positive cancer cells [13]. The study also showed that the MYCN gene amplification type of neuroblastoma is dependent on ASCT2 for maintaining sufficient levels of glutamate to activate TCA cycle.
Further, MYCN amplification type of neuroblastoma cells needs machinery that keeps metabolic demand of glutathione as is mainly necessary for activation of TCA cycle [13], [16]. Studies showed that the MYCN gene uses aerobic glycolysis for energy in neuroblastoma cells [17], [18]. MYCN also regulates so many cellular processes during development of normal cellular and cancer formation. MYCN increases glycolytic flux and glutaminolysis and that further helps to develop tumorigenesis in cancer like neuroblastoma [19].
P53 in neuroblastoma:
P53 is identified as the saviour of the genome and this p53 gene mutation leads to most malignancy to develop, but in the neuroblastoma mutation of this gene found rarely and surprisingly it accumulates in neuroblastoma [11].
As a prognostic factor:
The MYCN gene has no such reliable antibody that can be used in IHC. We have to detect MYCN amplification at the nucleic level [20]. Survival outcomes in neuroblastoma patients are usually affected by Schwann cell specific types of genes like (CALR, KLF10, UBL3) [21]. Neuroblastoma with MYCN positive expression or overexpression is classified as high-risk and needs a higher dose of chemotherapy than others [20]. High-risk neuroblastoma patients have a survival chance less than 50%, with therapy and chemo they survive less [18].
Targeted therapy options against MYCN gene:
MYCN gene drives the upregulation of ABC transported and also the metabolic enzymes that contribute to chemoresistance, this can be the reason for patients with MYCN-amplified gene neuroblastoma. They often respond poorly to chemotherapy [22].
Against MYCN gene small-molecular inhibitors like PI3K and GSK3 inhibitors have been identified as reduced viability specifically in MYCN-amplified cell line xenografts [23]. These GSK3 inhibitors act on a large scale on neuroblastoma cells and cause cell death [24]. PI3K/AkT/mTOR pathway is activated in most types of the neuroblastoma. It is a pro survival signaling pathway that prompts neuroblastoma cell survival and chemoresistance [25]. PI3K inhibitors alone showed results but cells over time developed clinical resistance, to overcome that study showed that therapy with multidrug is effective. Therapy with targeting PIM, PI3K and mTOR is effective after this therapy tumor showed lots of differentiation and cell death and tumor growth also reduced over time [26]. There is p53-MDM2 pathway where MDM2 inhibits the activity of p53 and blocks the effects of p53 also increases MYCN gene translation and tumorigenesis [25]. This pathway is associated with MYCN gene overexpression [27]. So, small molecular inhibitors that inhibit the p53-MDM2 pathway can be very useful for patients with high-risk MYCN-amplified neuroblastoma [28].
Alteration of ALK gene
ALK (anaplastic lymphoma kinase) is similar to an insulin receptor. It is a receptor of tyrosine kinase and belongs to a superfamily of insulin receptors and contains glycine rich domains. In neuroblastoma gain-of-function mutation in the kinase domain is seen [29]. In 85% of cases mutation is seen on F1174, F1245 and R1275. These mutations are found in both sporadic and familial types of neuroblastoma. Study showed that sometimes these ALK mutations are correlated with MYCN gene [29]. ALK signaling pathway is associated for activating PI3K-AKT, JAKSTAT and MAPK pathways. These pathways are able to cell proliferation, cell survival and some like PI3K-AkT shows chemoresistance also [30]. In neuroblastoma ALK signaling shares similarities with MYCN gene to growth of the tumor development so it is also a high-risk type of neuroblastoma [30]. In formation of neuroblastoma ALK gene abnormalities like mutation, amplification or translocation can cause proliferation of neuroblast cells. It is thought that during cell migration the ALK gene can increase their migration rate. The ALK gene is required only for migration and cell proliferation, however it is not required for differentiation so it only affects migration and proliferation [31]. As a treatment option ALK inhibitors like crizotinib and ceritinib are now developed but the tumor cell can develop clinical resistance and may need multiple therapy options [32].
Mutation and alteration in genes
PHOX2B gene
It is the first gene to be identified in neuroblastoma predisposition, it is believed that this PHOX2B gene encodes a very important transcription factor that is necessary for autonomic nervous system development [31]. High levels of the PHOX2B gene showed that it promotes cell proliferation and growth of neuroblast cells. It shows effects on early stages of neuroblasts growth and is likely associated with poor differentiation of cells [33]. There is BMP signaling that is done by dorsal aorta and it initiates the neural crest cells to express high levels of PHOX2B and that activates some proteins like Phox2A, GATA2 and GATA3 and that further promotes cell differentiation [34]. With mutation of the PHOX2B gene this process gets blocked. The PHOX2B protein is encoded by the PHOX2B gene that is located on chromosome 4p13. The PHOX2B mutation is seen on both familial and sporadic types of neuroblastoma. Study showed that it is found as undifferentiated and poorly differentiated and presents as an optimal diagnostic marker. It is sensitive for diagnosis for neuroblastoma not only on tissue specimens but cytological specimens also [35]. ATRX gene The ATRX gene is located on the long arm of X chromosome and it encodes ATP-dependent helicase SWI/SNF (switch/sucrose non-fermentable) that is chromatin remodeller family. It is involved in many functions like DNA repair, transcription regulation and nucleosome recognition. In the neuroblastoma there is point mutation or frameshift mutation that results in loss of function of the ATRX gene [36]. ATRX is also involved indirectly in inhibiting macroH2A1 deposition, removing R loops and also modifying histones. Some studies showed that 90% of ATRX deletion neuroblastoma also had 11q deletion [5].
Maybe 11q deletion existed before ATRX but there is no data about that. Why this occurs needs further research. MYCN gene amplification with ATRX mutation leads to suppression of the tumor suppressor gene found in neuroblastoma from patients of all types of stages and ages and MYCN and ATRX are incompatible and both leads to DNA replicative stress and ATRX mutation type of neuroblastoma have often worse outcome [19].
TERT gene
Telomerase are located at the end of the chromosomes in eukaryotes. The enzyme telomerase consists of two components, one is TERT it is telomerase reverse transcription protein that is responsible for catalytic activity within cells and other one is TERC that is RNA subunit and works as a template for synthesizing sequences of telomerase [37]. TERT is a reverse transcription that is expressed by stem cells. Its function is to use noncoding RNA templates and telomeric repeats at telomers, that prevents apoptosis mediated by telomers. DNA methylation can inhibit the expression of telomerase and MYCN expressed neuroblast cells express TERT [38]. In neuroblastoma there is induction of TERT gene and activation of ALT pathway is seen and MYCN gene also induces TERT gene and increases its effect in tumor development and combination of this leads to high-risk neuroblastoma with poor outcomes [37]. NALT is alternative lengthening of telomerase that is associated with ATRX mutation and can be seen with TERT gene mutation [36].
BARD1 gene
BARD1 gene mutation is often characterized as a rare type of mutation in neuroblastoma and is a high-risk and predicts worst outcomes. BARD1 gene works as a DNA repair it binds to BRCA1 and that further repairs DNA damage [39]. The BARD1 gene is associated with germline mutation and in neuroblastoma it is rarely found. With repairing of DNA, it is also associated with modulation of chromatin structure, hormone signaling and cell cycle regulation. The full length of the BARD1 gene is also found to be a tumor suppressor gene [40]. MYCN plays a main role in DNA repair and with DNA damage by BARD1 gene neuroblast cells must be synthesizing more MYCN genes [41].
NF1 gene
NF1 is a major mediator of peripheral neuronal nerve cells progenitors. It is studied that in MYCN expressed NF1 loss and activation of RAS-MAPK pathway alters neuroblastoma and drives tumorigenesis crazy [42], [43]. Binimetinib is the drug that inhibits MEK that indirectly inhibits the RAS-MAPK pathway that showed good results in NF1 gene mutated neuroblastoma [44]. The main function of the NF1 gene involves RAS proteins and its activation. Neurofibromin is a very long amino acid that GTPase activates proteins and GAP related protein and domains. The RAS proteins are most of the time bound to inactivate form of GDP and in time of activation they can form RAS-GTP and can activate one more pathway PI3K/AKT/mTOR and this pathway has one unique ability to protect the cells from apoptosis [45].
RAS-MAPK pathway alteration in neuroblastoma
The RAS-MAPK pathway is activated in the primary type of neuroblastoma and association of this pathway with neuroblastoma showed poor prognosis and worse outcomes. Mutation in genes like ALK showed activation of this pathway [46]. Although alteration of this pathway frequently occurs in relapsed neuroblastoma tumors [47]. PHOX2B gene also through various mutations found to activate MAPK pathway [48]. NF1 gene mutation found in neuroblastoma that is also associated with activation of the RAS/MAPK pathway [44]. This pathway is a signaling pathway and for cellular function sends different signals and alters cellular function, in dysregulation of this pathway cancerous event occurs. It regulates transcription of many genes for cellular function; it regulates it via phosphorylation [49]. This pathway contains two components RAS and MAPK, p44 is mainly associated with downstream signal cascade of the RAS protein and MAPK (p44/42 mitogen-activated protein kinase) is extracellular signal-regulated protein kinases that is the one that overexpressed in neuroblastoma and found in another type of cancers too [47].
For therapy MEK1/2 inhibitor drug-Binimetinb showed some possibilities. In that study specific MEK1/2 inhibitor drug-Binimetinb was sensitive with some of the cell lines and on that cell death were seen with cell rounding and detachment, however much more cell lines were resistant to treatment and showed no results [44]. Other analogues are Cobimetinib, Selumetinib and Trametinib can be given to inhibit the RAS-MAPK pathway in neuroblastoma [49].
PI3K/AKT/mTOR pathway
The ALK gene is one of the prognostic markers for high-risk neuroblastoma that activates this PI3K/AKT/mTOR pathway [25]. NF1 gene and many other genes can alter and activate this pathway [45]. This pathway prompts the neuroblastoma cell survival and protects them against chemotherapy so it makes tumors even stronger [25]. For targeted therapy against this pathway, multikinase PI3K/AKT/mTOR inhibition with IBL-202 (PIM/PI3K) and IBL-301 (PIM/PI3K/mTOR) and that showed cell death of neuroblast cells and reduced tumor growth however in MYCN-amplified high risk neuroblastoma had PIM3 expression that shows resistance against this therapy [26]. Chromosomal alterations in neuroblastoma In neuroblastoma deletion of the 1q chromosome is common in most primary neuroblastoma tumors and it is characterized by loss of heterogeneity [50]. MYCN gene is found on chromosome 2 and gain of chromosome 2 can be a very very high risk because it increases MYCN gene expression, together with ALK gene [51]. With 11q gene alteration there is a study showing development of resistance against chemotherapy and 11q gene alteration and MYCN gene amplification is not linked at all [52]. Gain of the 17q chromosome is found out to be more occurrence than 11q chromosome alteration and 17q gain although identified in the smallest region but it’s associated with high-risk and relapse neuroblastoma [53].
Targeted therapy options
Therapy with low risk neuroblastoma non-MYCN amplified usually involves localized surgical resection with standard chemotherapy. This type of risk doesn’t metastasize and doesn’t spread after resection. For stage 1 patients with low risk is usually effective treatment [1]. With high risk neuroblastoma treatment is involved in several phases: induction phase, consolidation phase and the maintenance phase. In induction phase treatment is given with chemotherapy drugs like etoposide, vincristin, doxorubicin, cyclophosphamide and others. The consolidation phase includes chemotherapy along with radiotherapy and the maintenance phase is focused on retinoic acid treatment and immune activator drugs or cytokines that activate the immune system [54].
In conclusion, there was a lot of heterogeneity of MYCN genes and this type of heterogeneity often leads to high-risk neuroblastoma. There was also a lot of correlation of MYCN gene overexpression/amplification with different types of genes and with different molecular pathways. Although we mentioned many molecular mechanisms of genes and pathways and targeted therapy options that are related with neuroblastoma, there is still need for further research against targeted therapies and molecular mechanisms.
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Dear Editorial Coordinator of the Journal of Nutrition and Food Processing! "I would like to thank the Journal of Nutrition and Food Processing for including and publishing my article. The peer review process was very quick, movement and precise. The Editorial Board has done an extremely conscientious job with much help, valuable comments and advices. I find the journal very valuable from a professional point of view, thank you very much for allowing me to be part of it and I would like to participate in the future!”
Dealing with The Journal of Neurology and Neurological Surgery was very smooth and comprehensive. The office staff took time to address my needs and the response from editors and the office was prompt and fair. I certainly hope to publish with this journal again.Their professionalism is apparent and more than satisfactory. Susan Weiner
My Testimonial Covering as fellowing: Lin-Show Chin. The peer reviewers process is quick and effective, the supports from editorial office is excellent, the quality of journal is high. I would like to collabroate with Internatioanl journal of Clinical Case Reports and Reviews.
My experience publishing in Psychology and Mental Health Care was exceptional. The peer review process was rigorous and constructive, with reviewers providing valuable insights that helped enhance the quality of our work. The editorial team was highly supportive and responsive, making the submission process smooth and efficient. The journal's commitment to high standards and academic rigor makes it a respected platform for quality research. I am grateful for the opportunity to publish in such a reputable journal.
My experience publishing in International Journal of Clinical Case Reports and Reviews was exceptional. I Come forth to Provide a Testimonial Covering the Peer Review Process and the editorial office for the Professional and Impartial Evaluation of the Manuscript.
I would like to offer my testimony in the support. I have received through the peer review process and support the editorial office where they are to support young authors like me, encourage them to publish their work in your esteemed journals, and globalize and share knowledge globally. I really appreciate your journal, peer review, and editorial office.
Dear Agrippa Hilda- Editorial Coordinator of Journal of Neuroscience and Neurological Surgery, "The peer review process was very quick and of high quality, which can also be seen in the articles in the journal. The collaboration with the editorial office was very good."
I would like to express my sincere gratitude for the support and efficiency provided by the editorial office throughout the publication process of my article, “Delayed Vulvar Metastases from Rectal Carcinoma: A Case Report.” I greatly appreciate the assistance and guidance I received from your team, which made the entire process smooth and efficient. The peer review process was thorough and constructive, contributing to the overall quality of the final article. I am very grateful for the high level of professionalism and commitment shown by the editorial staff, and I look forward to maintaining a long-term collaboration with the International Journal of Clinical Case Reports and Reviews.
To Dear Erin Aust, I would like to express my heartfelt appreciation for the opportunity to have my work published in this esteemed journal. The entire publication process was smooth and well-organized, and I am extremely satisfied with the final result. The Editorial Team demonstrated the utmost professionalism, providing prompt and insightful feedback throughout the review process. Their clear communication and constructive suggestions were invaluable in enhancing my manuscript, and their meticulous attention to detail and dedication to quality are truly commendable. Additionally, the support from the Editorial Office was exceptional. From the initial submission to the final publication, I was guided through every step of the process with great care and professionalism. The team's responsiveness and assistance made the entire experience both easy and stress-free. I am also deeply impressed by the quality and reputation of the journal. It is an honor to have my research featured in such a respected publication, and I am confident that it will make a meaningful contribution to the field.
"I am grateful for the opportunity of contributing to [International Journal of Clinical Case Reports and Reviews] and for the rigorous review process that enhances the quality of research published in your esteemed journal. I sincerely appreciate the time and effort of your team who have dedicatedly helped me in improvising changes and modifying my manuscript. The insightful comments and constructive feedback provided have been invaluable in refining and strengthening my work".
I thank the ‘Journal of Clinical Research and Reports’ for accepting this article for publication. This is a rigorously peer reviewed journal which is on all major global scientific data bases. I note the review process was prompt, thorough and professionally critical. It gave us an insight into a number of important scientific/statistical issues. The review prompted us to review the relevant literature again and look at the limitations of the study. The peer reviewers were open, clear in the instructions and the editorial team was very prompt in their communication. This journal certainly publishes quality research articles. I would recommend the journal for any future publications.
Dear Jessica Magne, with gratitude for the joint work. Fast process of receiving and processing the submitted scientific materials in “Clinical Cardiology and Cardiovascular Interventions”. High level of competence of the editors with clear and correct recommendations and ideas for enriching the article.
We found the peer review process quick and positive in its input. The support from the editorial officer has been very agile, always with the intention of improving the article and taking into account our subsequent corrections.
My article, titled 'No Way Out of the Smartphone Epidemic Without Considering the Insights of Brain Research,' has been republished in the International Journal of Clinical Case Reports and Reviews. The review process was seamless and professional, with the editors being both friendly and supportive. I am deeply grateful for their efforts.
To Dear Erin Aust – Editorial Coordinator of Journal of General Medicine and Clinical Practice! I declare that I am absolutely satisfied with your work carried out with great competence in following the manuscript during the various stages from its receipt, during the revision process to the final acceptance for publication. Thank Prof. Elvira Farina
Dear Jessica, and the super professional team of the ‘Clinical Cardiology and Cardiovascular Interventions’ I am sincerely grateful to the coordinated work of the journal team for the no problem with the submission of my manuscript: “Cardiometabolic Disorders in A Pregnant Woman with Severe Preeclampsia on the Background of Morbid Obesity (Case Report).” The review process by 5 experts was fast, and the comments were professional, which made it more specific and academic, and the process of publication and presentation of the article was excellent. I recommend that my colleagues publish articles in this journal, and I am interested in further scientific cooperation. Sincerely and best wishes, Dr. Oleg Golyanovskiy.
Dear Ashley Rosa, Editorial Coordinator of the journal - Psychology and Mental Health Care. " The process of obtaining publication of my article in the Psychology and Mental Health Journal was positive in all areas. The peer review process resulted in a number of valuable comments, the editorial process was collaborative and timely, and the quality of this journal has been quickly noticed, resulting in alternative journals contacting me to publish with them." Warm regards, Susan Anne Smith, PhD. Australian Breastfeeding Association.
Dear Jessica Magne, Editorial Coordinator, Clinical Cardiology and Cardiovascular Interventions, Auctores Publishing LLC. I appreciate the journal (JCCI) editorial office support, the entire team leads were always ready to help, not only on technical front but also on thorough process. Also, I should thank dear reviewers’ attention to detail and creative approach to teach me and bring new insights by their comments. Surely, more discussions and introduction of other hemodynamic devices would provide better prevention and management of shock states. Your efforts and dedication in presenting educational materials in this journal are commendable. Best wishes from, Farahnaz Fallahian.
Dear Maria Emerson, Editorial Coordinator, International Journal of Clinical Case Reports and Reviews, Auctores Publishing LLC. I am delighted to have published our manuscript, "Acute Colonic Pseudo-Obstruction (ACPO): A rare but serious complication following caesarean section." I want to thank the editorial team, especially Maria Emerson, for their prompt review of the manuscript, quick responses to queries, and overall support. Yours sincerely Dr. Victor Olagundoye.
Dear Ashley Rosa, Editorial Coordinator, International Journal of Clinical Case Reports and Reviews. Many thanks for publishing this manuscript after I lost confidence the editors were most helpful, more than other journals Best wishes from, Susan Anne Smith, PhD. Australian Breastfeeding Association.
Dear Agrippa Hilda, Editorial Coordinator, Journal of Neuroscience and Neurological Surgery. The entire process including article submission, review, revision, and publication was extremely easy. The journal editor was prompt and helpful, and the reviewers contributed to the quality of the paper. Thank you so much! Eric Nussbaum, MD
Dr Hala Al Shaikh This is to acknowledge that the peer review process for the article ’ A Novel Gnrh1 Gene Mutation in Four Omani Male Siblings, Presentation and Management ’ sent to the International Journal of Clinical Case Reports and Reviews was quick and smooth. The editorial office was prompt with easy communication.
Dear Erin Aust, Editorial Coordinator, Journal of General Medicine and Clinical Practice. We are pleased to share our experience with the “Journal of General Medicine and Clinical Practice”, following the successful publication of our article. The peer review process was thorough and constructive, helping to improve the clarity and quality of the manuscript. We are especially thankful to Ms. Erin Aust, the Editorial Coordinator, for her prompt communication and continuous support throughout the process. Her professionalism ensured a smooth and efficient publication experience. The journal upholds high editorial standards, and we highly recommend it to fellow researchers seeking a credible platform for their work. Best wishes By, Dr. Rakhi Mishra.
Dear Jessica Magne, Editorial Coordinator, Clinical Cardiology and Cardiovascular Interventions, Auctores Publishing LLC. The peer review process of the journal of Clinical Cardiology and Cardiovascular Interventions was excellent and fast, as was the support of the editorial office and the quality of the journal. Kind regards Walter F. Riesen Prof. Dr. Dr. h.c. Walter F. Riesen.
Dear Ashley Rosa, Editorial Coordinator, International Journal of Clinical Case Reports and Reviews, Auctores Publishing LLC. Thank you for publishing our article, Exploring Clozapine's Efficacy in Managing Aggression: A Multiple Single-Case Study in Forensic Psychiatry in the international journal of clinical case reports and reviews. We found the peer review process very professional and efficient. The comments were constructive, and the whole process was efficient. On behalf of the co-authors, I would like to thank you for publishing this article. With regards, Dr. Jelle R. Lettinga.
Dear Clarissa Eric, Editorial Coordinator, Journal of Clinical Case Reports and Studies, I would like to express my deep admiration for the exceptional professionalism demonstrated by your journal. I am thoroughly impressed by the speed of the editorial process, the substantive and insightful reviews, and the meticulous preparation of the manuscript for publication. Additionally, I greatly appreciate the courteous and immediate responses from your editorial office to all my inquiries. Best Regards, Dariusz Ziora
Dear Chrystine Mejia, Editorial Coordinator, Journal of Neurodegeneration and Neurorehabilitation, Auctores Publishing LLC, We would like to thank the editorial team for the smooth and high-quality communication leading up to the publication of our article in the Journal of Neurodegeneration and Neurorehabilitation. The reviewers have extensive knowledge in the field, and their relevant questions helped to add value to our publication. Kind regards, Dr. Ravi Shrivastava.
Dear Clarissa Eric, Editorial Coordinator, Journal of Clinical Case Reports and Studies, Auctores Publishing LLC, USA Office: +1-(302)-520-2644. I would like to express my sincere appreciation for the efficient and professional handling of my case report by the ‘Journal of Clinical Case Reports and Studies’. The peer review process was not only fast but also highly constructive—the reviewers’ comments were clear, relevant, and greatly helped me improve the quality and clarity of my manuscript. I also received excellent support from the editorial office throughout the process. Communication was smooth and timely, and I felt well guided at every stage, from submission to publication. The overall quality and rigor of the journal are truly commendable. I am pleased to have published my work with Journal of Clinical Case Reports and Studies, and I look forward to future opportunities for collaboration. Sincerely, Aline Tollet, UCLouvain.
Dear Ms. Mayra Duenas, Editorial Coordinator, International Journal of Clinical Case Reports and Reviews. “The International Journal of Clinical Case Reports and Reviews represented the “ideal house” to share with the research community a first experience with the use of the Simeox device for speech rehabilitation. High scientific reputation and attractive website communication were first determinants for the selection of this Journal, and the following submission process exceeded expectations: fast but highly professional peer review, great support by the editorial office, elegant graphic layout. Exactly what a dynamic research team - also composed by allied professionals - needs!" From, Chiara Beccaluva, PT - Italy.
Dear Maria Emerson, Editorial Coordinator, we have deeply appreciated the professionalism demonstrated by the International Journal of Clinical Case Reports and Reviews. The reviewers have extensive knowledge of our field and have been very efficient and fast in supporting the process. I am really looking forward to further collaboration. Thanks. Best regards, Dr. Claudio Ligresti
Dear Chrystine Mejia, Editorial Coordinator, Journal of Neurodegeneration and Neurorehabilitation. “The peer review process was efficient and constructive, and the editorial office provided excellent communication and support throughout. The journal ensures scientific rigor and high editorial standards, while also offering a smooth and timely publication process. We sincerely appreciate the work of the editorial team in facilitating the dissemination of innovative approaches such as the Bonori Method.” Best regards, Dr. Matteo Bonori.
I recommend without hesitation submitting relevant papers on medical decision making to the International Journal of Clinical Case Reports and Reviews. I am very grateful to the editorial staff. Maria Emerson was a pleasure to communicate with. The time from submission to publication was an extremely short 3 weeks. The editorial staff submitted the paper to three reviewers. Two of the reviewers commented positively on the value of publishing the paper. The editorial staff quickly recognized the third reviewer’s comments as an unjust attempt to reject the paper. I revised the paper as recommended by the first two reviewers.
Dear Maria Emerson, Editorial Coordinator, Journal of Clinical Research and Reports. Thank you for publishing our case report: "Clinical Case of Effective Fetal Stem Cells Treatment in a Patient with Autism Spectrum Disorder" within the "Journal of Clinical Research and Reports" being submitted by the team of EmCell doctors from Kyiv, Ukraine. We much appreciate a professional and transparent peer-review process from Auctores. All research Doctors are so grateful to your Editorial Office and Auctores Publishing support! I amiably wish our article publication maintained a top quality of your International Scientific Journal. My best wishes for a prosperity of the Journal of Clinical Research and Reports. Hope our scientific relationship and cooperation will remain long lasting. Thank you very much indeed. Kind regards, Dr. Andriy Sinelnyk Cell Therapy Center EmCell
Dear Editorial Team, Clinical Cardiology and Cardiovascular Interventions. It was truly a rewarding experience to work with the journal “Clinical Cardiology and Cardiovascular Interventions”. The peer review process was insightful and encouraging, helping us refine our work to a higher standard. The editorial office offered exceptional support with prompt and thoughtful communication. I highly value the journal’s role in promoting scientific advancement and am honored to be part of it. Best regards, Meng-Jou Lee, MD, Department of Anesthesiology, National Taiwan University Hospital.
Dear Editorial Team, Journal-Clinical Cardiology and Cardiovascular Interventions, “Publishing my article with Clinical Cardiology and Cardiovascular Interventions has been a highly positive experience. The peer-review process was rigorous yet supportive, offering valuable feedback that strengthened my work. The editorial team demonstrated exceptional professionalism, prompt communication, and a genuine commitment to maintaining the highest scientific standards. I am very pleased with the publication quality and proud to be associated with such a reputable journal.” Warm regards, Dr. Mahmoud Kamal Moustafa Ahmed
Dear Maria Emerson, Editorial Coordinator of ‘International Journal of Clinical Case Reports and Reviews’, I appreciate the opportunity to publish my article with your journal. The editorial office provided clear communication during the submission and review process, and I found the overall experience professional and constructive. Best regards, Elena Salvatore.
Dear Mayra Duenas, Editorial Coordinator of ‘International Journal of Clinical Case Reports and Reviews Herewith I confirm an optimal peer review process and a great support of the editorial office of the present journal
Dear Editorial Team, Clinical Cardiology and Cardiovascular Interventions. I am really grateful for the peers review; their feedback gave me the opportunity to reflect on the message and impact of my work and to ameliorate the article. The editors did a great job in addition by encouraging me to continue with the process of publishing.
Dear Cecilia Lilly, Editorial Coordinator, Endocrinology and Disorders, Thank you so much for your quick response regarding reviewing and all process till publishing our manuscript entitled: Prevalence of Pre-Diabetes and its Associated Risk Factors Among Nile College Students, Sudan. Best regards, Dr Mamoun Magzoub.
International Journal of Clinical Case Reports and Reviews is a high quality journal that has a clear and concise submission process. The peer review process was comprehensive and constructive. Support from the editorial office was excellent, since the administrative staff were responsive. The journal provides a fast and timely publication timeline.
Dear Maria Emerson, Editorial Coordinator of International Journal of Clinical Case Reports and Reviews, What distinguishes International Journal of Clinical Case Report and Review is not only the scientific rigor of its publications, but the intellectual climate in which research is evaluated. The submission process is refreshingly free of unnecessary formal barriers and bureaucratic rituals that often complicate academic publishing without adding real value. The peer-review system is demanding yet constructive, guided by genuine scientific dialogue rather than hierarchical or authoritarian attitudes. Reviewers act as collaborators in improving the manuscript, not as gatekeepers imposing arbitrary standards. This journal offers a rare balance: high methodological standards combined with a respectful, transparent, and supportive editorial approach. In an era where publishing can feel more burdensome than research itself, this platform restores the original purpose of peer review — to refine ideas, not to obstruct them Prof. Perlat Kapisyzi, FCCP PULMONOLOGIST AND THORACIC IMAGING.
Dear Grace Pierce, International Journal of Clinical Case Reports and Reviews I appreciate the opportunity to review for Auctore Journal, as the overall editorial process was smooth, transparent and professionally managed. This journal maintains high scientific standards and ensures timely communications with authors, which is truly commendable. I would like to express my special thanks to editor Grace Pierce for his constant guidance, promt responses, and supportive coordination throughout the review process. I am also greatful to Eleanor Bailey from the finance department for her clear communication and efficient handling of all administrative matters. Overall, my experience with Auctore Journal has been highly positive and rewarding. Best regards, Sabita sinha
Dear Mayra Duenas, Editorial Coordinator of the journal IJCCR, I write here a little on my experience as an author submitting to the International Journal of Clinical Case Reports and Reviews (IJCCR). This was my first submission to IJCCR and my manuscript was inherently an outsider’s effort. It attempted to broadly identify and then make some sense of life’s under-appreciated mysteries. I initially had responded to a request for possible submissions. I then contacted IJCCR with a tentative topic for a manuscript. They quickly got back with an approval for the submission, but with a particular requirement that it be medically relevant. I then put together a manuscript and submitted it. After the usual back-and-forth over forms and formality, the manuscript was sent off for reviews. Within 2 weeks I got back 4 reviews which were both helpful and also surprising. Surprising in that the topic was somewhat foreign to medical literature. My subsequent updates in response to the reviewer comments went smoothly and in short order I had a series of proofs to evaluate. All in all, the whole publication process seemed outstanding. It was both helpful in terms of the paper’s content and also in terms of its efficient and friendly communications. Thank you all very much. Sincerely, Ted Christopher, Rochester, NY.
