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Biomedicines
Special Issues
State-of-the-Art Cell Biology and Pathology in Poland
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State-of-the-Art Cell Biology and Pathology in Poland

A special issue of Biomedicines (ISSN 2227-9059). This special issue belongs to the section "Cell Biology and Pathology".

Deadline for manuscript submissions: closed (30 September 2023) | Viewed by 14517

Special Issue Editors

Dr. Bartłomiej Tomasik

E-Mail Website
Guest Editor
Department of Oncology and Radiotherapy, Faculty of Medicine, Medical University of Gdańsk, Gdańsk, Poland
Interests: biomarkers; cancer; cell biology; cell cycle; DNA repair; epigenetics; genetics; immunotherapy; molecular biology; radiation oncology
Special Issues, Collections and Topics in MDPI journals
Dr. Marcin Braun

E-Mail Website
Guest Editor
Department of Pathology, Chair of Oncology, Medical University of Łódź, Łódź, Poland
Interests: pathology; breast cancer; cell cycle
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

This Special Issue will provide a comprehensive overview on the state of the art of cell biology and pathology in Poland. We are inviting you to submit manuscripts that will consolidate our understanding in these areas. Full research articles and in-depth reviews will be considered. Topics of interest include, but are not limited to, the following research areas:

  • Artificial intelligence and machine learning;
  • Cancer biology and pathology stem cells;
  • CAR-T cell research;
  • Cell physiology: cell growth, metabolism, protein synthesis, division, movement of proteins, active/passive transport, intra- and extracellular signaling, adhesion, DNA repair, etc.;
  • Cell signaling;
  • Cell techniques: cell and tissue culture, isolation, and fractionation of cells, immunocytochemistry (ICC), in situ hybridization (ISH), transfection, and optogenetics;
  • Computational biology and pathology;
  • Digital pathology;
  • Immune microenvironment and immunotherapy;
  • OMICS: transcriptomics, genomics, proteomics, metabolomics, glycomics, lipidomics, interactomics, fluxomics, and biomics;
  • Predictive and prognostic biomarkers;
  • Stem cell biology.

Dr. Bartłomiej Tomasik
Dr. Marcin Braun
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. Biomedicines 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 2600 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

  • artificial intelligence
  • biomarkers
  • cell cycle
  • immune environment
  • molecular biology
  • molecular pathology
  • pathology
  • pathobiology

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Further information on MDPI's Special Issue polices can be found here.

Published Papers (3 papers)

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Review

18 pages, 1835 KiB  
Review
Updates in KMT2A Gene Rearrangement in Pediatric Acute Lymphoblastic Leukemia
by Mateusz Górecki, Ilona Kozioł, Agnieszka Kopystecka, Julia Budzyńska, Joanna Zawitkowska and Monika Lejman
Biomedicines 2023, 11(3), 821; https://doi.org/10.3390/biomedicines11030821 - 8 Mar 2023
Cited by 19 | Viewed by 6038
Abstract
The KMT2A (formerly MLL) encodes the histone lysine-specific N-methyltransferase 2A and is mapped on chromosome 11q23. KMT2A is a frequent target for recurrent translocations in acute myeloid leukemia (AML), acute lymphoblastic leukemia (ALL), or mixed lineage (biphenotypic) leukemia (MLL). Over 90 KMT2A [...] Read more.
The KMT2A (formerly MLL) encodes the histone lysine-specific N-methyltransferase 2A and is mapped on chromosome 11q23. KMT2A is a frequent target for recurrent translocations in acute myeloid leukemia (AML), acute lymphoblastic leukemia (ALL), or mixed lineage (biphenotypic) leukemia (MLL). Over 90 KMT2A fusion partners have been identified until now, including the most recurring ones—AFF1, MLLT1, and MLLT3—which encode proteins regulating epigenetic mechanisms. The presence of distinct KMT2A rearrangements is an independent dismal prognostic factor, while very few KMT2A rearrangements display either a good or intermediate outcome. KMT2A-rearranged (KMT2A-r) ALL affects more than 70% of new ALL diagnoses in infants (<1 year of age), 5–6% of pediatric cases, and 15% of adult cases. KMT2A-rearranged (KMT2A-r) ALL is characterized by hyperleukocytosis, a relatively high incidence of central nervous system (CNS) involvement, an aggressive course with early relapse, and early relapses resulting in poor prognosis. The exact pathways of fusions and the effects on the final phenotypic activity of the disease are still subjects of much research. Future trials could consider the inclusion of targeted immunotherapeutic agents and prioritize the identification of prognostic factors, allowing for the less intensive treatment of some infants with KMT2A ALL. The aim of this review is to summarize our knowledge and present current insight into the mechanisms of KMT2A-r ALL, portray their characteristics, discuss the clinical outcome along with risk stratification, and present novel therapeutic strategies. Full article
(This article belongs to the Special Issue State-of-the-Art Cell Biology and Pathology in Poland)
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13 pages, 894 KiB  
Review
The Interplay between Finasteride-Induced Androgen Imbalance, Endoplasmic Reticulum Stress, Oxidative Stress, and Liver Disorders in Paternal and Filial Generation
by Sylwia Rzeszotek, Agnieszka Kolasa, Anna Pilutin, Kamila Misiakiewicz-Has, Katarzyna Sielatycka and Barbara Wiszniewska
Biomedicines 2022, 10(11), 2725; https://doi.org/10.3390/biomedicines10112725 - 27 Oct 2022
Cited by 3 | Viewed by 5159
Abstract
Finasteride (Fin) causes androgen imbalance by inhibiting the conversion of testosterone (T) to its more active metabolite, dihydrotestosterone (DHT). Androgen receptors (AR) are present (e.g., in hepatocytes), which have well-developed endoplasmic reticulum (ERet). Cellular protein quality control is carried out by ERet in [...] Read more.
Finasteride (Fin) causes androgen imbalance by inhibiting the conversion of testosterone (T) to its more active metabolite, dihydrotestosterone (DHT). Androgen receptors (AR) are present (e.g., in hepatocytes), which have well-developed endoplasmic reticulum (ERet). Cellular protein quality control is carried out by ERet in two paths: (i) unfolded protein response (UPR) and/or (ii) endoplasmic reticulum associated degradation (ERAD). ERet under continuous stress can generate changes in the UPR and can direct the cell on the pathway of life or death. It has been demonstrated that genes involved in ERet stress are among the genes controlled by androgens in some tissues. Oxidative stress is also one of the factors affecting the functions of ERet and androgens are one of the regulators of antioxidant enzyme activity. In this paper, we discuss/analyze a possible relationship between androgen imbalance in paternal generation with ERet stress and liver disorders in both paternal and filial generation. In our rat model, hyperglycemia and subsequent higher accumulation of hepatic glycogen were observed in all filial generation obtained from females fertilized by Fin-treated males (F1:Fin). Importantly, genes encoding enzymes involved in glucose and glycogen metabolism have been previously recognized among UPR targets. Full article
(This article belongs to the Special Issue State-of-the-Art Cell Biology and Pathology in Poland)
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Graphical abstract

13 pages, 910 KiB  
Review
Subtype-Specific Tumour Immune Microenvironment in Risk of Recurrence of Ductal Carcinoma In Situ: Prognostic Value of HER2
by Julia Solek, Jedrzej Chrzanowski, Adrianna Cieslak, Aleksandra Zielinska, Dominika Piasecka, Marcin Braun, Rafal Sadej and Hanna M. Romanska
Biomedicines 2022, 10(5), 1061; https://doi.org/10.3390/biomedicines10051061 - 3 May 2022
Cited by 2 | Viewed by 2287
Abstract
Increasing evidence suggests that the significance of the tumour immune microenvironment (TIME) for disease prognostication in invasive breast carcinoma is subtype-specific but equivalent studies in ductal carcinoma in situ (DCIS) are limited. The purpose of this paper is to review the existing data [...] Read more.
Increasing evidence suggests that the significance of the tumour immune microenvironment (TIME) for disease prognostication in invasive breast carcinoma is subtype-specific but equivalent studies in ductal carcinoma in situ (DCIS) are limited. The purpose of this paper is to review the existing data on immune cell composition in DCIS in relation to the clinicopathological features and molecular subtype of the lesion. We discuss the value of infiltration by various types of immune cells and the PD-1/PD-L1 axis as potential markers of the risk of recurrence. Analysis of the literature available in PubMed and Medline databases overwhelmingly supports an association between densities of infiltrating immune cells, traits of immune exhaustion, the foci of microinvasion, and overexpression of HER2. Moreover, in several studies, the density of immune infiltration was found to be predictive of local recurrence as either in situ or invasive cancer in HER2-positive or ER-negative DCIS. In light of the recently reported first randomized DCIS trial, relating recurrence risk with overexpression of HER2, we also include a closing paragraph compiling the latest mechanistic data on a functional link between HER2 and the density/composition of TIME in relation to its potential value in the prognostication of the risk of recurrence. Full article
(This article belongs to the Special Issue State-of-the-Art Cell Biology and Pathology in Poland)
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