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Molecular Pathology in Cancer Research
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Molecular Pathology in Cancer Research

A special issue of Journal of Personalized Medicine (ISSN 2075-4426). This special issue belongs to the section "Personalized Therapy in Clinical Medicine".

Deadline for manuscript submissions: closed (25 November 2025) | Viewed by 2123

Special Issue Editors

Dr. Maurizio Martini

E-Mail Website
Guest Editor
Department of Human Pathology of the Adult and Developmental Age “Gaetano Barresi”, University of Messina, 90128 Messina, Italy
Interests: blood and lymphatic pathology; pathology of the central and peripheral nervous system; thyroid and endocrinological pathology; urological and male genital pathology; molecular pathology with a diagnostic and prognostic-therapeutic orientation; gastrointestinal pathology
Dr. Giuseppe Giuffré

E-Mail Website
Guest Editor
Department of Human Pathology of the Adult and Developmental Age “Gaetano Barresi”, University of Messina, 90128 Messina, Italy
Interests: molecular pathology; diagnostic pathology

Special Issue Information

Dear Colleagues,

Molecular pathology combines aspects of pathology and molecular biology to understand diseases at a molecular level. It is an emerging discipline that encompasses the development of molecular and genetic approaches in the diagnosis and classification of various diseases.

Molecular pathology has become a cornerstone in cancer research due to its ability to provide detailed insights into the molecular mechanisms driving cancer development, progression, and response to treatment. Applications of molecular pathology in cancer include the identification of genetic mutations, classification of tumors, discovery of diagnostic, prognostic, and predictive biomarkers, and development of targeted therapies. Overall, it enhances the precision of diagnoses and improves the understanding of disease mechanisms.

This Special Issue aims to provide a deeper understanding of the molecular mechanisms of cancers and discuss the role of molecular pathology and biomarkers in the diagnosis, prognosis, and treatment of cancers. We encourage authors to submit original articles or reviews focusing on this topic.

Dr. Maurizio Martini
Dr. Giuseppe Giuffré
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 250 words) can be sent to the Editorial Office for assessment.

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. Journal of Personalized Medicine 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

  • molecular pathology
  • diagnostic pathology
  • cancer diagnosis
  • biomarkers
  • targeted therapy
  • genomics

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

Published Papers (2 papers)

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Research

13 pages, 2829 KB  
Article
Gene Expression Profiling Provides an Improved Characterization of CD79B-Mutated Diffuse Large B-Cell Lymphomas
by Luis Grossmann, Wolfgang Jagla, Marcus Bettstetter, Simone Bertz, Stephan Schwarz-Furlan, Thomas Richter, Tobias Dechow, Thomas Decker, Martin Dreyling, Karl Sotlar, Harald Bartsch, Arndt Hartmann, Julius Honecker and Andreas Gaumann
J. Pers. Med. 2025, 15(11), 548; https://doi.org/10.3390/jpm15110548 - 10 Nov 2025
Viewed by 544
Abstract
Background and Objectives: Diffuse large B-cell lymphomas (DLBCLs) are heterogeneous neoplasms. CD79B and MYD88 mutations are associated with the activated B-cell-like (ABC) subtype of DLBCL and often co-occur and lead to constitutive activation of the NF-κB pathway. Several different genetic classifications to [...] Read more.
Background and Objectives: Diffuse large B-cell lymphomas (DLBCLs) are heterogeneous neoplasms. CD79B and MYD88 mutations are associated with the activated B-cell-like (ABC) subtype of DLBCL and often co-occur and lead to constitutive activation of the NF-κB pathway. Several different genetic classifications to date have recognized CD79B- and MYD88-mutated DLBCLs as a unique subtype with poor response to therapy and unfavorable survival. However, little is known about gene expression in DLBCLs with mutated CD79B (and MYD88) in comparison to their wild type counterparts. The objective of this study was to compare the gene expression in DLBCLs according to their CD79B mutational status. Methods: A total of 48 primary, treatment-naïve DLBCLs (CD79B-mutated: 35%/n = 17, CD79B-wild type: 65%/n = 31) were investigated using RNA expression profiling (770 genes), followed by immunohistochemical analysis of the up-regulated genes and survival analysis. Results: The gene expression analysis revealed that downstream of CD79B CARD11 and the NF-κB targets NFKBIZ, IL10, IL12A, PIM1 and BCL2A1 were up-regulated in CD79B-mutated DLBCLs. The strongest up-regulation was detected for ARNT2 and WNT11. Other up-regulated genes included the apoptosis-related BID and granzyme B, as well as genes of cell cycle regulation such as RUNX1, RUNX1T1 and RASGRF1. Up-regulation was also found for IL7, STAT3, MLLT4, CD14 and the HSP90B1 subunit. TP53 mutation showed an association with poorer overall survival in a secondary analysis, consistent with prior reports, while survival by CD79B/MYD88 mutation status and the differentially expressed genes showed no significant differences in this cohort. Conclusions: In conclusion, the current study identified novel up-regulated genes in CD79B-mutated DLBCLs beyond NF-κB pathway signaling, which may contribute to a better definition of potential therapeutic targets and further improves the characterization of this distinct and aggressive DLBCL subgroup. Full article
(This article belongs to the Special Issue Molecular Pathology in Cancer Research)
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12 pages, 12885 KB  
Article
The Prognostic Impact of the Tumor Immune Microenvironment in Synovial Sarcoma: An Immunohistochemical Analysis Using Digital Pathology and Conventional Interpretation
by Emilio Medina-Ceballos, Francisco Giner, Isidro Machado, Begoña Heras-Morán, Mónica Espino, Samuel Navarro and Antonio Llombart-Bosch
J. Pers. Med. 2025, 15(5), 169; https://doi.org/10.3390/jpm15050169 - 25 Apr 2025
Cited by 3 | Viewed by 1091
Abstract
Background and Objectives: Innate and adaptive immune responses serve a crucial role in neoplasms. The interaction of immune cells with the neoplastic tissue influences tumor behavior, resulting in either pro-tumorigenic or anti-tumorigenic effects. However, the prognostic significance of the tumor immune microenvironment (TIME) [...] Read more.
Background and Objectives: Innate and adaptive immune responses serve a crucial role in neoplasms. The interaction of immune cells with the neoplastic tissue influences tumor behavior, resulting in either pro-tumorigenic or anti-tumorigenic effects. However, the prognostic significance of the tumor immune microenvironment (TIME) in synovial sarcoma (SS) remains poorly studied. This study aimed to analyze the TIME of SS to determine its impact on the prognosis by examining the intratumoral lymphocytic and macrophagic infiltrate and its potential correlation with survival and recurrence. Methods: We conducted a retrospective observational study of 49 fusion-confirmed SS cases collected from two different institutions. We obtained clinical and follow-up data, and SSs were histologically classified according to WHO criteria. Immunohistochemical analysis, including of CD163, CD68, CD3, CD8, and CD20, was conducted in tissue microarrays using an analog scale. We examined the whole-slide tissue for the 23 cases with sufficient material available and then assessed the positive area by scanning the slides and analyzing the images using QuPath (0.4.4, Belfast, Northern Ireland) to calculate the positive area in an immune hotspot. We correlated the expression of these markers with clinical outcomes. A log-rank test and Kaplan–Meyer curves were used as appropriate (significance: p ≤ 0.05). Results: The most frequent morphological subtype was monophasic (59.6%), followed by biphasic (26.9%) and undifferentiated (7%). The mean disease specific survival (DSS) was 55.3 months, with a median of 33 months. The median overall survival (OS) was 50 months (range: 2–336 months). Both evaluation methods showed a good correlation for all antibodies, with Chi-square values of p < 0.05. All cases showed variable amounts of CD163-positive macrophages. The cases that showed a higher density of CD163-positive macrophages in whole-slide images subjected to digital analysis demonstrated an improved OS and DSS on Kaplan–Meier curves. Cases with lower CD8 and CD3 positivity showed a tendency toward faster progression and a slightly worse prognosis. Conclusions: The tumor immune microenvironment in sarcomas is a complex system that requires further investigation to fully understand its impact on tumorigenesis and patient clinical outcomes. Our results demonstrate that a higher amount of intratumoral CD163-positive macrophage infiltrate is associated with an increased OS and DSS. Our findings show that digital pathology is more precise than subjective quantitative analysis. Full article
(This article belongs to the Special Issue Molecular Pathology in Cancer Research)
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