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Molecular Mechanisms and Therapeutic Resistance in Hematological Malignancies

A special issue of Cancers (ISSN 2072-6694).

Deadline for manuscript submissions: 31 August 2026 | Viewed by 654

Editor


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Guest Editor
1. Centro Hospitalar e Universitário São João, Porto, Portugal
2. Clinical Hematology, FMUP–Faculty of Medicine of the University of Porto, Porto, Portugal
3. 1i3S–Instituto de Investigação e Inovação em Saúde, University of Porto, Porto, Portugal
Interests: EVs; microRNAs; drug resistance; immunotherapy; multiple myeloma
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

We are pleased to invite you to contribute to an upcoming Special Issue entitled “Molecular Mechanisms and Therapeutic Resistance in Hematological Malignancies,” to be published in Cancers. This Special Issue aims to highlight cutting-edge research exploring the molecular, cellular, and immunological determinants that govern disease evolution, therapeutic response, and resistance across hematologic cancers.

This Special Issue seeks to gather original research articles, reviews, and perspectives that provide mechanistic insights or translational relevance, ultimately aiming to support the development of more effective and precise therapeutic strategies.

While substantial advances have been achieved through targeted agents and immunotherapies, treatment resistance remains a central clinical challenge. Increasing evidence indicates that resistance is driven not only by tumor-intrinsic genetic and epigenetic alterations but also by dynamic immune escape mechanisms and microenvironmental remodeling that collectively shape therapeutic vulnerability.

By integrating molecular oncology, immunobiology, and translational therapeutics, this Special Issue aims to advance a more comprehensive framework for understanding resistance as a multidimensional process involving tumor genetics, immune competence, and microenvironmental context.

We welcome original research, mechanistic studies, translational analyses, and state-of-the-art reviews that provide biological insight or therapeutic innovation, with the ultimate goal of informing precision medicine approaches and improving long-term outcomes in hematological malignancies. We look forward to your valuable contribution to this timely and impactful collection.

Dr. Rui Bergantim
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 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-anonymized peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Cancers 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 2900 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

  • genomic and epigenomic alterations
  • signaling pathway dysregulation
  • non-coding RNAs
  • metabolic reprogramming
  • antigen escape mechanisms
  • antigen presentation defects
  • interferon signaling impairment
  • T-cell exhaustion
  • memory T-cell dysfunction
  • myeloid-mediated immunosuppression
  • bone marrow immune microenvironment
  • spatial immune architecture
  • CAR-T cell therapy
  • next-generation CAR engineering
  • bispecific antibodies and T-cell engagers
  • antibody-drug conjugates
  • NK-cell and macrophage immunotherapy
  • immune checkpoint modulation
  • combination immunotherapy strategies
  • liquid biopsy–guided precision therapy

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Published Papers (1 paper)

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Research

20 pages, 2451 KB  
Article
Breaking the Balance: Baseline Oxidative Stress and DNA Repair Capacity in Multiple Myeloma Therapy
by Panagiotis Malamos, Elisavet Deligianni, Konstantinos Voutetakis, Konstantinos Koutoulogenis, Olga Papadodima, Evangelos Terpos and Vassilis L. Souliotis
Cancers 2026, 18(12), 1995; https://doi.org/10.3390/cancers18121995 - 19 Jun 2026
Viewed by 411
Abstract
Background/Objectives: Disruption of cellular redox balance and DNA damage response (DDR) signals represents a key driver of cancer development, influencing tumor progression and therapeutic response. Here, we investigated the interplay between DDR-related parameters and oxidative stress in relation to treatment response in patients [...] Read more.
Background/Objectives: Disruption of cellular redox balance and DNA damage response (DDR) signals represents a key driver of cancer development, influencing tumor progression and therapeutic response. Here, we investigated the interplay between DDR-related parameters and oxidative stress in relation to treatment response in patients with multiple myeloma (MM). Methods: Oxidative stress and DDR signals were evaluated in primary cells, including peripheral blood mononuclear cells (PBMCs) and bone marrow plasma cells (BMPCs), collected at diagnosis from MM patients who were subsequently classified as responders (n = 35) or non-responders (n = 41) to melphalan-based therapy. Results: PBMCs and BMPCs from non-responders exhibited a distinct biological profile characterized by lower baseline DNA damage, reduced oxidative stress, increased nucleotide excision repair and double-strand break repair capacity, and reduced apoptotic sensitivity compared with responders (all p < 0.001). In addition, non-responders displayed increased chromatin relaxation. Differential gene expression patterns involving DDR-related pathways further distinguished BMPCs between the two clinical outcome groups. Conclusions: Collectively, these findings indicate that alterations in oxidative stress and DDR signals play a crucial role in determining response to melphalan-based therapy in MM. The identification of these molecular alterations in an easily accessible tissue, such as peripheral blood, underscores their potential clinical relevance and warrants further validation. Full article
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