https://journaljcti.com/index.php/JCTI <p style="text-align: justify;"><strong>Journal of Cancer and Tumor International (ISSN: 2454-7360)</strong>&nbsp;aims to publish high quality papers (<a href="/index.php/JCTI/general-guideline-for-authors">Click here for Types of paper</a>) in all areas of&nbsp;‘Cancer and&nbsp;Tumor research’. By not excluding papers based on novelty, this journal facilitates the research and wishes to publish papers as long as they are technically correct and scientifically motivated. The journal also encourages the submission of useful reports of negative results. This is a quality controlled, OPEN peer-reviewed, open-access INTERNATIONAL journal.</p> SCIENCEDOMAIN international en-US Journal of Cancer and Tumor International 2454-7360 https://journaljcti.com/index.php/JCTI/article/view/347 <p>Hyperthermic intrathoracic chemotherapy (HITHOC) has emerged as a significant multimodal therapeutic adjunct for the management of aggressive pleural malignancies, primarily malignant pleural mesothelioma and stage IVA thymoma. By combining surgical cytoreduction with the local administration of heated chemotherapeutic agents, HITHOC aims to eliminate microscopic residual disease while minimizing systemic toxicity. A comprehensive Boolean search was conducted using PubMed/Medline, Google Scholar, Embase and Scopus to identify relevant studies on the use of HITHOC for pleural malignancies. Findings were summarised regarding HITHOC’s biological rationale, applications, integration with surgery and methodological challenges. While large retrospective analyses suggest meaningful improvements in overall survival and locoregional control, the technique is currently characterized by a high degree of protocol heterogeneity across global centers. This review synthesizes current evidence on the biological rationale, clinical outcomes across various histologies, safety profiles, and the methodological barriers that must be addressed for the formal consolidation of HITHOC into international treatment guidelines.</p> Swarnava Chanda Abdul Quadir Rahmani Dhairya Gupta Copyright (c) 2026 Author(s). The licensee is the journal publisher. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. 2026-03-23 2026-03-23 16 2 1 13 10.9734/jcti/2026/v16i2347 https://journaljcti.com/index.php/JCTI/article/view/348 <p>Stem cell fate has traditionally been viewed as a product of intrinsic transcriptional programs and epigenetic regulation operating within specialized tissue niches. However, growing evidence suggests that immune-derived signals constitute a powerful and underappreciated force shaping stem cell behavior across both physiological and pathological contexts. In parallel, the concept of cancer immunoediting has revealed how immune pressure selects for tumor cell variants capable of survival, dormancy, and immune evasion. This review integrates these paradigms to propose immune editing of stem cell fate as a unifying framework linking inflammation, cellular plasticity, and malignant evolution. Recent studies demonstrate that immune-derived cytokines, inflammatory mediators, and checkpoint signaling pathways such as IL-6/STAT3, NF-κB, TGF-β/SMAD, and PI3K/AKT signaling actively reprogram stem and progenitor cells, promoting dedifferentiation, quiescence, epithelial-mesenchymal plasticity, and the persistence of stem-like phenotypes. In normal tissues, immune regulation helps balance regeneration and stem cell exhaustion, whereas under chronic inflammatory conditions and within the tumor microenvironment, immune-mediated selective pressures favor the emergence and maintenance of cancer stem cell-like states. This review further discusses how immune checkpoints such as programmed death-ligand 1 (PD-L1) and CD47 function beyond immune evasion by directly contributing to stemness maintenance and therapy resistance. Advances in single-cell transcriptomics, spatial profiling, and systems-level analyses are increasingly revealing the complex immune-stem cell interactions that shape tumor evolution. Finally, this review examines how chemotherapy and immunotherapy can inadvertently impose immune-selective pressures that enrich resistant stem-like populations, ultimately driving relapse and metastasis. By reframing stem cell fate as an immunologically sculpted and dynamically edited process, this review highlights emerging conceptual and therapeutic opportunities to disrupt immune-stem cell signaling networks and develop more effective strategies for durable cancer control.</p> Dickens Agie Michael Sakha Copyright (c) 2026 Author(s). The licensee is the journal publisher. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. 2026-03-25 2026-03-25 16 2 14 31 10.9734/jcti/2026/v16i2348