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Special Issue Editor

Dr. Hyonchol Jang

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Guest Editor

Division of Cancer Biology, National Cancer Center, Korea & Department of Cancer Biomedical Science, National Cancer Center Graduate School of Cancer Science and Policy, Korea
Interests: cancer stemness, molecular changes in relapse after standard therapy, metabolism of malignant tumor population, circulating tumor cell, translational research, posttranslational modification

Special Issue Information

Dear Colleagues,

Despite many advances, cancer deaths continue to increase every year worldwide. One of the leading causes of cancer death is relapse after standard therapy. For cancer cells to relapse after standard therapy, therapy-resistant cancer cells must migrate to the recurrence site and proliferate. In this process, cancer cells must survive in adhesion-independent situations, such as circulating tumor cells, and remain resistant to standard therapy. Increasing evidence suggests that not all cells in a heterogenous cancer cell population have the same capacity for it, but certain cells have a higher capacity for it. And, the certain cells that have higher capacity for relapse after standard therapy are often described as having more stem cell-like characteristics, stemness. In this special issue, we will address studies that ultimately aim to control the process of cancer relapse after standard therapy. Original manuscripts and reviews covering the molecular mechanisms of this process, new molecular targets, or new strategies to control this process are welcome. Original manuscripts and reviews dealing with regulation of cancer stemness and studies that can control the survival of circulating tumor cells are also welcome.

Dr. Hyonchol Jang
Guest Editor

Manuscript Submission Information

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Keywords

cancer stemness
standard therapy resistance
cancer relapse
circulating tumor cells
tumor plasticity
metastasis
cancer cell differentiation
cancer relapse inhibitors

Published Papers (2 papers)

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Research

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15 pages, 2355 KiB

Open AccessArticle

Fusion Cell Markers in Circulating Tumor Cells from Patients with High-Grade Ovarian Serous Carcinoma

by Anna Paula Carreta Ruano, Andrea Paiva Gadelha Guimarães, Alexcia C. Braun, Bianca C. T. C. P. Flores, Milena Shizue Tariki, Emne A. Abdallah, Jacqueline Aparecida Torres, Diana Noronha Nunes, Bruna Tirapelli, Vladmir C. Cordeiro de Lima, Marcello Ferretti Fanelli, Pierre-Emmanuel Colombo, Alexandre André Balieiro Anastácio da Costa, Catherine Alix-Panabières and Ludmilla Thomé Domingos Chinen

Int. J. Mol. Sci. 2022, 23(23), 14687; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms232314687 - 24 Nov 2022

Cited by 6 | Viewed by 1868

Abstract

Cancer is primarily a disease in which late diagnosis is linked to poor prognosis, and unfortunately, detection and management are still challenging. Circulating tumor cells (CTCs) are a potential resource to address this disease. Cell fusion, an event discovered recently in CTCs expressing carcinoma and leukocyte markers, occurs when ≥2 cells become a single entity (hybrid cell) after the merging of their plasma membranes. Cell fusion is still poorly understood despite continuous evaluations in in vitro/in vivo studies. Blood samples from 14 patients with high-grade serous ovarian cancer (A.C. Camargo Cancer Center, São Paulo, Brazil) were collected with the aim to analyze the CTCs/hybrid cells and their correlation to clinical outcome. The EDTA collected blood (6 mL) from patients was used to isolate/identify CTCs/hybrid cells by ISET. We used markers with possible correlation with the phenomenon of cell fusion, such as MC1-R, EpCAM and CD45, as well as CEN8 expression by CISH analysis. Samples were collected at three timepoints: baseline, after one month (first follow-up) and after three months (second follow-up) of treatment with olaparib (total sample = 38). Fourteen patients were included and in baseline and first follow-up all patients showed at least one CTC. We found expression of MC1-R, EpCAM and CD45 in cells (hybrid) in at least one of the collection moments. Membrane staining with CD45 was found in CTCs from the other cohort, from the other center, evaluated by the CellSearch^® system. The presence of circulating tumor microemboli (CTM) in the first follow-up was associated with a poor recurrence-free survival (RFS) (5.2 vs. 12.2 months; p = 0.005). The MC1-R expression in CTM in the first and second follow-ups was associated with a shorter RFS (p = 0.005). CEN8 expression in CTCs was also related to shorter RFS (p = 0.035). Our study identified a high prevalence of CTCs in ovarian cancer patients, as well as hybrid cells. Both cell subtypes demonstrate utility in prognosis and in the assessment of response to treatment. In addition, the expression of MC1-R and EpCAM in hybrid cells brings new perspectives as a possible marker for this phenomenon in ovarian cancer. Full article

(This article belongs to the Special Issue Study on “Stemness” of Cancer Cells and Main Cause of Cancer Relapse after Standard Therapy)

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Review

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15 pages, 2798 KiB

Open AccessReview

Stemness, Inflammation and Epithelial–Mesenchymal Transition in Colorectal Carcinoma: The Intricate Network

by Inese Briede, Dainis Balodis, Janis Gardovskis and Ilze Strumfa

Int. J. Mol. Sci. 2021, 22(23), 12891; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms222312891 - 29 Nov 2021

Cited by 9 | Viewed by 2505

Abstract

In global cancer statistics, colorectal carcinoma (CRC) ranks third by incidence and second by mortality, causing 10.0% of new cancer cases and 9.4% of oncological deaths worldwide. Despite the development of screening programs and preventive measures, there are still high numbers of advanced cases. Multiple problems compromise the treatment of metastatic colorectal cancer, one of these being cancer stem cells—a minor fraction of pluripotent, self-renewing malignant cells capable of maintaining steady, low proliferation and exhibiting an intriguing arsenal of treatment resistance mechanisms. Currently, there is an increasing body of evidence for intricate associations between inflammation, epithelial–mesenchymal transition and cancer stem cells. In this review, we focus on inflammation and its role in CRC stemness development through epithelial–mesenchymal transition. Full article

(This article belongs to the Special Issue Study on “Stemness” of Cancer Cells and Main Cause of Cancer Relapse after Standard Therapy)

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