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Liver tumors represent a serious clinical health problem that threatens human life. Previous studies have demonstrated that the pathogenesis of liver tumors is complex and influenced by various factors, highlighting limitations in both basic pathological research and clinical treatment. Traditional research methods often begin with the discovery of phenomena and gradually progress to the development of animal models and human trials. Among these, liver tumor animal models play a critical role in advancing related research. The zebrafish liver closely resembles the human liver in structure, function, and regenerative capacity. Additionally, the high transparency and rapid development of zebrafish embryos and larvae make them ideal model organisms for studying liver tumors. This review systematically summarizes recent methods for constructing zebrafish liver tumor models, including transplantation, transgenesis, induction, and gene knockout. Furthermore, the present paper explores the applications of these models in the study of liver cancer pathogenesis, metastasis, the tumor microenvironment, drug screening, and other related areas. By comparing the advantages and limitations of various models and integrating their distinct characteristics, this review provides insights for developing a novel liver tumor model that better aligns with clinical needs. This approach will offer valuable reference information for further in-depth studies of the pathological mechanisms of liver tumors and the development of new therapeutic drugs or strategies. [ABSTRACT FROM AUTHOR]

During the celebration of the 50th anniversary of the founding of the Korean Cancer Association, articles published in Cancer Research and Treatment from 2004 to 2023 were assessed based on the subject and design of each study. Based on this analysis, trends in domestic cancer research were inferred and directions were suggested for the future development of Cancer Research and Treatment. [ABSTRACT FROM AUTHOR]

ABSTRACT In cancer research, the term epigenetics was used in the 1970s in its modern sense encompassing non‐genetic events modifying the chromatin state, mainly to oppose the emerging oncogene paradigm. However, starting from the establishment of this prominent concept, the importance of these epigenetic phenomena in cancer rarely led to questioning the causal role of genetic alterations. Only in the last 10 years, the accumulation of problematic data, better experimental technologies, and some ambitious models pushed the idea that epigenetics could be at least as important as genetics in early oncogenesis. Until this year, a direct demonstration of epigenetic oncogenesis was still lacking. Now, Parreno, Cavalli and colleagues, using a refined experimental model in the fruit fly Drosophila melanogaster, enforced the initiation of tumors solely by imposing a transient loss of Polycomb repression, leading to a purely epigenetic oncogenesis phenomenon. Despite a few caveats that we discuss, this pioneering work represents a major breakpoint in cancer research. We are led to consider the theoretical and conceptual implications on oncogenesis and to search for links between this artificial experimental model and naturally occurring processes, while revisiting cancer theories that were previously proposed as alternatives to the oncogene‐centered paradigm. [ABSTRACT FROM AUTHOR]

AbstractProfessional painters represent an occupational population group that deserves attention for study in the field of occupational toxicology due to the wide range of complex chemical mixtures they are exposed to. It is imperative to underscore that the International Agency for Research on Cancer has classified commercial painting as a high-risk occupation for the development of cancer. Given this context, the primary objective of the present study was to conduct a systematic review aimed at addressing the following question: are car painters at occupational risk regarding potential genotoxicity? To address this question, a selection process was undertaken, with three reviewers carefully selecting, reading, and analyzing full manuscripts from 26 studies included in this review. The technical rigor of these studies underwent meticulous scrutiny, culminating in the classification of six studies as Strong, eight as Moderate, and 12 as Weak, predicated on the extent of confounders considered. Taken together, the findings suggest that chemical substances from paints may indeed pose a risk of genotoxicity for professionals in this field, as all studies indicated genotoxicity among professional painters through various tests. [ABSTRACT FROM AUTHOR]

Cancer and brain research have historically followed concrete pathways and converged mostly to studying brain cancer. Nowadays, the fields of neuro‐oncology and neuroendocrine regulation of tumorigenesis are both emerging fields of intense research and promising applications. An increasing body of evidence suggests that somatic mutations in cancer‐related genes are prevalent in several noncancerous brain disorders. These findings highlighting that certain aspects of cancer development/progression and pathologies of the nervous system share molecular alterations, could assist in elucidating the unique hallmarks of cancer and in cancer drugs repurposing for brain disorders. In so doing, identifying the commonalities in these conditions could be crucial not only for better understanding the basis of these pathologies but also for considering the previously underappreciated and/or neglected possibility of using drugs known to be effective in one type of pathology for the other type. [ABSTRACT FROM AUTHOR]

Mitochondrial heat shock protein 90 (mtHsp90), including Tumor necrosis factor receptor-associated protein 1 (TRAP1) and Hsp90 translocated from cytoplasm, modulating cellular metabolism and signaling pathways by altering the conformation, activity, and stability of numerous client proteins, and is highly expressed in tumors. mtHsp90 inhibition results in the destabilization and eventual degradation of its client proteins, leading to interference with various tumor-related pathways and efficient control of cancer cell development. Among these compounds, gamitrinib, a specific mtHsp90 inhibitor, has demonstrated its safety and efficacy in several preclinical investigations and is currently undergoing evaluation in clinical trials. This review aims to provide a comprehensive overview of the present knowledge pertaining to mtHsp90, encompassing its structure and function. Moreover, our main emphasis is on the development of mtHsp90 inhibitors for various cancer therapies, to present a thorough overview of the recent pre-clinical and clinical advancements in this field. [ABSTRACT FROM AUTHOR]

Anchorage-independent 3D-cultures of multicellular tumour spheroids (MCTS) and in vitro microtumours of cancer cells can provide upfront information on the effects of anticancer drug candidates, tantamount to that obtained from animal xenograft studies. Unlike 2D cancer cell cultures, 3D-models take into account the influence of the tumour microenvironment and the location dependence of drug effects and accumulation. We exemplified this by comparison of the effects of two new dual-mode anticancer agents, Troxbam and Troxham, and their monomodal congeners SAHA (suberoylanilide hydroxamic acid) and CA-4 (combretastatin A-4). We assessed the growth of MCTS of HCT116wt human colon carcinoma cells exposed to these compounds, as well as the spatial distribution of dead HCT116wt cells in these MCTS. Also, fluorescence imaging of live and fixed MCTS was used to assess the type of cellular death induced by test compounds. Furthermore, an innovative perfusion bioreactor system was used to grow microtumours in the presence or absence of test compounds. Both new investigational compounds led to significant reductions of the size of such MCTS and also of corresponding in vitro microtumours by inducing caspase-9 dependent apoptosis and elevated levels of reactive oxygen species. 3D multicellular tumour spheroids are easy to grow and employ for compound tests in the familiar well-plate set-up. Together with 3D microtumours grown at scaffolds in continuously perfused bioreactors they allow to study, early on in the course of drug evaluations, the communication of tumour cells with their microenvironment to an extent hitherto available only in animal experiments. [ABSTRACT FROM AUTHOR]

Cancer continues to threaten human health regardless of novel therapeutic options. Over the last two decades, targeted therapy has emerged as a significant advancement in treating malignancies, surpassing standard chemoradiotherapy and surgical procedures. Gynecological malignancies, including cervical, endometrial, and ovarian carcinoma, have a bad prognosis in advanced or metastatic stages and are difficult to treat. The advancements in understanding the molecular pathways behind cancer development offer valuable insights into promising targeted medicines, and researchers have always searched for a superior and safe technique to target cancer-related oncoproteins because of the limited therapeutic benefit, drug resistance, and off-target effects of current targeted treatments. Recently, proteolysis-targeting chimeras (PROTACs) have been developed to selectively degrade proteins using the natural ubiquitin-proteasome system (UPS). These approaches have garnered significant attention in the field of cancer research. The rapid progress in PROTACs has also eased the targeting of various oncoproteins in gynecological cancer. Therefore, this review aims to elucidate the mechanism and research advancements of PROTACs and provide a comprehensive overview of their use in gynecological tumors. [ABSTRACT FROM AUTHOR]

This poster demonstrates the development of drug-resistant cancer cell lines and their application in cancer research. [ABSTRACT FROM AUTHOR]

Cancer is a major disease endangering human health. More and more studies have shown that microorganisms play an extremely important role in the occurrence, development and treatment of tumors. As a very promising tumor treatment strategy, immunotherapy has also been proved to have a great relationship with microorganisms. Here, the authors review the contribution of the microbiota to cancer and the research on its impact on cancer immunotherapy. We also highlight the possible mechanism of their interaction and outlined the potential application of microbiota in tumor immunotherapy. [ABSTRACT FROM AUTHOR]

Circular RNAs (circRNAs) are non-coding single-stranded covalently closed circular RNA, mainly produced by reverse splicing of exons of precursor mRNAs (pre-mRNAs). The characteristics of high abundance, strong specificity, and good stability of circRNAs have been discovered. A large number of studies have reported its various functions and mechanisms in biological events, such as the occurrence and development of cancer. In this review, we focus on the classification, characterization, biogenesis, functions of circRNAs, and the latest advances in cancer research. The development of circRNAs as biomarkers in cancer diagnosis and treatment also provides new ideas for studying circRNAs research. [ABSTRACT FROM AUTHOR]

Human sterile α motif and HD domain-containing protein 1 (SAMHD1), originally described as the major cellular deoxyribonucleoside triphosphate triphosphohydrolase (dNTPase) balancing the intracellular deoxynucleotide (dNTP) pool, has come recently into focus of cancer research. As outlined in this review, SAMHD1 has been reported to be mutated in a variety of cancer types and the expression of SAMHD1 is dysregulated in many cancers. Therefore, SAMHD1 is regarded as a tumor suppressor in certain tumors. Moreover, it has been proposed that SAMHD1 might fulfill the requirements of a driver gene in tumor development or might promote a so-called mutator phenotype. Besides its role as a dNTPase, several novel cellular functions of SAMHD1 have come to light only recently, including a role as negative regulator of innate immune responses and as facilitator of DNA end resection during DNA replication and repair. Therefore, SAMHD1 can be placed at the crossroads of various cellular processes. The present review summarizes the negative role of SAMHD1 in chemotherapy sensitivity, highlights reported SAMHD1 mutations found in various cancer types, and aims to discuss functional consequences as well as underlying mechanisms of SAMHD1 dysregulation potentially involved in cancer development. [ABSTRACT FROM AUTHOR]

The founding of the National Cancer Institute in 1937 was attended by the formation of the National Advisory Council on Cancer. A seminal action by this Council was the funding of the First National Cancer Survey, the first population-based cancer surveillance activity of the federal government. Francis Carter Wood, distinguished cancer researcher and editor of the American Journal of Cancer (predecessor to Cancer Research), was a member of that Council, through which he was a prime mover in the funding of this survey. This action reflected Wood's commitment to population-based cancer surveillance, voiced over more than two decades. Such commitment reflected his view that only such data could identify the optimal treatment modality for cancer patients. The implications of this view, with epidemiologic data providing insights on treatment rather than prevention of disease, as the basis for the development of cancer epidemiology are then considered. [ABSTRACT FROM AUTHOR]

Background: Every year, the American Thyroid Association (ATA) Annual Meeting opening session features presentations covering the most recent advances in the three major areas of thyroidology: basic, clinical, and surgical. As the ATA did not have an annual meeting in 2020, because of the COVID19 pandemic, the 2021 meeting opened with a special "Two Years in Thyroidology" session. Methods: A PubMed electronic search was conducted to identify original basic science research studies on thyroid cancer published between October 2019 and September 2021. Methodologically rigorous studies that were deemed most likely to influence the field of basic science research in thyroid cancer were grouped into three thematic units: Genetics and Genomics, Molecular Biology and Signaling, and Preclinical and Translational Science. Four publications for each category were chosen for discussion. Results: Selected studies covered topics ranging from the genetics of thyroid cancer predisposition to the genomics of anaplastic thyroid cancer evolution, from novel molecular pathways involved in thyroid cancer pathogenesis to potentially game-changing imaging and therapeutic innovations. Conclusions: The past two years, in the face of unique COVID19 pandemic-associated hurdles, have witnessed a large number of important developments in basic and translational thyroid cancer research. These studies not only have shed novel light on a number of long-standing scientific questions but have also highlighted the major challenges and open questions that still remain to be addressed in the coming years. [ABSTRACT FROM AUTHOR]

Objective: The objective of this review was to examine the comprehensive role of microbiota in epithelial ovarian carcinogenesis. Methods: A scoping review method was used, and relevant databases were searched using combinations of key terms. Human and animal studies were selected that met inclusion criteria and critical appraisal tools were used to assess study quality. Results: A total of 10 international studies (human n = 8; animal n = 2) were included with total samples sizes varying from 16 to 580. Mean/median ages of women with epithelial ovarian cancer (EOC) were 50.5 to 66 years, and controls were 47.3 to 56 years. Compared to the ovaries and fallopian tubes of women without disease, tissue collected from women with EOC were characterized by differing proportions of bacterial phyla including Actinobacteria, Bacteroidetes, Chlamydiae, Firmicutes, and Proteobacteria. Intestinal depletions and reduced diversity of genera Lactobacillus accelerated ovarian tumor growth in animal models. Cytomegalovirus and human papillomavirus types 6, 16, 18, and 45 had a significantly higher prevalence in women with disease and represented up to 70% of cases with high-grade serous ovarian carcinoma. Colonized bacteria were detected in fallopian tubes, peritoneal fluid, and ovarian tissue similar to that of commensal GI tract and vaginal bacteria. Conclusion: The EOC microenvironment harbors diverse microbes. Due to the heterogeneity of microbiota identified between studies, additional research is needed to reconcile findings and ascertain clinical applicability. Future investigations should also examine potential associations between EOC tumor, gut, and vaginal microbiota, patient symptoms throughout disease, chemotherapy response, recurrence, and survival. [ABSTRACT FROM AUTHOR]

Complex heterogeneity is an important characteristic in the development of prostate cancer (PCa), which further leads to the failure of known therapeutic options. PCa research has been hampered by the current in vitro model systems that cannot fully reflect the biological characteristics and clinical diversity of PCa. The tumor organoid model in three-dimensional culture retains the heterogeneity of primary tumor tissues in vitro well and enables high-throughput screening and genome editing. Therefore, the establishment of a PCa organoid model that recapitulates the diverse heterogeneity observed in clinical settings is of great significance for the study of PCa. In this review, we summarize the culture conditions, establishments, and limitations of PCa organoids and further review their application for the study of pathogenesis, drug screening, mechanism of drug resistance, and individualized treatment for PCa. Additionally, we look forward to other potential developmental directions of PCa organoids, such as the interaction between prostate cancer tumor cells and their microenvironment, clinical individualized treatments, heterogeneous transformation model, tumor immunotherapy, and organoid models combined with liquid biopsy. Through this, we provide more effective preclinical experimental schemes using the PCa organoid model. [ABSTRACT FROM AUTHOR]

Scientists engaged in prostate cancer research have been conducting experiments using two‐dimensional cultures of prostate cancer cell lines for decades. However, these experiments fail to reproduce and reflect the clinical course of individual patients with prostate cancer, or the molecular and genetic characteristics of prostate cancer, the basic requirement for most of the preclinical studies on prostate cancer. The use of human prostate cancer tissues in experiments has enabled the collection and verification of clinically relevant data, including chemical reactions, changes in proteins, and specific gene expression. Tissue recombination models have been employed for studying prostate development, the initiation and progression of prostate cancer, and the tumor microenvironment. Notably, the epithelial–stromal interaction, which might play a critical role in prostate cancer pathogenesis, can be reproduced in this model. Patient‐derived xenograft models have been developed as powerful avatars comprising patient‐derived prostate cancer tissues implanted in immunocompromised mice and could serve as a precision medicine approach for each prostate cancer patient. Spheroid and organoid assays, representative of modern three‐dimensional cultures, can replicate the conditions in human prostate tumors and the prostate organ itself as a miniature model. Although an intact immune system against the tumor is missing from the models aimed at investigating immuno‐oncological reagents in various malignancies, all these experimental models can help researchers in developing new drugs and selecting appropriate treatment strategies for prostate cancer patients. [ABSTRACT FROM AUTHOR]

Glucose regulated protein 78 (GRP 78), a master regulator of endoplasmic reticulum stress has been reported to be up regulated in various cancers and remains a crucial link between tumor glycolysis and tumor microenvironment. Overexpressed GRP78 has also shown to induce immune suppressive molecules and thereby tumor immune evasion. On the other hand emerging reports indicates that the next generation hallmarks viz., metabolic reprogramming and immune evasion, the two distinct processes are suggested to be fundamentally linked which is yet to be explored. Our concern is, if GRP78 is considered as a connecting link between these two different processes then targeting this triangle would be a promising approach in anticancer drug discovery. Lack of sufficient literature on this aspect represents GRP78 as an under explored target in anti-cancer research. The objective of this review is to provide a concise and integrated information on GRP78 and its association with tumor glycolysis and immune evasion which will revive and draw attention of the researchers to consider GRP78 as a potential drug target for cancer intervention and it also highlights few potential natural products investigated so far as GRP78 inhibitors. Image 1 • GRP78 overexpression is reported in various cancers. • Emerging hall marks of cancer includes metabolic reprogramming and immune evasion. • Increased GRP78 influence energy metabolism and immune evasion. • Crosstalk might exist between GRP78-tumor glycolysis-immune evasion. • Very few natural products have been investigated as GRP78 modulators. [ABSTRACT FROM AUTHOR]

RIO (right open reading frame) family of kinases including RIOK1, RIOK2 and RIOK3 are known for their role in the ribosomal biogenesis. Dysfunction of RIO kinases have been implicated in malignancies, including acute myeloid leukemia, glioma, breast, colorectal, lung and prostatic adenocarcinoma suggesting RIO kinases as potential targets in cancer. In vitro , in vivo and clinical studies have demonstrated that RIO kinases are overexpressed in various types of cancers suggesting important roles in tumorigenesis, especially in metastasis. In the context of malignancies, RIO kinases are involved in cancer-promoting pathways including AKT/mTOR, RAS, p53 and NF-κB and cell cycle regulation. Here we review the role of RIO kinases in cancer development emphasizing their potential as therapeutic target and encouraging further development and investigation of inhibitors in the context of cancer. [ABSTRACT FROM AUTHOR]

This document is a correction notice for an article titled "Helicobacter pylori CagA promotes epithelial mesenchymal transition in gastric carcinogenesis via triggering oncogenic YAP pathway" published in the Journal of Experimental & Clinical Cancer Research. The correction states that duplicate images were found in Figure 7b and Figure 7d of the original article. The correct figure is provided in the correction notice. The authors of the article are listed as Nianshuang Li, Yan Feng, Yi Hu, Cong He, Chuan Xie, Yaobin Ouyang, Stephen C. Artim, Deqiang Huang, Yin Zhu, Zhijun Luo, Zhongming Ge, and Nonghua Lu. [Extracted from the article]