Individualized Molecular Mechanisms and Treatment in Tumor Metastasis

Topic Information

Dear Colleagues,

The purpose and scope of tumor metastasis are still a challenge for personalized tumor therapy and an important reason for the poor prognosis of tumor patients. In recent years, researchers have attempted to apply genomics, transcriptomic, and proteomic techniques to establish reasonably stable animal tumor metastasis models to explore the internal tumor microenvironment and molecular mechanisms during the process of metastasis and subsequently study the potential drug targets in metastatic tumors. However, even the metastatic process of a specific tumor has individual characteristics. With the progress of research in this field, more and more mechanisms related to the metastatic process have been reported, such as exosomes, the tumor metabolism, etc. Therefore, the complexity of tumor metastasis brings difficulties and challenges, and more advanced research is urgently needed. This Special Collection aims to collect recent advances in the pathogenesis and treatment strategies of metastatic neoplastic processes. Potential submissions include but are not limited to:

• The latest research on the process of tumor metastasis, such as vascular invasion, pre-metastatic niche formation, engraftment of metastases, and resistance to anoikis;
• The latest research on the role of the tumor microenvironment in tumor metastasis, including the interaction of tumor cells and non-tumor cells, spatiotemporal changes of the tumor microenvironment, multi-omics-based exploration of the tumor microenvironment, and drug resistance in metastatic tumors.

Dr. Dong Tang
Dr. Chen Liu
Prof. Dr. Bin Cheng
Topic Editors

Keywords

Participating Journals

Journal Name	Impact Factor	CiteScore	Launched Year	First Decision (median)	APC
Biomedicines biomedicines	4.7	3.7	2013	15.4 Days	CHF 2600	Submit
Cancers cancers	5.2	7.4	2009	17.9 Days	CHF 2900	Submit
Current Oncology curroncol	2.6	2.6	1994	18 Days	CHF 2200	Submit
Onco onco	-	-	2021	18.3 Days	CHF 1000	Submit
Pathophysiology pathophysiology	-	2.8	1994	22.6 Days	CHF 1400	Submit

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Published Papers (4 papers)

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All Biomedicines Cancers Current Oncology Onco Pathophysiology

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Open AccessArticle

Patient Derived Xenografts (PDX) Models as an Avatar to Assess Personalized Therapy Options in Uveal Melanoma: A Feasibility Study

by Fariba Nemati, Leanne de Koning, David Gentien, Franck Assayag, Emilie Henry, Khadija Ait Rais, Gaelle Pierron, Odette Mariani, Michèle Nijnikoff, Gabriel Champenois, André Nicolas, Didier Meseure, Sophie Gardrat, Nicolas Servant, Philippe Hupé, Maud Kamal, Christophe Le Tourneau, Sophie Piperno-Neumann, Manuel Rodrigues, Sergio Roman-Roman, Didier Decaudin, Pascale Mariani and Nathalie Cassouxadd Show full author list remove Hide full author list

Curr. Oncol. 2023, 30(10), 9090-9103; https://doi.org/10.3390/curroncol30100657 - 11 Oct 2023

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Abstract

Uveal melanoma is the most common primary intraocular malignancy in adults. Up to 50% of UM patients develop metastatic disease, usually in the liver. When metastatic, the prognosis is poor, and few treatment options exist. Here, we investigated the feasibility of establishing patient-derived [...] Read more.

Uveal melanoma is the most common primary intraocular malignancy in adults. Up to 50% of UM patients develop metastatic disease, usually in the liver. When metastatic, the prognosis is poor, and few treatment options exist. Here, we investigated the feasibility of establishing patient-derived xenografts (PDXs) from a patient’s tumor in order to screen for therapies that the patient could benefit from. Samples obtained from 29 primary tumors and liver metastases of uveal melanoma were grafted into SCID mice. PDX models were successfully established for 35% of primary patient tumors and 67% of liver metastases. The tumor take rate was proportional to the risk of metastases. PDXs showed the same morphology, the same GNAQ/11, BAP1, and SF3B1 mutations, and the same chromosome 3 and 8q status as the corresponding patient samples. Six PDX models were challenged with two compounds for 4 weeks. We show that, for 31% of patients with high or intermediate risk of metastasis, the timing to obtain efficacy results on PDX models derived from their primary tumors was compatible with the selection of the therapy to treat the patient after relapse. PDXs could thus be a valid tool (“avatar”) to select the best personalized therapy for one third of patients that are most at risk of relapse. Full article

(This article belongs to the Topic Individualized Molecular Mechanisms and Treatment in Tumor Metastasis)

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15 pages, 7800 KiB  

Open AccessArticle

ATF4 Transcriptionally Activates SHH to Promote Proliferation, Invasion, and Migration of Gastric Cancer Cells

by Yang Wang, Muhammad Ali, Qi Zhang, Qiannan Sun, Jun Ren, Wei Wang, Dong Tang and Daorong Wang

Cancers 2023, 15(5), 1429; https://doi.org/10.3390/cancers15051429 - 23 Feb 2023

Cited by 3 | Viewed by 1632

Abstract

Activating transcription factor 4 (ATF4) is a DNA-binding protein widely generated in mammals, which has two biological characteristics that bind the cAMP response element (CRE). The mechanism of ATF4 as a transcription factor in gastric cancer affecting the Hedgehog pathway remains unclear. Here, [...] Read more.

Activating transcription factor 4 (ATF4) is a DNA-binding protein widely generated in mammals, which has two biological characteristics that bind the cAMP response element (CRE). The mechanism of ATF4 as a transcription factor in gastric cancer affecting the Hedgehog pathway remains unclear. Here, we observed that ATF4 was markedly upregulated in gastric cancer (GC) using immunohistochemistry and Western blotting assays in 80 paraffin-embedded GC samples and 4 fresh samples and para-cancerous tissues. ATF4 knockdown using lentiviral vectors strongly inhibited the proliferation and invasion of GC cells. ATF4 upregulation using lentiviral vectors promoted the proliferation and invasion of GC cells. We predicted that the transcription factor ATF4 is bound to the SHH promoter via the JASPA database. Transcription factor ATF4 is bound to the promoter region of SHH to activate the Sonic Hedgehog pathway. Mechanistically, rescue assays showed that ATF4 regulated gastric cancer cells’ proliferation and invasive ability through SHH. Similarly, ATF4 enhanced the tumor formation of GC cells in a xenograft model. Full article

(This article belongs to the Topic Individualized Molecular Mechanisms and Treatment in Tumor Metastasis)

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15 pages, 3165 KiB  

Open AccessArticle

Expression Profiles of Cuproptosis-Related Genes Determine Distinct Subtypes of Pancreatic Ductal Adenocarcinoma

by Yusheng Chen, Xuan Zou, Mingjian Ma, Yu Liu, Ruijie Wang, Zhengjie Dai, Yesiboli Tashiheng, Yu Yan, Xianjun Yu, Xu Wang, Chen Liu, Xuan Lin and He Cheng

Curr. Oncol. 2023, 30(2), 1648-1662; https://doi.org/10.3390/curroncol30020126 - 29 Jan 2023

Cited by 1 | Viewed by 2077

Abstract

Background: Pancreatic ductal adenocarcinoma (PDAC) is the most prevalent subtype of pancreatic cancer and one of the most malignant tumors worldwide. Due to the heterogeneity of its genomics and proteomics, the prognosis of PDAC remains disappointing despite advances in surgery and medicines. Recently, [...] Read more.

Background: Pancreatic ductal adenocarcinoma (PDAC) is the most prevalent subtype of pancreatic cancer and one of the most malignant tumors worldwide. Due to the heterogeneity of its genomics and proteomics, the prognosis of PDAC remains disappointing despite advances in surgery and medicines. Recently, a novel form of programmed cell death, cuproptosis, was proposed, although its role in PDAC has not been investigated. This study aimed to quantify the expression of cuproptosis-related genes and characterize the novel subtypes of PDAC. Methods: To evaluate the pattern of cuproptosis in PDAC, the gene expression data and clinical information of 372 samples were collected from the Cancer Genome Atlas (TCGA) and Gene Expression Omnibus (GEO) databases. A consensus cluster analysis was performed using the transcriptional levels, genetic alterations, and individual prognostic values of seven pre-selected cuproptosis-related genes (DLAT, LIPT1, FDX1, DLD, PDHB, PDHA1, and LIAS) to identify the novel subtypes associated with cuproptosis in PDAC. A univariate Cox regression analysis was used to determine the significant prognostic indicators and cuproptosis scores among the differentially expressed genes (DEGs) between the dividing subclusters, followed by a principal component analysis. The prognostic values, immune profiles, treatment sensitivities, and cuproptosis scores were evaluated between the different subgroups. Results: Seven cuproptosis-related genes showed aberrant expression levels and genetic alterations in the PDAC tumor microenvironment. Among them, LIPT1, LIAS, DLAT, PDHA1, and DLD were significantly correlated with overall survival. Based on the expression profiles of the seven cuproptosis-related genes, three cuproptosis clusters (Clusters A, B, and C) were identified, which were represented by different clinicopathologic features, gene expression levels, and biological processes. A total of 686 DEGs were identified among the three cuproptosis clusters, of which 35 prognosis-related DEGs were selected to further classify the PDAC samples into two subgroups with different survival rates, clinicopathologic features, immune infiltration levels, and drug sensitivities. Higher cuproptosis scores were associated with a significantly poorer prognosis. Conclusion: The cuproptosis subtypes, scores, and relevant genes represent valuable information for assessing the heterogeneity, treatment, and prognosis of PDAC. Full article

(This article belongs to the Topic Individualized Molecular Mechanisms and Treatment in Tumor Metastasis)

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Open AccessReview

Intestinal Microbiota: The Driving Force behind Advances in Cancer Immunotherapy

by Zhujiang Dai, Jihong Fu, Xiang Peng, Dong Tang and Jinglue Song

Cancers 2022, 14(19), 4796; https://doi.org/10.3390/cancers14194796 - 30 Sep 2022

Cited by 4 | Viewed by 2136

Abstract

In recent years, cancer immunotherapy has become a breakthrough method to solve solid tumors. It uses immune checkpoint inhibitors to interfere with tumor immune escape to coordinate anti-tumor therapy. However, immunotherapy has an individualized response rate. Moreover, immune-related adverse events and drug resistance [...] Read more.

In recent years, cancer immunotherapy has become a breakthrough method to solve solid tumors. It uses immune checkpoint inhibitors to interfere with tumor immune escape to coordinate anti-tumor therapy. However, immunotherapy has an individualized response rate. Moreover, immune-related adverse events and drug resistance are still urgent issues that need to be resolved, which may be attributed to the immune imbalance caused by immune checkpoint inhibitors. Microbiome research has fully revealed the metabolic-immune interaction relationship between the microbiome and the host. Surprisingly, sequencing technology further proved that intestinal microbiota could effectively intervene in tumor immunotherapy and reduce the incidence of adverse events. Therefore, cancer immunotherapy under the intervention of intestinal microbiota has innovatively broadened the anti-tumor landscape and is expected to become an active strategy to enhance individualized responses. Full article

(This article belongs to the Topic Individualized Molecular Mechanisms and Treatment in Tumor Metastasis)

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