Search for Articles:
Title / Keyword
Author / Affiliation / Email
Journal
Article Type
 
 
Advanced Search
 
Section
Special Issue
Volume
Issue
Number
Page
 
8.0
4.5
Journals
Cancers
Special Issues
Advances in Personalized Medicine of Cancers
share announcement

Advances in Personalized Medicine of Cancers

A special issue of Cancers (ISSN 2072-6694). This special issue belongs to the section "Molecular Cancer Biology".

Deadline for manuscript submissions: closed (28 February 2025) | Viewed by 7423

Special Issue Editor

Dr. Shigenori Kadowaki

E-Mail Website
Guest Editor
Department of Clinical Oncology, Aichi Cancer Center Hospital, Nagoya 464-8681, Aichi, Japan
Interests: trastuzumab; chemotherapy; gastric cancer

Special Issue Information

Dear Colleagues,

Personalized medicine (PM), also referred to as precision medicine in oncology, is an emerging approach to tumor treatment and prevention. The evolving field of personalized medicine is playing an increasingly important role in cancer prevention, diagnosis, prognosis, and therapeutics.

Personalized cancer medicine focuses on human genes and the genes in different cancers, and the research results make the treatment more effective. Moreover, genetic information can be used to develop tests for cancer and ways to prevent it.

In addition, the field of personalized medicine has become extremely active in the identification of predictive biomarkers, which is the essence of personalized oncology. These biomarkers can be from tissue, serum, urine, or imaging and must be validated. Genomics and proteomics have provided a means for molecular profiling to identify biomarkers. The rapid development of newer technologies in omics and platforms provides hope for personalized medicine.

The aim of this Special Issue is to analyze the evolution of cancer treatment toward a precision approach and its role in cancer prevention and treatment, as well as its future direction in oncology.

Dr. Shigenori Kadowaki
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 100 words) can be sent to the Editorial Office for announcement on this website.

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-blind 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

  • personalized medicine
  • biomarkers
  • genomics
  • proteomics
  • personalized oncology

Benefits of Publishing in a Special Issue

  • Ease of navigation: Grouping papers by topic helps scholars navigate broad scope journals more efficiently.
  • Greater discoverability: Special Issues support the reach and impact of scientific research. Articles in Special Issues are more discoverable and cited more frequently.
  • Expansion of research network: Special Issues facilitate connections among authors, fostering scientific collaborations.
  • External promotion: Articles in Special Issues are often promoted through the journal's social media, increasing their visibility.
  • Reprint: MDPI Books provides the opportunity to republish successful Special Issues in book format, both online and in print.

Further information on MDPI's Special Issue policies can be found here.

Published Papers (3 papers)

Download All Papers
Order results
Result details
Show export options expand_more Show export options expand_less
Select all
Export citation of selected articles as:

Research

15 pages, 1266 KiB  
Article
Dkk1 as a Prognostic Marker for Neoadjuvant Chemotherapy Response in Breast Cancer Patients
by Mariz Kasoha, Anna K. Steinbach, Rainer M. Bohle, Barbara Linxweiler, Bashar Haj Hamoud, Merle Doerk, Meletios P. Nigdelis, Lisa Stotz, Julia S. M. Zimmermann, Erich-Franz Solomayer, Askin C. Kaya and Julia C. Radosa
Cancers 2024, 16(2), 419; https://doi.org/10.3390/cancers16020419 - 18 Jan 2024
Cited by 1 | Viewed by 1776
Abstract
Purpose: To investigate the role of Dkk1 as a predictor of response to NACT in BC patients. Methods: This retrospective monocentric study included 145 women who had undergone NACT followed by breast surgery. Dkk1 protein expression was assessed using immunohistochemistry staining in core [...] Read more.
Purpose: To investigate the role of Dkk1 as a predictor of response to NACT in BC patients. Methods: This retrospective monocentric study included 145 women who had undergone NACT followed by breast surgery. Dkk1 protein expression was assessed using immunohistochemistry staining in core needle biopsies and mammary carcinoma specimens. Results: Dkk1 levels were lower in treated BC tumours than in untreated tumours. The outcomes of 68 matched pre- and post-therapy tissues showed that Dkk1 levels in mammary carcinoma tissues were significantly predicted by levels in core needle biopsies and that Dkk1 expression was reduced in 83% of cases. Smaller cT stage, positive Her2 expression, and decreased Dkk1-IRS in core needle biopsy tissues were all independent predictors of regression grade (R4), according to Sinn. However, the percentage of Dkk1 expression differences prior to and following NACT had no effect on PFS or OS. Conclusions: In this study, we demonstrated for the first time that Dkk1 could be identified as an independent predictor of NACT response in BC patients, particularly those with TNBC. Further research with a multicentric expanded (pre-/post-therapy) sample set and better-defined populations in terms of molecular subtypes, therapy modality, and long-term follow-up is recommended to obtain more solid evidence. Full article
(This article belongs to the Special Issue Advances in Personalized Medicine of Cancers)
►▼ Show Figures

Figure 1

11 pages, 850 KiB  
Communication
Technological Convergence: Highlighting the Power of CRISPR Single-Cell Perturbation Toolkit for Functional Interrogation of Enhancers
by Reza Ghamsari, Joseph Rosenbluh, A Vipin Menon, Nigel H. Lovell and Hamid Alinejad-Rokny
Cancers 2023, 15(14), 3566; https://doi.org/10.3390/cancers15143566 - 11 Jul 2023
Cited by 1 | Viewed by 2453
Abstract
Higher eukaryotic enhancers, as a major class of regulatory elements, play a crucial role in the regulation of gene expression. Over the last decade, the development of sequencing technologies has flooded researchers with transcriptome-phenotype data alongside emerging candidate regulatory elements. Since most methods [...] Read more.
Higher eukaryotic enhancers, as a major class of regulatory elements, play a crucial role in the regulation of gene expression. Over the last decade, the development of sequencing technologies has flooded researchers with transcriptome-phenotype data alongside emerging candidate regulatory elements. Since most methods can only provide hints about enhancer function, there have been attempts to develop experimental and computational approaches that can bridge the gap in the causal relationship between regulatory regions and phenotypes. The coupling of two state-of-the-art technologies, also referred to as crisprQTL, has emerged as a promising high-throughput toolkit for addressing this question. This review provides an overview of the importance of studying enhancers, the core molecular foundation of crisprQTL, and recent studies utilizing crisprQTL to interrogate enhancer-phenotype correlations. Additionally, we discuss computational methods currently employed for crisprQTL data analysis. We conclude by pointing out common challenges, making recommendations, and looking at future prospects, with the aim of providing researchers with an overview of crisprQTL as an important toolkit for studying enhancers. Full article
(This article belongs to the Special Issue Advances in Personalized Medicine of Cancers)
►▼ Show Figures

Figure 1

18 pages, 6104 KiB  
Article
RBM38 Reverses Sorafenib Resistance in Hepatocellular Carcinoma Cells by Combining and Promoting lncRNA-GAS5
by Xing Gao, Cheng Lu, Ziyu Liu, Yan Lin, Julu Huang, Lu Lu, Shuanghang Li, Xi Huang, Minchao Tang, Shilin Huang, Ziqin He, Xiaomin She, Rong Liang and Jiazhou Ye
Cancers 2023, 15(11), 2897; https://doi.org/10.3390/cancers15112897 - 24 May 2023
Cited by 4 | Viewed by 2358
Abstract
Background: Hepatocellular carcinoma (HCC) is a life-threatening human malignancy and the fourth leading cause of cancer-related deaths worldwide. Patients with HCC are often diagnosed at an advanced stage with a poor prognosis. Sorafenib is a multikinase inhibitor used as the first-line treatment for [...] Read more.
Background: Hepatocellular carcinoma (HCC) is a life-threatening human malignancy and the fourth leading cause of cancer-related deaths worldwide. Patients with HCC are often diagnosed at an advanced stage with a poor prognosis. Sorafenib is a multikinase inhibitor used as the first-line treatment for patients with advanced HCC. However, acquired resistance to sorafenib in HCC leads to tumor aggression and limits the drug’s survival benefits; the underlying molecular mechanisms for this resistance remain unclear. Methods: This study aimed to examine the role of the tumor suppressor RBM38 in HCC, and its potential to reverse sorafenib resistance. In addition, the molecular mechanisms underlying the binding of RBM38 and the lncRNA GAS5 were examined. The potential involvement of RBM38 in sorafenib resistance was examined using both in vitro and in vivo models. Functional assays were performed to assess whether RBM38: binds to and promotes the stability of the lncRNA GAS5; reverses the resistance of HCC to sorafenib in vitro; and suppresses the tumorigenicity of sorafenib-resistant HCC cells in vivo. Results: RBM38 expression was lower in HCC cells. The IC50 value of sorafenib was significantly lower in cells with RBM38 overexpression than in control cells. RBM38 overexpression improved sorafenib sensitivity in ectopic transplanted tumors and suppressed the growth rate of tumor cells. RBM38 could bind to and stabilize GAS5 in sorafenib-resistant HCC cells. In addition, functional assays revealed that RBM38 reversed sorafenib resistance both in vivo and in vitro in a GAS5-dependent manner. Conclusions: RBM38 is a novel therapeutic target that can reverse sorafenib resistance in HCC by combining and promoting the lncRNA GAS5. Full article
(This article belongs to the Special Issue Advances in Personalized Medicine of Cancers)
►▼ Show Figures

Figure 1

Show export options expand_more Show export options expand_less
Select all
Export citation of selected articles as:
 
Displaying articles 1-3
Back to TopTop