Search for Articles:
Title / Keyword
Author / Affiliation / Email
Journal
Article Type
 
 
Advanced Search
 
Section
Special Issue
Volume
Issue
Number
Page
 
7.4
5.2
Journals
Cancers
Special Issues
Molecular Insights into Drug Resistance in Cancer
share announcement

Molecular Insights into Drug Resistance in Cancer

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

Deadline for manuscript submissions: 30 June 2024 | Viewed by 4908

Special Issue Editor

Dr. Yang Yuqi

E-Mail Website
Guest Editor
Department of Pharmaceutical Sciences, College of Pharmacy and Health Sciences, St. John's University, Queens, NY 11439, USA
Interests: multidrug resistance in cancer

Special Issue Information

Dear Colleagues,

Accumulating evidence from research and clinics has suggested that cancer cells can become resistant to cancer therapy, resulting in treatment failure and poor prognosis. Because of resistance, exploring molecular mechanisms and developing therapeutic strategies are necessary to overcome drug resistance in cancer treatment.

We are pleased to invite you to submit a research article or review that fall within the scope of this special issue.

This Special Issue aims to investigate novel mechanisms of action on drug resistance in cancer, and/or potential strategies for overcoming drug resistance in cancer patients.

In this Special Issue, original research articles and reviews are welcome. Research areas may include (but are not limited to) the following:

  • Insights into molecular mechanism involved in drug resistance in cancer.
  • Crosstalk between drug resistance and cancer treatment.
  • Strategies for improving the efficacy of current FDA-approved anticancer drugs.
  • Development of new drugs against drug resistance in cancer.
  • Combination therapy strategies against tumor resistance.
  • Approaches that can improve prognosis and the quality of cancer patient’s life during cancer treatment.

We look forward to receiving your contributions. In addition, you may share this special issue with your team members and colleagues; student co-authors are most welcome. It would be great if you were interested in participating, and I hope to continue this endeavor together.

Dr. Yang Yuqi
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 short 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

  • drug resistance
  • cancer treatment
  • molecular mechanism
  • chemotherapeutic therapy
  • small molecules
  • biologics/large molecules
  • leukemia
  • solid tumor

Published Papers (4 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

Jump to: Review, Other

9 pages, 609 KiB  
Communication
Are We Losing the Final Fight against Cancer?
by Guy Storme
Cancers 2024, 16(2), 421; https://doi.org/10.3390/cancers16020421 - 19 Jan 2024
Viewed by 996
Abstract
Despite our increasing understanding of the biology and evolution of the cancer process, it is indisputable that the natural process of cancer creation has become increasingly difficult to cure, as more mutations are found with age. It is significantly more difficult to challenge [...] Read more.
Despite our increasing understanding of the biology and evolution of the cancer process, it is indisputable that the natural process of cancer creation has become increasingly difficult to cure, as more mutations are found with age. It is significantly more difficult to challenge the curative method when there is heterogeneity within the tumor, as it hampers clinical and genetic categorization. With advances in diagnostic technologies and screening leading to progressive tumor shrinkage, it becomes more difficult over time to evaluate the effects of treatment on overall survival. New treatments are often authorized based on early evidence, such as tumor response; disease-free, progression-free, meta-static-free, and event-free survival; and, less frequently, based on clinical endpoints, such as overall survival or quality of life, when standard guidelines are not available to approve pharmaceuticals. These clearances usually happen quite rapidly. Although approval takes longer, relative survival demonstrates the genuine worth of a novel medication. Pressure is being applied by pharmaceutical companies and patient groups to approve “new” treatments based on one of the above-listed measures, with results that are frequently insignificantly beneficial and frequently have no impact on quality of life. Full article
(This article belongs to the Special Issue Molecular Insights into Drug Resistance in Cancer)
►▼ Show Figures

Figure 1

23 pages, 4745 KiB  
Article
A Comprehensive Bioinformatic Analysis of RNA-seq Datasets Reveals a Differential and Variable Expression of Wildtype and Variant UGT1A Transcripts in Human Tissues and Their Deregulation in Cancers
by Dong Gui Hu, Shashikanth Marri, Julie-Ann Hulin, Ross A. McKinnon, Peter I. Mackenzie and Robyn Meech
Cancers 2024, 16(2), 353; https://doi.org/10.3390/cancers16020353 - 13 Jan 2024
Viewed by 1051
Abstract
The UGT1A locus generates over 60 different alternatively spliced transcripts and 30 circular RNAs. To date, v2 and v3 transcripts are the only variant UGT1A transcripts that have been functionally characterized. Both v2 and v3 transcripts encode the same inactive variant UGT1A proteins [...] Read more.
The UGT1A locus generates over 60 different alternatively spliced transcripts and 30 circular RNAs. To date, v2 and v3 transcripts are the only variant UGT1A transcripts that have been functionally characterized. Both v2 and v3 transcripts encode the same inactive variant UGT1A proteins (i2s) that can negatively regulate glucuronidation activity and influence cancer cell metabolism. However, the abundance and interindividual variability in the expression of v2 and v3 transcripts in human tissues and their potential deregulation in cancers have not been comprehensively assessed. To address this knowledge gap, we quantified the expression levels of v1, v2, and v3 transcripts using RNA-seq datasets with large cohorts of normal tissues and paired normal and tumor tissues from patients with six different cancer types (liver, kidney, colon, stomach, esophagus, and bladder cancer). We found that v2 and v3 abundance varied significantly between different tissue types, and that interindividual variation was also high within the same tissue type. Moreover, the ratio of v2 to v3 variants varied between tissues, implying their differential regulation. Our results showed higher v2 abundance in gastrointestinal tissues than liver and kidney tissues, suggesting a more significant negative regulation of glucuronidation by i2 proteins in gastrointestinal tissues than in liver and kidney tissues. We further showed differential deregulation of wildtype (v1) and variant transcripts (v2, v3) in cancers that generally increased the v2/v1 and/or v3/v1 expression ratios in tumors compared to normal tissues, indicating a more significant role of the variants in tumors. Finally, we report ten novel UGT1A transcripts with novel 3′ terminal exons, most of which encode variant proteins with a similar structure to UGT1A_i2 proteins. These findings further emphasize the diversity of the UGT1A transcriptome and proteome. Full article
(This article belongs to the Special Issue Molecular Insights into Drug Resistance in Cancer)
►▼ Show Figures

Figure 1

Review

Jump to: Research, Other

22 pages, 332 KiB  
Review
Ocular Surface Side Effects of Novel Anticancer Drugs
by Livio Vitiello, Filippo Lixi, Giulia Coco and Giuseppe Giannaccare
Cancers 2024, 16(2), 344; https://doi.org/10.3390/cancers16020344 - 13 Jan 2024
Viewed by 1285
Abstract
Surgery, anticancer drugs (chemotherapy, hormonal medicines, and targeted treatments), and/or radiation are common treatment strategies for neoplastic diseases. Anticancer drugs eliminate malignant cells through the inhibition of specific pathways that contribute to the formation and development of cancer. Given the ability of such [...] Read more.
Surgery, anticancer drugs (chemotherapy, hormonal medicines, and targeted treatments), and/or radiation are common treatment strategies for neoplastic diseases. Anticancer drugs eliminate malignant cells through the inhibition of specific pathways that contribute to the formation and development of cancer. Given the ability of such pharmacological medications to combat cancerous cells, their role in the management of neoplastic diseases has become essential. However, these drugs may also lead to undesirable systemic and ocular adverse effects due to cyto/neuro-toxicity and inflammatory reactions. Ocular surface side effects are recognized to significantly impact patient’s quality of life and quality of vision. Blepharoconjunctivitis is known to be a common side effect caused by oxaliplatin, cyclophosphamide, cytarabine, and docetaxel, while anastrozole, methotrexate, and 5-fluorouracil can all determine dry eye disease. However, the potential processes involved in the development of these alterations are yet not fully understood, especially for novel drugs currently available for cancer treatment. This review aims at analyzing the potential ocular surface and adnexal side effects of novel anticancer medications, trying to provide a better understanding of the underlying pharmacological processes and useful insights on the choice of proper management. Full article
(This article belongs to the Special Issue Molecular Insights into Drug Resistance in Cancer)

Other

Jump to: Research, Review

14 pages, 2244 KiB  
Systematic Review
Non-Vitamin K Antagonist Oral Anticoagulants versus Low Molecular Weight Heparin for Cancer-Related Venous Thromboembolic Events: Individual Patient Data Meta-Analysis
by Chun En Yau, Chen Ee Low, Natasha Yixuan Ong, Sounak Rana, Lucas Jun Rong Chew, Sara Moiz Tyebally, Ping Chai, Tiong-Cheng Yeo, Mark Y. Chan, Matilda Xinwei Lee, Li-Ling Tan, Chieh-Yang Koo, Ainsley Ryan Yan Bin Lee and Ching-Hui Sia
Cancers 2023, 15(24), 5887; https://doi.org/10.3390/cancers15245887 - 18 Dec 2023
Viewed by 1009
Abstract
Venous thromboembolism (VTE) is a leading cause of morbidity and mortality in cancer patients. Low molecular weight heparin (LMWH) has been the standard of care but new guidelines have approved the use of non-vitamin K antagonist oral anticoagulants (NOAC). By conducting an individual [...] Read more.
Venous thromboembolism (VTE) is a leading cause of morbidity and mortality in cancer patients. Low molecular weight heparin (LMWH) has been the standard of care but new guidelines have approved the use of non-vitamin K antagonist oral anticoagulants (NOAC). By conducting an individual patient data (IPD) meta-analysis of randomised controlled trials (RCTs) comparing the outcomes of NOAC versus LMWH in cancer patients, we aim to determine an ideal strategy for the prophylaxis of VTE and prevention of VTE recurrence. Three databases were searched from inception until 19 October 2022. IPD was reconstructed from Kaplan–Meier curves. Shared frailty, stratified Cox and Royston–Parmar models were fit to compare the outcomes of venous thromboembolism recurrence and major bleeding. For studies without Kaplan–Meier curves, aggregate data meta-analysis was conducted using random-effects models. Eleven RCTs involving 4844 patients were included. Aggregate data meta-analysis showed that administering NOACs led to a significantly lower risk of recurrent VTE (RR = 0.65; 95%CI: 0.50–0.84) and deep vein thrombosis (DVT) (RR = 0.60; 95%CI: 0.40–0.90). In the IPD meta-analysis, NOAC when compared with LMWH has an HR of 0.65 (95%CI: 0.49–0.86) for VTE recurrence. Stratified Cox and Royston–Parmar models demonstrated similar results. In reducing risks of recurrent VTE and DVT among cancer patients, NOACs are superior to LMWHs without increased major bleeding. Full article
(This article belongs to the Special Issue Molecular Insights into Drug Resistance in Cancer)
►▼ Show Figures

Figure 1

Show export options expand_more Show export options expand_less
Select all
Export citation of selected articles as:
 
Displaying articles 1-4
Back to TopTop