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Pharmaceuticals
Special Issues
Adjuvant Therapies for Cancer Treatment
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Adjuvant Therapies for Cancer Treatment

A special issue of Pharmaceuticals (ISSN 1424-8247). This special issue belongs to the section "Pharmacology".

Deadline for manuscript submissions: 20 October 2024 | Viewed by 4321

Special Issue Editors

Prof. Dr. Fuyi Wang

E-Mail Website
Guest Editor
CAS Key Laboratory of Analytical Chemistry for Living Biosystems, Institute of Chemistry, Chinese Academy of Sciences, Beijing 100190, China
Interests: anticancer drug design; nutural bioactive products; interactomics of drugs; chemical biology of drugs; mass spectrometry; mass spectrometry imaging; chemical proteomics
Dr. Andréia Machado Leopoldino

E-Mail Website
Guest Editor
Department of Clinical Analyses, Toxicology and Food Sciences, School of Pharmaceutical Sciences of Ribeirão Preto, Universidade de São Paulo (USP), Sao Paulo 14040-903, Brazil
Interests: new therapies; targeting signaling pathways; biomarkers; drug resistance; cancer stem cell; adjuvant therapy

Special Issue Information

Dear Colleagues,

To improve cancer survival and prevent the recurrence of the disease and metastasis, we still need to find new compounds and therapeutic strategies, as well as apply drug repurposing and combined therapies. This means finding better adjuvant therapy to improve cancer cures in the next decade.

Adjuvant therapy may take the form of chemotherapy, radiotherapy, biological therapy, hormone therapy, and targeted therapy.

Adjuvant therapy is used after an initial treatment (such as surgery) or before as a neoadjuvant. Both applications have advantages (such as reducing the tumor size, preventing tumor cells to spread/metastasis, and eliminating any remaining malignant cells after surgery and disease recurrence) and disadvantages (such as serious side effects). 

Omics studies and biological approaches have brought a lot of knowledge about alterations and signaling deregulations in several cancer types and profiles related to outcome and drug efficacy. Cancer resistance occurs in different types of tumors and patients under different treatments where some therapies are associated with specific resistance mechanisms (such as drug efflux, autophagy, apoptosis blockage, metabolism reprogramming, mutations, and stemness). However, the next steps in oncology will be to connect molecular data with clinical practice and offer a potential and specific protocol to the patient for cancer treatment. 

This Special Issue is dedicated to illustrating the new findings in adjuvant therapy applied for cancer treatment and highlights the gaps and new directions in this field.

Prof. Dr. Fuyi Wang
Dr. Andréia Machado Leopoldino
Guest Editors

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. Pharmaceuticals is an international peer-reviewed open access monthly 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 repurposing
  • combined therapies
  • new compounds
  • drug resistance
  • chemosensitization
  • antitumoral strategies

Published Papers (4 papers)

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Research

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20 pages, 3874 KiB  
Article
Potential Antitumor Activity of Combined Lycopene and Sorafenib against Solid Ehrlich Carcinoma via Targeting Autophagy and Apoptosis and Suppressing Proliferation
by Thanaa A. El-Masry, Maysa M. F. El-Nagar, Nageh A. El Mahdy, Fatemah A. Alherz, Reham Taher and Enass Y. Osman
Pharmaceuticals 2024, 17(4), 527; https://doi.org/10.3390/ph17040527 - 19 Apr 2024
Viewed by 396
Abstract
An FDA-approved kinase inhibitor called sorafenib (SOR) is used to treat primary kidney and liver cancer as well as to stop the spread of advanced breast cancer. Side effects from SOR, such as palmar–plantar erythrodysesthesia syndrome, can negatively impact an individual’s quality of [...] Read more.
An FDA-approved kinase inhibitor called sorafenib (SOR) is used to treat primary kidney and liver cancer as well as to stop the spread of advanced breast cancer. Side effects from SOR, such as palmar–plantar erythrodysesthesia syndrome, can negatively impact an individual’s quality of life. There are a lot of data supporting the importance of lycopene (LYC) in preventing cancer. The antitumor properties of the combination of sorafenib and lycopene were examined in this study. A viability test against MDA-MB-231 was used to assess the anticancer efficacy of sorafenib, lycopene, and their combination in vitro. Moreover, a cell cycle analysis and Annexin-V/PI double staining were performed by using flow cytometry. In addition, the protein level of JNK-1, ERK-1, Beclin-1, P38, and P53 of the MDA-MB-231 cell line was estimated using ELISA kits. In addition, mice with SEC were divided into four equal groups at random (n = 10) to investigate the possible processes underlying the in vivo antitumor effect. Group IV (SEC-SOR-LYC) received SOR (30 mg/kg/day, p.o.) and LYC (20 mg/kg/day, p.o.); Group I received the SEC control; Group II received SEC-SOR (30 mg/kg/day, p.o.); and Group III received SEC-LYC (20 mg/kg/day, p.o.). The findings demonstrated that the combination of sorafenib and lycopene was superior to sorafenib and lycopene alone in causing early cell cycle arrest, suppressing the viability of cancer cells, and increasing cell apoptosis and autophagy. Likewise, the combination of sorafenib and lycopene demonstrated inhibition of the levels of Bcl-2, Ki-67, VEGF, IL-1β, and TNF-α protein. Otherwise, the quantities of the proteins BAX, P53, and caspase 3 were amplified. Furthermore, the combined treatment led to a substantial increase in TNF-α, caspase 3, and VEGF gene expression compared to the equivalent dosages of monotherapy. The combination of sorafenib and lycopene enhanced apoptosis and reduced inflammation, as seen by the tumor’s decreased weight and volume, hence demonstrating its potential anticancer effect. Full article
(This article belongs to the Special Issue Adjuvant Therapies for Cancer Treatment)
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11 pages, 473 KiB  
Article
Relation of Statin Use with Esophageal Cancer
by Sarang Jang, Hyo Geun Choi, Mi Jung Kwon, Ji Hee Kim, Joo-Hee Kim and So Young Kim
Pharmaceuticals 2023, 16(6), 900; https://doi.org/10.3390/ph16060900 - 19 Jun 2023
Viewed by 1125
Abstract
The present study evaluated the association of long-term statin use with the diagnosis and mortality of esophageal cancer in a Korean population. The Korean National Health Insurance Service-Health Screening Cohort from 2002 to 2019 was enrolled. Esophageal cancer patients were matched with control [...] Read more.
The present study evaluated the association of long-term statin use with the diagnosis and mortality of esophageal cancer in a Korean population. The Korean National Health Insurance Service-Health Screening Cohort from 2002 to 2019 was enrolled. Esophageal cancer patients were matched with control participants for demographic variables. The statin prescription histories were collected and grouped into <180 days, 180 to 545 days, and >545 days of duration. Propensity score overlap weighting was applied to minimize the bias between the esophageal cancer and control groups. The odds ratios (ORs) of the duration of statin use for esophageal cancer were analyzed using propensity score overlap weighted multivariable logistic regression analysis. The esophageal cancer group was classified as dead and surviving patients, and the ORs of the duration of statin use for the mortality of esophageal cancer were analyzed in an identical manner. Secondary analyses were conducted according to comorbid factors. Patients with esophageal cancer did not show lower odds for the duration of statin prescription in the overall study population (OR = 1.30, 95% CI = 1.03–1.65, p = 0.027 for 180 to 545 days and OR = 1.29, 95% CI = 1.08–1.55, p = 0.006 for >545 days). Subgroups of nonsmokers, past and current smokers, alcohol consumption ≥ 1 time a week, SBP < 140 mmHg and DBP < 90 mmHg, fasting blood glucose ≥ 100 mg/dL, total cholesterol ≥ 200 mg/dL, CCI score = 0, and nondyslipidemia history demonstrated low odds for the duration of statin prescription. Both types of statins, hydrophilic and lipophilic statins, were not related to a lower rate of esophageal cancer. The mortality of esophageal cancer was not associated with the duration of statin prescription. A subgroup with total cholesterol ≥ 200 mg/dL showed lower odds of statin prescription for mortality of esophageal cancer. The duration of statin prescription was not related to a lower rate or mortality of esophageal cancer in the adult Korean population. Full article
(This article belongs to the Special Issue Adjuvant Therapies for Cancer Treatment)
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Review

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21 pages, 1504 KiB  
Review
Advances in IL-7 Research on Tumour Therapy
by Chunxue Fu, Xinqiang Zhang, Xinyu Zhang, Dan Wang, Shuxin Han and Zhenghai Ma
Pharmaceuticals 2024, 17(4), 415; https://doi.org/10.3390/ph17040415 - 25 Mar 2024
Viewed by 714
Abstract
Interleukin-7 (IL-7) is a versatile cytokine that plays a crucial role in regulating the immune system’s homeostasis. It is involved in the development, proliferation, and differentiation of B and T cells, as well as being essential for the differentiation and survival of naïve [...] Read more.
Interleukin-7 (IL-7) is a versatile cytokine that plays a crucial role in regulating the immune system’s homeostasis. It is involved in the development, proliferation, and differentiation of B and T cells, as well as being essential for the differentiation and survival of naïve T cells and the production and maintenance of memory T cells. Given its potent biological functions, IL-7 is considered to have the potential to be widely used in the field of anti-tumour immunotherapy. Notably, IL-7 can improve the tumour microenvironment by promoting the development of Th17 cells, which can in turn promote the recruitment of effector T cells and NK cells. In addition, IL-7 can also down-regulate the expression of tumour growth factor-β and inhibit immunosuppression to promote anti-tumour efficacy, suggesting potential clinical applications for anti-tumour immunotherapy. This review aims to discuss the origin of IL-7 and its receptor IL-7R, its anti-tumour mechanism, and the recent advances in the application of IL-7 in tumour therapy. Full article
(This article belongs to the Special Issue Adjuvant Therapies for Cancer Treatment)
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24 pages, 2579 KiB  
Review
Exploring the mTOR Signalling Pathway and Its Inhibitory Scope in Cancer
by Suhail Ahmad Mir, Ashraf Dar, Saad Ali Alshehri, Shadma Wahab, Laraibah Hamid, Mohammad Ali Abdullah Almoyad, Tabasum Ali and Ghulam Nabi Bader
Pharmaceuticals 2023, 16(7), 1004; https://doi.org/10.3390/ph16071004 - 14 Jul 2023
Cited by 2 | Viewed by 1663
Abstract
Mechanistic target of rapamycin (mTOR) is a protein kinase that regulates cellular growth, development, survival, and metabolism through integration of diverse extracellular and intracellular stimuli. Additionally, mTOR is involved in interplay of signalling pathways that regulate apoptosis and autophagy. In cells, mTOR is [...] Read more.
Mechanistic target of rapamycin (mTOR) is a protein kinase that regulates cellular growth, development, survival, and metabolism through integration of diverse extracellular and intracellular stimuli. Additionally, mTOR is involved in interplay of signalling pathways that regulate apoptosis and autophagy. In cells, mTOR is assembled into two complexes, mTORC1 and mTORC2. While mTORC1 is regulated by energy consumption, protein intake, mechanical stimuli, and growth factors, mTORC2 is regulated by insulin-like growth factor-1 receptor (IGF-1R), and epidermal growth factor receptor (EGFR). mTOR signalling pathways are considered the hallmark in cancer due to their dysregulation in approximately 70% of cancers. Through downstream regulators, ribosomal protein S6 kinase β-1 (S6K1) and eukaryotic translation initiation factor 4E binding protein 1 (4E-BP1), mTORC1 influences various anabolic and catabolic processes in the cell. In recent years, several mTOR inhibitors have been developed with the aim of treating different cancers. In this review, we will explore the current developments in the mTOR signalling pathway and its importance for being targeted by various inhibitors in anti-cancer therapeutics. Full article
(This article belongs to the Special Issue Adjuvant Therapies for Cancer Treatment)
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