Oral Cancer Therapy Research Articles

Hyaluronic acid/chitosan-coated poly (lactic-co-glycolic acid) nanoparticles to deliver single and co-loaded paclitaxel and temozolomide for CD44+oral cancer cells

Oral cancer has a poor survival rate despite comprehensive therapy. Current treatments result in acute side effects and fail to eliminate an aggressive group of cells overexpressing CD44. Such cells are capable of tumour initiating, self-renewal, invasion and metastasis, resulting in tumour relapse and resistance. This study aims to synthesise and characterise hyaluronic acid/chitosan-coated poly (lactic-co-glycolic acid) nanoparticles and assess their effectiveness in delivering Paclitaxel and Temozolomide to human tongue squamous cell carcinoma cell line that expresses high CD44 levels, in terms of cell cytotoxicity and apoptosis. This study also assesses the coordinated administration of Paclitaxel and Temozolomide and whether they exhibit significant synergistic cell inhibition effects with reduced introduced drug concentration if co-delivered simultaneously. Nanoparticles were synthesised with solvent evaporation method and characterised to assess their size, homogeneity, and zeta potential. Cell viability assay and real-time cell analysis were performed to examine the cell inhibitory effect of the drug-loaded nanoparticles. Cell apoptosis and cell cycle alteration were detected, and reactive oxygen species induction, mitochondrial membrane potential, and expressed genes associated with cell inhibition and death were evaluated. The synthesised nanoparticles had a nano-sized diameter of 260.40±11.54 nm, a positive zeta potential of +14.31±1.37 mV and a low polydispersity index value of 0.15±0.03. Paclitaxel, Temozolomide, and their combination have inhibited cell proliferation with half maximal inhibitory concentrations of 4 nM, 1000 μM and 2nM:300 μM, respectively. Compared to free drugs, the single-loaded and co-loaded drugs induced more cytotoxicity. Paclitaxel and Temozolomide showed a considerable synergistic inhibitory effect which was discovered to be more significant when the drugs were loaded in the nanoparticles. Drug-loaded nanoparticles were verified to induce higher cell apoptosis rates, cell proportion arrested at the S-phase of the cell cycle, reactive oxygen species generation, mitochondrial collapse and expression of genes associated with cellular inhibition and death than free drugs. These results demonstrate that the established nanoparticles could be a potential candidate for oral cancer therapy since they could deliver and improve the efficacy of single and dual drugs against oral cancer cells.

Flash dissolving nanofiber membranes for chemo/cascade chemodynamic therapy of oral cancer

Cellular glucose and glutathione (GSH)-responsive nanofiber (NF) membrane system was developed for combined chemo/cascade chemodynamic therapy. Glucose oxidase (GOx), MnO2, and rapamycin were encapsulated in polyvinyl alcohol (PVA) NF for glucose decomposition/H2O2 generation, OH radical production based on Fenton-like reaction/GSH depletion/O2-induced hypoxia relief, and antiproliferation in cancer therapy, respectively. Restriction in the physicochemical properties of drug cargos, such as lower dispersibility of MnO2 and lower solubility of rapamycin in water, was overcome with the electrospinning process and homogeneous NF membrane was successfully fabricated. Designed NF mat structure exhibited immediate wetting, disintegrating, and drug releasing characteristics, which can be ideal requisites for oral cavity administration. In oral cancer cells (YD-9 cells), GOx in NF mat decomposed highly accumulated glucose to H2O2. MnO2 reduced cellular GSH level in cancer cells and generated O2 for hypoxia relief, in addition, Mn2+ successfully transformed H2O2 into OH radical. With these cascade catalytic reaction strategies, incorporated rapamycin in NF mat had an antiproliferation potential in oral cancer cells. Combination effects between GOx/MnO2 and rapamycin entrapped in NF mat were also demonstrated in 3D-cultured YD-9 tumor spheroid model. Designed PVA/GOx/MnO2/rapamycin NF mat can be used safely and conveniently as an anticancer drug delivery platform.

Combination Therapy as a Promising Way to Fight Oral Cancer.

Oral cancer is a highly aggressive tumor with invasive properties that can lead to metastasis and high mortality rates. Conventional treatment strategies, such as surgery, chemotherapy, and radiation therapy, alone or in combination, are associated with significant side effects. Currently, combination therapy has become the standard practice for the treatment of locally advanced oral cancer, emerging as an effective approach in improving outcomes. In this review, we present an in-depth analysis of the current advancements in combination therapies for oral cancer. The review explores the current therapeutic options and highlights the limitations of monotherapy approaches. It then focuses on combinatorial approaches that target microtubules, as well as various signaling pathway components implicated in oral cancer progression, namely, DNA repair players, the epidermal growth factor receptor, cyclin-dependent kinases, epigenetic readers, and immune checkpoint proteins. The review discusses the rationale behind combining different agents and examines the preclinical and clinical evidence supporting the effectiveness of these combinations, emphasizing their ability to enhance treatment response and overcome drug resistance. Challenges and limitations associated with combination therapy are discussed, including potential toxicity and the need for personalized treatment approaches. A future perspective is also provided to highlight the existing challenges and possible resolutions toward the clinical translation of current oral cancer therapies.

Uniting Dual‐Modal MRI/Chemiluminescence Nanotheranostics: Spatially and Sensitively Self‐Reporting Photodynamic Therapy in Oral Cancer

AbstractUnpredictable in vivo therapeutic feedback of reactive oxygen species (ROS) efficiency is the major bottleneck of photodynamic therapy (PDT). Herein, novel PDT‐based nanotheranostics Pa–Mn&CH‐A@P are elaborately constructed for in vivo tracking biodistribution and in situ self‐reporting PDT, which innovatively unites magnetic resonance imaging (MRI) and chemiluminescence (CL) signals. Taking advantages of the versatility of lanthanide coordination chemistry and flash nanoprecipitation (FNP) technology, photosensitizers, MRI, and CL agents are unprecedently integrated within a stable and uniform nanotheranostic. Specifically, MRI signal offers detailed dose distribution of nanotheranostics with high‐spatial resolution, and CL signal timely performs in situ evaluation of ROS generation with high sensitivity. This dual‐modal MRI/CL nanotheranostic makes a breakthrough in high fidelity feedback for oral tumor, conquering the inherent unpredictable obstacles on spatially and sensitively reporting PDT.

Effectiveness of a pharmaceutical consultation in the care of cancer patients receiving oral anti-cancer therapy: PHACON study.

e13670 Background: The emergence of oral cancer therapies (OCT) has improved the management of cancer patients. However, the specific toxicities of these OCT and their outpatient management raise many challenges, such as compliance and drug interactions. Pharmaceutical consultation (PC) takes into account all the medications taken and to be taken by the patient when a new prescription is issued. It involves the patient and is based on information sharing and multi-professional coordination. It prevents medication errors by facilitating the transmission of complete information between healthcare professionals. Despite these benefits, this PC is barely implemented in patient care. Methods: This prospective study was conducted at the Military Hospital Bégin. All patients with an OCT were eligible for PC. The PCcircuit was as follows. 1) PC was prescribed by the referring oncologist via the prescription software. 2) The patient was contacted by the hospital pharmacy to schedule an appointment. 3) On the day of the PC, the patient was greeted by the pharmacist in the hospital's outpatient department. The objectives of the PC were presented. The pharmacist reviewed with the patient all the treatments taken and also the herbal medicine. He presented the OCT, its objective and the recommended times of intake in a personalized manner. 4) Patient's local pharmacy was contacted by phone to ensure a close follow-up. A patient-centered multidisciplinary update is performed regularly. The objective of our study was to evaluate the feasibility of this PC and its acceptance by patients and health-caregivers. Results: 53 patients were enrolled between October 1st 2021 and January 31st 2023. The median age was 70 years (range 27-89). 80% presented a metastatic stage, and the most represented cancer was prostate (27%), breast (25%), lung (13%), and kidney (11%). The OCT were mainly TKI (62%) and hormonotherapy (30%). 47% of PC led to pharmaceutical interventions, notably to adapt the dosage and/or the choice of the molecule, in order to limit interactions and side effects. 41 city pharmacies were contacted (77%). Only 5 pharmacists were aware of these treatments (12%). 98% appreciated to be informed about the OCT received by their patient. All the patients were satisfied with this treatment and in particular with the information they received about herbal medicine. All practitioners reported a marked improvement in the management of their patients since the implementation of PC. Conclusions: Our study demonstrated the feasibility of the implementation of PC. This consultation allowed an adaptation and a therapeutic follow-up. All patients were satisfied and had a better adherence to their care. This secured the patient's care in order to maintain the therapeutic benefit and limit the side effects. Our study also shows the importance of the link between the city and the hospital in patient care via pharmacists.

Recent and advanced therapy for oral cancer.

Oral cancer is a common and deadly kind of tissue invasion, has a high death rate, and may induce metastasis that mostly affects adults over the age of 40. Most in vitro traditional methods for studying cancer have included the use of monolayer cell cultures and several animal models. There is a worldwide effort underway to reduce the excessive use of laboratory animals since, although being physiologically adequate, animal models rarely succeed in exactly mimicking human models. 3D culture models have gained great attention in the area of biomedicine because of their capacity to replicate parent tissue. There are many benefits to using a drug delivery approach based on nanoparticles in cancer treatment. Because of this, in vitro test methodologies are crucial for evaluating the efficacy of prospective novel nanoparticle drug delivery systems. This review discusses current advances in the utility of 3D cell culture models including multicellular spheroids, patient-derived explant cultures, organoids, xenografts, 3D bioprinting, and organoid-on-a-chip models. Aspects of nanoparticle-based drug discovery that have utilized 2D and 3D cultures for a better understanding of genes implicated in oral cancers are also included in this review.

Photodynamic Therapy in Oral Cancer: A Narrative Review.

Methods: A comprehensive search in PubMed, Scopus, and Google Scholar was performed using relevant keywords to structure this narrative review. Only English articles were included and assessed according to titles, abstracts, and full texts. Background: Photodynamic therapy (PDT) is applied for targeting pre-malignancy and malignancies in the head and neck, skin, lungs, and gastrointestinal tract and has been greatly promising in reducing disfigurement and morbidity. This method includes a light-sensitive medicine known as a photosensitizer and a light source used through a minimally invasive surgical tool. Objective: This study aimed to review the application of PDT in managing head and neck cancers (HNCs) and provide an overview of the most recent advances in PDT and its efficiency in increasing the long-term life quality of patients with HNC. Results: The light source irradiates light at an appropriate wavelength that can be absorbed by the sensitizer and produce cytotoxic free radicals that can kill tumor cells, impair microvasculature in the tumor microenvironment, and stimulate further inflammatory responses of the immune system. Patients with either early lesions or advanced disease conveniently accept to receive PDT in outpatient clinics. Therefore, this simple technique is considered a novel and promising approach that can be used either individually or in association with other methods. However, its application as a management method in oral malignancies has yet to be studied. PDT is also suggested as a promising adjuvant treatment with better functional results. Then, it is possible to conclude that PDT's effectiveness in treating various tumors has been shown to depend on the depth of the lesion location. Its safety is acceptable, but its limited irradiation depth confines its application in the advanced stages of cancer. Conclusions: PDT is critically applicable in the early diagnosed cancers and superficial tumors where many heads and neck lesions settle as an ideal candidate for PDT because of the possibility of accurate evaluation of lesions and providing appropriate irradiation at these sites.

Exploring animal models in oral cancer research and clinical intervention: A critical review.

Cancer is a leading cause of death worldwide, but advances in treatment, early detection, and prevention have helped to reduce its impact. To translate cancer research findings into clinical interventions for patients, appropriate animal experimental models, particularly in oral cancer therapy, can be helpful. In vitro experiments using animal or human cells can provide insight into cancer's biochemical pathways. This review discusses the various animal models used in recent years for research and clinical intervention in oral cancer, along with their advantages and disadvantages. We highlight the advantages and limitations of the used animal models in oral cancer research and therapy by searching the terms of animal models, oral cancer, oral cancer therapy, oral cancer research, and animals to find all relevant publications during 2010-2023. Mouse models, widely used in cancer research, can help us understand protein and gene functions in vivo and molecular pathways more deeply. To induce cancer in rodents, xenografts are often used, but companion animals with spontaneous tumours are underutilized for rapid advancement in human and veterinary cancer treatments. Like humans with cancer, companion animals exhibit biological behaviour, treatment responses, and cytotoxic agent responses similar to humans. In companion animal models, disease progression is more rapid, and the animals have a shorter lifespan. Animal models allow researchers to study how immune cells interact with cancer cells and how they can be targeted specifically. Additionally, animal models have been extensively used in research on oral cancers, so researchers can use existing knowledge and tools to better understand oral cancers using animal models.

Pomegranate extract mechanism in inhibiting the development of oral cancer: A review

Background: Oral cancer is one of the most aggressive and invasive cancers with high metastatic potential. Oral cancer is cancer with the 11th highest number of cases in the world. Oral cancer is treated with chemotherapy and radiotherapy. However, this therapy causes side effects in the form of damage to normal cells in the surrounding tissue. Pomegranate extract contains polyphenols which may be great for inhibiting the development of oral cancer. Purpose: This article presents a systematic and comprehensive review of the potential of pomegranate extract as a natural product to inhibit the development of oral cancer. Review: Pomegranate extract was obtained by ethanol extraction using maceration method. The main content of pomegranate is polyphenolic compounds such as punicalagin, tannins, flavonoids, and ellagic acid. This compound reduces ATP formation, shortens the subG1 phase, and increases apoptosis. At the microcellular level, pomegranate extract can inhibit the activity of MMP-2 or MMP-9 to produce anti-proliferative, anti-angiogenesis and pro-apoptotic processes of cancer cells at concentrations of 25 and 50 μg/ml. Anti-proliferative and pro-apoptotic effects are produced through mitochondrial damage mechanisms. Exposure after 72 hours can reduce oral cell viability greater than exposure after 24 hours. Conclusion: Pomegranate extract is likely has four mechanisms to oral cancer: inhibiting the invasion, migration and growth of oral cancer cells, increasing oral cancer cell apoptosis and regulating antioxidant genes. So that this material can be used as a candidate for oral cancer therapy.

Longitudinal changes in swallowing function after surgery and proactive swallowing therapy for oral cancer.

This study aimed to describe and explore the longitudinal changes in swallowing function among patients with oral cancer who underwent surgery and proactive swallowing therapy from baseline to 1-year postoperation. We retrospectively studied 118 patients over a 4.5-year duration. Swallowing functional assessment including 10-item Eating Assessment Tool (EAT-10), Functional Oral Intake Scale (FOIS), M. D. Anderson Dysphagia Inventory, and Modified Barium Swallow Impairment Profile (MBSImP™) was performed at baseline, 1-month, 6-month, and 1-year postoperatively. All swallowing parameters worsened 1-month postoperation. EAT-10, FOIS, and MBSImP™ oral and pharyngeal impairment scores improved significantly compared with 1-month postoperation at 6 months. Other swallowing parameters, except for weight, did not differ significantly from baseline at 6 months. The rate of tube-feeding dependency was 11.5% and 5.6% at 1 and 6 months postoperation, respectively. Periodic swallowing functional assessments help delineate the longitudinal changes in swallowing functional outcomes.

Synergistic Effect of Anethole and Platinum Drug Cisplatin against Oral Cancer Cell Growth and Migration by Inhibiting MAPKase, Beta-Catenin, and NF-κB Pathways.

Cisplatin is a common drug used to treat patients with oral squamous cell carcinoma. However, cisplatin-induced chemoresistance poses a major challenge to its clinical application. Our recent study has shown that anethole possesses an anti-oral cancer effect. In this study, we examined the combined effect of anethole and cisplatin on oral cancer therapy. Gingival cancer cells Ca9-22 were cultured in the presence of various concentrations of cisplatin with or without anethole. The cell viability/proliferation and cytotoxicity were evaluated, respectively, by MTT, Hoechst staining, and LDH assay, while colony formation was measured by crystal violet. Oral cancer cell migration was evaluated by the scratch method. Apoptosis, caspase activity, oxidative stress, MitoSOX, and mitochondrial membrane potential (ΔΨm) levels were evaluated by flow cytometry, and the inhibition of signaling pathways was investigated by Western blot. Our results show that anethole (3 µM) potentiates cisplatin-induced inhibition of cell proliferation and decreases the ΔΨm on Ca9-22 cells. Furthermore, drug combination was found to inhibit cell migration and enhanced cisplatin cytotoxicity. The combination of anethole and cisplatin potentiates cisplatin-induced oral cancer cell apoptosis through the activation of caspase, while we also found anethole and cisplatin to enhance the cisplatin-induced generation of reactive oxygen species (ROS) and mitochondrial stress. In addition, major cancer signaling pathways were inhibited by the combination of anethole and cisplatin such as MAPKase, beta-catenin, and NF-κB pathways. This study reports that the combination of anethole and cisplatin might provide a beneficial effect in enhancing the cisplatin cancer cell-killing effect, thus lowering the associated side effects.

Tunable Nanoparticles with Aggregation-Induced Emission Heater for Precise Synergistic Photothermal and Thermodynamic Oral Cancer Therapy of Patient-Derived Tumor Xenograft.

The fluorophores in the second near-infrared (NIR-II) biological window (1000 - 1700nm) show great application prospects in the fields of biology and optical communications. However, both excellent radiative transition and nonradiative transition cannot be achieved simultaneously for the majority of traditional fluorophores. Herein, tunable nanoparticles formulated with aggregation-induced emission (AIE) heater are developed rationally. The system can be implemented via the development of an ideal synergistic system that can not only produce photothermal from nonspecific triggers but also trigger carbon radical release. Once accumulating in tumors and subsequently being irradiated with 808nm laser, the nanoparticles (NMB@NPs) encapsulated with NMDPA-MT-BBTD (NMB) are splitted due to the photothermal effect of NMB, leading to the decomposition of azo bonds in the nanoparticle matrix to generate carbon radical. Accompanied by second near-infrared (NIR-II) window emission from the NMB, fluorescence image-guided thermodynamic therapy (TDT) and photothermal therapy (PTT) which significantly inhibited the growth of oral cancer and negligible systemic toxicity is achieved synergistically. Taken together, this AIE luminogens-based synergistic photothermal-thermodynamic strategy brings a new insight into the design of superior versatile fluorescent NPs for precise biomedical applications and holds great promise to enhance the therapeutic efficacy of cancer therapy.

The Regulatory Mechanism of Cold Plasma in Relation to Cell Activity and Its Application in Biomedical and Animal Husbandry Practices.

As an innovative technology in biological applications, cold plasma is widely used in oral treatment, tissue regeneration, wound healing, and cancer therapy, etc., because of the adjustable composition and temperature which allow the plasma to react with bio-objects safely. Reactive oxygen species (ROS) produced by cold plasma regulate cell activity in an intensity- and time-dependent manner. A low level of ROS produced by cold plasma treatment within the appropriate intensities and times promotes proliferation of skin-related cells and increases angiogenesis, which aid in the acceleration of the wound healing process, while a high level of ROS produced by cold plasma treatment performed at a high intensity or over a long period of time inhibits the proliferation of endothelial cells, keratinocytes, fibroblasts, and cancer cells. Moreover, cold plasma can regulate stem cell proliferation by changing niche interface and producing nitric oxide directly. However, the molecular mechanism of cold plasma regulating cell activity and its potential application in the field of animal husbandry remain unclear in the literature. Therefore, this paper reviews the effects and possible regulatory mechanisms of cold plasma on the activities of endothelial cells, keratinocytes, fibroblasts, stem cells, and cancer cells to provide a theoretical basis for the application of cold plasma to skin-wound healing and cancer therapy. In addition, cold plasma exposure at a high intensity or an extended time shows excellent performances in killing various microorganisms existing in the environment or on the surface of animal food, and preparing inactivated vaccines, while cold plasma treatment within the appropriate conditions improves chicken growth and reproductive capacity. This paper introduces the potential applications of cold plasma treatment in relation to animal-breeding environments, animal health, their growth and reproduction, and animal food processing and preservation, which are all beneficial to the practice of animal husbandry and guarantee good animal food safety results.

Abstract 1109: Effects of radiation therapy on the hardness of enamel and dentin

Abstract Introduction: Radiation therapy is often used as the main or adjunctive treatment for cancer in the oral cavity. Unfortunately, prolonged exposure to radiation has adverse effects on tissues of the oral cavity, including a decrease in the hardness of dentin. Consequently, patients who receive radiation therapy are susceptible to tooth sensitivity and caries. Fluoride treatments have proven to be effective in restoring the hardness of dentin as it remineralizes the tooth. The aim of this study was to determine the optimal fluoride treatment for restoring the hardness of irradiated teeth. Methods: 100 teeth were extracted, cleaned, and mounted in acrylic resin. The teeth were ground and polished to expose the dentin and enamel. The initial Knoop hardness of the teeth was measured and split equally among five groups and treated as follows: (1) sodium fluoride varnish (SF), (2) MI varnish (MI), (3) silver diamine fluoride and potassium iodide (SDFKI), (4) silver diamine fluoride (SDF), and (5) no treatment (NT). All groups were subjected to 2 grays of daily radiation treatment for 6 weeks. The hardness of the dentin was measured immediately following radiation. Afterwards, the 5 treatments were applied weekly for 6 weeks. Hardness was measured 1 week after each treatment. Kruskal-Wallis one way analysis of variance on ranks was used to compare the different groups. Results: After 6 weeks of fluoride treatment, there was a significant difference (p = 0.013) between the hardness of the irradiated enamel, with Group 4 resulting in the largest median measurement (263.4). Similarly, 5 weeks of fluoride application resulted in a mean hardness of dentin that was 15.8%, 13.6%, 16.2%, and 19.4% higher than the control for groups 1, 2, 3, and 4, respectively. Again, Group 4 had the highest hardness measurement. Conclusions: Radiation therapy decreases the hardness of enamel and dentin. SDF treatment resulted in the highest hardness for both irradiated dentin and enamel, suggesting that SDF is promising as a fluoride treatment for those undergoing radiation therapy for oral cancer. Citation Format: Rachel Kulchar, Florin Eggmann, Celine Mina, Steven Szewczyk, Kakiuchi Yusuke, Jie Deng, Francis Mante. Effects of radiation therapy on the hardness of enamel and dentin [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2023; Part 1 (Regular and Invited Abstracts); 2023 Apr 14-19; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2023;83(7_Suppl):Abstract nr 1109.

Role and regulation of GLUT1/3 during oral cancer progression and therapy resistance

ObjectiveThis study aimed to determine whether glucose transporter-1/3 (GLUT1/3) increased expression could contribute to oral tumor severity. Furthermore, this study detected whether GLUT1/3 mRNA/protein was associated with oncogenic transcription factors (HIF1α, AP1 and NFκB) and whether by blocking GLUT1 along with cisplatin could sensitize drug-resistant OSCC cells. DesignWe used 120 post-operated human tissue samples, including 35 primary tumors (PT), 43 invasive tumors (N1‐3), 17 recurrent chemoradiation-resistant tumors (RCRT), and 25 PT-adjacent normal tissues (AN). The cisplatin-resistant (CisR-SCC4/9) cells were generated using a drug escalation strategy from parental SCC4/9 cells. The BAY-876 treatment blocked GLUT1 in OSCC cells. Western Blot, Immunohistochemistry, and reverse transcription polymerase chain reaction (RT-PCR) were used to detect various proteins and mRNA. Cell survival was determined by MTT assay. ResultsGLUT1/3 expression was observed more in PT over AN tissue (PT > AN), N1–3 > PT, and .RCRT > PT. GLUT1 expression was maximum in the RCRT group and CisR-SCC4/9 cells over their parental counterpart, linked with tumor size (p=0.0037) and loco-regional invasiveness (p=0.0422). GLUT1/3 mRNA/protein was correlated (positively) with oncogenic transcription factors (TFs) like HIF1α, AP1 and NFκB. We found the degree of positive correlation of these TFs with GLUT1/3 was in the order c-Jun > HIF1α > Fra-2 > NFκB > c-Fos. Treatment of BAY-876 and cisplatin-induced cell death in both CisR-SCC4/9 cells, possibly by triggering apoptosis and autophagy. ConclusionCollectively, our results demonstrated increased GLUT1/3 overexpression linked with oral tumor severity like invasion and therapy resistance, and it was powered mainly by c-Jun (AP1). Blocking GLUT1 receptors and cisplatin application can sensitize CisR-OSCC cells.

Knowledge of and willingness for dispensing oral anticancer drug therapy among community pharmacists: a cross-sectional study from Jordan

Abstract Objectives This study aimed to assess the knowledge of and willingness for dispensing oral anticancer drugs (OADs) among community pharmacists in Jordan. Methods A cross-sectional survey was conducted among pharmacists in community pharmacies. Key findings Five hundred pharmacists completed the questionnaire. The mean age of respondents was 30.4 ± 6.2 years (range 21–61). Most pharmacists had a bachelor’s degree in pharmacy (80.8%) and were staff pharmacists (61.6%). Two hundred and ten (42.0%) pharmacists indicated not receiving adequate education on OADs at the undergraduate level. The majority of respondents (79.8%) did not attend continuing education events in oncology in the past 2 years. Further, 44.6% of pharmacists never dispensed OADs in their pharmacies. The mean score of knowledge of OADs was 1.7 ± 1.9 out of 12 points (range 0–9). The vast majority of pharmacists surveyed (97.6%) had poor knowledge of OADs. Almost half of the pharmacists (49.8%) agreed or strongly agreed to be comfortable answering questions regarding cancer treatments. More than half of respondents (52.2%) feel comfortable providing patient education on OADs. Half of the respondents (49.6%) disagreed that their current pharmacy settings are equipped with the necessary tools to handle OADs. Conclusions A large number of community pharmacists in Jordan lack the foundational knowledge regarding OADs. A substantial proportion of pharmacists never dispensed OADs and were not satisfied with the level of undergraduate education received regarding oncology and oral cancer therapies. Nevertheless, most pharmacists were willing to handle OADs and were positive about receiving further training/education on dispensing OADs. Collectively, efforts are needed to improve pharmacy education on oral chemotherapy and cancer care along with continuous training for pharmacists in their community settings.

PENGEMBANGAN MOBILE APLIKASI OBAT ORAL ANTI KANKER DALAM PENERAPAN PATIENT CENTER CARE: A LITERATUR REVIEW

Anti-cancer drugs have been developed in oral form. It is reported that the types of oral anti-cancer drug that are often used for the most cancer cases in the world such as hormonal groups, genetic mutation targets, and cytotoxic types. There are many benefits of this oral anti-cancer drug for patients, health workers, and drug providers. However, there are still challenges and obstacles such as the lack of patient understanding about drugs, low patient adherence to oral cancer therapy, and the limited number of health workers compared to the speed of increasing cancer cases. The purpose of this study was to determine the development of an Oral Agent for Cancer (OAC) mobile application for patient-centred care. This study uses a literature review method. The four databases used are ClinicalKey Nursing, ScienceDirect, EBSCOhost, and Scopus, using the keywords Cellular Application, Oral Agent for Cancer, Patient Centre Care and Technology. Literature review result shows that the use of mobile OAC applications increases patient motivation, actively participates in therapy, cost efficiency, time effectiveness, patient independence in managing side effects. From the nurse's point of view, although the number of personnel is limited, it’s show optimal quality of nursing care. The use of the OAC mobile application is effective in patient-centred care.

Imaging and Histopathological Analysis of Microvascular Angiogenesis in Photodynamic Therapy for Oral Cancer.

The objective of this study is to use imaging and histopathological analysis to characterize and monitor microvascular responses to photodynamic therapy (PDT). In vivo chicken chorioallantoic membranes (CAMs) and a stimulated malignant oral lesions animal model were used to determine the blood flow and the biological activities of Photofrin® (2.5 mg/kg) exposed to different laser power densities at 630 nm. The vascular changes, the velocity of the blood flow, the speckle flow index (SFI) of fluorescence changes, and ultrastructure damage in the microvasculature before and after PDT were recorded. The subcellular localization of Photofrin® revealed satisfactory uptake throughout the cytoplasm of human red blood cells at 10 s and 20 s before PDT. The mean blood-flow velocities of the veins and arteries were 500 ± 40 and 1500 ± 100 μm/s, respectively. A significant decrease in the velocities of the blood flow in the veins and arteries was detected in the CAM model after PDT. The veins and arteries of CAMs, exposed to the power densities of 80, 100, and 120 mW/cm2, had average blood-flow velocities of 100 ± 20, 60 ± 10, and 0 μm/s and 300 ± 50, 150 ± 30, and 0 μm/s, respectively. In the stimulated malignant oral lesions animal model, the treated tumors exhibited hemorrhage and red blood cell extravasation after PDT. The oxyhemoglobin and total hemoglobin levels decreased, which resulted in a decrease in tissue oxygen saturation, while the deoxyhemoglobin levels increased. PDT using Photofrin® has the ability to cause the destruction of the targeted microvasculature under nonthermal mechanisms selectively.

Photodynamic therapy in oral cancer: a review of clinical studies.

A significant mortality rate is associated with oral cancer, particularly in cases of late-stage diagnosis. Since the last decades, oral cancer survival rates have only gradually improved despite advances in treatment. This poor success rate is mainly due to the development of secondary tumors, local recurrence, and regional failure. Invasive treatments frequently have a negative impact on the aesthetic and functional outcomes of survivors. Novel approaches are thus needed to manage this deadly disease in light of these statistics. In photodynamic therapy (PDT), a light-sensitive medication called a photosensitizer is given first, followed by exposure to light of the proper wavelength that matches the absorbance band of the photosensitizer. The tissue oxygen-induced cytotoxic free radicals kill tumor cells directly, harm the microvascular structure, and cause inflammatory reactions at the targeted sites. In the case of early lesions, PDT can be used as a stand-alone therapy, and in the case of advanced lesions, it can be used as adjuvant therapy. The current review article discussed the uses of PDT in oral cancer therapy based on recent advances in this field.

LINC01296 promotes cancer stemness traits in oral carcinomas by sponging miR-143

Background/purposeEmerging evidence has shown that various failures in cancer therapy, such as drug resistance, metastasis, and cancer relapse are attributed to cancer stem cells (CSCs). Also, growing attention has been paid to the regulation of non-coding RNAs in cancer stemness. Here, we aimed to investigate the contribution of LINC01296 in the modulation of oral CSCs. Materials and methodsThe phenotypic assays including migration, invasion, and colony-forming abilities were carried out in CSCs of two types of oral cancer cells (SAS and GNM) following the knockdown of LINC01296. In addition, the percentage of cells expressing stemness marker, ALDH1, and drug resistance marker, ABCG2, was examined as well as the self-renewal capacity after silencing of LINC01296. Moreover, a luciferase reporter was used to validate the direct interaction between LINC01296 and miR-143. ResultsOur results showed that LINC01296 was significantly overexpressed in oral cancer tissues and positively correlated with stemness markers. The phenotypic and flow cytometry assays demonstrated that suppression of LINC01296 reduced the aggressiveness, cancer stemness features, and colony-forming and self-renewal abilities in oral CSCs. Furthermore, we demonstrated that LINC01296 may enhance cancer stemness features through suppression of the effect of miR-143. ConclusionSilencing of LINC01296 may be a promising direction for oral cancer therapy by reducing cancer stemness via regulation of miR-143.