Automated Detection of Oral Malignant Lesions Using Deep Learning: Scoping Review and Meta-Analysis.

Objective: Oral diseases, specifically malignant lesions, are serious global health concerns requiring early diagnosis for effective treatment. In recent years, deep learning (DL) has emerged as a powerful tool for the automated detection and classification of oral lesions. This research, by conducting a scoping review and meta-analysis, aims to provide an overview of the progress and achievements in the field of automated detection of oral lesions using DL.

Towards explainable oral cancer recognition: Screening on imperfect images via Informed Deep Learning and Case-Based Reasoning.

Oral squamous cell carcinoma recognition presents a challenge due to late diagnosis and costly data acquisition. A cost-efficient, computerized screening system is crucial for early disease detection, minimizing the need for expert intervention and expensive analysis. Besides, transparency is essential to align these systems with critical sector applications.

Reduction of MRONJ risk after exodontia by virtue of ozone infiltration: A randomized clinical trial.

Introduction: Exodontia is commonly considered as a risk factor for the development of medication-related osteonecrosis of the jaw (MRONJ) in individuals exposed to bone modifying agents. This study was aimed at assessing the efficiency and safety of a gaseous oxygen-ozone mixture as an adjuvant to a standard exodontia to reduce the risk of MRONJ development.

Methods: A randomized, open-label, phase II, single-center clinical trial involving 117 patients at risk of MRONJ was conducted.

Improving the cancer adult patient support network (iCAN): a pilot study on a communication model and modified focus group.

Background: Many consider that cancer has the greatest impact of any disease in the world, and it can drastically limit patients' quality of life. Combating such a life-threatening disease can pose many challenges to daily life, highlighted by demonstrating the need to discuss one's health status within a focus group and encourage treatment compliance.

Aim: the purposes of this study were to share the authors' experience of a modified focus group in an Oral Medicine Unit, termed "Improving Cancer Adult Patients Support Network" (iCAN), and to evaluate how effective communication could improve patients' quality of life and empower them by virtue of enhanced knowledge and an awareness of cancer management.

Doctoral: A smartphone-based decision support tool for the early detection of oral potentially malignant disorders.

Oral potentially malignant disorders can be defined as mucosal lesions and conditions with an increased risk of malignant transformation. Oral potentially malignant disorders are a significant health burden, and they are often diagnosed late due to scant attention to routine dental practice and the low number of specialized oral medicine centres. This report summarizes the DoctOral experience, a research initiative, providing a free smartphone-based decision support tool for the general medical/dental practitioner; the tool is based on the clinical appearance of oral lesions.

Ozone Infiltration for Osteonecrosis of the Jaw Therapy: A Case Series.

Medication-related osteonecrosis of the jaw (MRONJ) is a serious adverse reaction, mainly due to bone-modifying agents (BMA), and it is a potentially painful and debilitating condition. To date, the literature has reported a 90% rate of successful outcomes for MRONJ patients undergoing surgical treatment. Particularly for patients with advanced disease stages who are unsuitable for surgery, prolonged medical treatment is required, with a consequent risk of the overuse of antibiotics and antibiotic resistance.

Mutation of the Conserved Threonine 8 within the Human ARF Tumour Suppressor Protein Regulates Autophagy.

Background: The ARF tumour suppressor plays a well-established role as a tumour suppressor, halting cell growth by both p53-dependent and independent pathways in several cellular stress response circuits. However, data collected in recent years challenged the traditional role of this protein as a tumour suppressor. Cancer cells expressing high ARF levels showed that its expression, far from being dispensable, is required to guarantee tumour cell survival.

Pancreatic Progenitor Commitment Is Marked by an Increase in Ink4a/Arf Expression.

The identification of the molecular mechanisms controlling early cell fate decisions in mammals is of paramount importance as the ability to determine specific lineage differentiation represents a significant opportunity for new therapies. Pancreatic Progenitor Cells (PPCs) constitute a regenerative reserve essential for the maintenance and regeneration of the pancreas. Besides, PPCs represent an excellent model for understanding pathological pancreatic cellular remodeling.

Clinical use of BCG and its complications: a case series.

Bacillus Calmette-Guérin (BCG), a live, attenuated strain of Mycobacterium bovis, is the essential constituent of the vaccine against tuberculosis and the gold-standard adjuvant treatment for urothelial cancer of the bladder. Being a live, attenuated strain with a potential pathogenic action, bacilli can cause several complications, both locally near the inoculation site and remotely through blood dissemination. BCG-related disease can represent a side effect of anti-TB vaccination in patient with congenital or acquired immunodeficiency or a complication of the therapeutic schedule in oncologic patients.

Dual Role of the Alternative Reading Frame ARF Protein in Cancer.

The CDKN2a/ARF locus expresses two partially overlapping transcripts that encode two distinct proteins, namely p14ARF (p19Arf in mouse) and p16INK4a, which present no sequence identity. Initial data obtained in mice showed that both proteins are potent tumor suppressors. In line with a tumor-suppressive role, ARF-deficient mice develop lymphomas, sarcomas, and adenocarcinomas, with a median survival rate of one year of age.

Oxidative Stress Causes Enhanced Secretion of YB-1 Protein that Restrains Proliferation of Receiving Cells.

The prototype cold-shock Y-box binding protein 1 (YB-1) is a multifunctional protein that regulates a variety of fundamental biological processes including cell proliferation and migration, DNA damage, matrix protein synthesis and chemotaxis. The plethora of functions assigned to YB-1 is strictly dependent on its subcellular localization. In resting cells, YB-1 localizes to cytoplasm where it is a component of messenger ribonucleoprotein particles.

PKC Dependent p14ARF Phosphorylation on Threonine 8 Drives Cell Proliferation.

ARF role as tumor suppressor has been challenged in the last years by several findings of different groups ultimately showing that its functions can be strictly context dependent. We previously showed that ARF loss in HeLa cells induces spreading defects, evident as rounded morphology of depleted cells, accompanied by a decrease of phosphorylated Focal Adhesion Kinase (FAK) protein levels and anoikis. These data, together with previous finding that a PKC dependent signalling pathway can lead to ARF stabilization, led us to the hypothesis that ARF functions in cell proliferation might be regulated by phosphorylation.

Sumoylation and ubiquitylation crosstalk in the control of ΔNp63α protein stability.

ΔNp63α is finely and strictly regulated during embryogenesis and differentiation. ΔNp63α is the only p63 isoform degraded by the proteasome after Ubiquitin and SUMO (Small Ubiquitin-like MOdifier) conjugation. Here, we show that p63 ubiquitylation per se is not the signal triggering p63 proteasomal degradation.

p14ARF interacts with the focal adhesion kinase and protects cells from anoikis.

The ARF protein functions as an important sensor of hyper-proliferative stimuli restricting cell proliferation through both p53-dependent and -independent pathways. Although to date the majority of studies on ARF have focused on its anti-proliferative role, few studies have addressed whether ARF may also have pro-survival functions. Here we show for the first time that during the process of adhesion and spreading ARF re-localizes to sites of active actin polymerization and to focal adhesion points where it interacts with the phosphorylated focal adhesion kinase.

ΔNp63α controls YB-1 protein stability: evidence on YB-1 as a new player in keratinocyte differentiation.

Y-box binding protein 1 (YBX-1 or YB-1) is an oncoprotein that promotes replicative immortality, tumor cell invasion and metastasis. The increase in the abundance of YB-1 in the cell or YB-1 translocation from the cytoplasm to the nucleus is characteristic of malignant cell growth. We have previously reported that ΔNp63α, a transcription factor that is known to play a pivotal role in keratinocyte proliferation and differentiation, promotes YB-1 nuclear accumulation.

MDM2-mediated degradation of p14ARF: a novel mechanism to control ARF levels in cancer cells.

We here show a new relationship between the human p14ARF oncosuppressor and the MDM2 oncoprotein. MDM2 overexpression in various cancer cell lines causes p14ARF reduction inducing its degradation through the proteasome. The effect does not require the ubiquitin ligase activity of MDM2 and preferentially occurs in the cytoplasm.

Y-box Binding Protein-1 Is Part of a Complex Molecular Network Linking ΔNp63α to the PI3K/akt Pathway in Cutaneous Squamous Cell Carcinoma.

Cutaneous squamous cell carcinomas (SCCs) typically lack somatic oncogene-activating mutations and most of them contain p53 mutations. However, the presence of p53 mutations in skin premalignant lesions suggests that these represent early events during tumor progression and additional alterations may be required for SCC development. SCC cells frequently express high levels of ΔNp63α and Y-box binding 1 (YB-1 or YBX1) oncoproteins.

Mimicking p14ARF phosphorylation influences its ability to restrain cell proliferation.

The INK4a/ARF locus on the short arm of chromosome 9 is one of the most frequently altered loci in human cancer. It is generally accepted that ARF is involved in oncogenic checkpoint pathways by sensitizing incipient cancer cells to undergo growth arrest or apoptosis through both p53-dependent and independent pathways. While intensive studies have been focused on ARF activation at the transcriptional level, only recently mechanisms governing ARF turnover have been identified.

The p63 protein isoform ΔNp63α modulates Y-box binding protein 1 in its subcellular distribution and regulation of cell survival and motility genes.

The Y-box binding protein 1 (YB-1) belongs to the cold-shock domain protein superfamily, one of the most evolutionarily conserved nucleic acid-binding proteins currently known. YB-1 performs a wide variety of cellular functions, including transcriptional and translational regulation, DNA repair, drug resistance, and stress responses to extracellular signals. Inasmuch as the level of YB-1 drastically increases in tumor cells, this protein is considered to be one of the most indicative markers of malignant tumors.

A regulatory mechanism involving TBP-1/Tat-Binding Protein 1 and Akt/PKB in the control of cell proliferation.

TBP-1 /Tat-Binding Protein 1 (also named Rpt-5, S6a or PSMC3) is a multifunctional protein, originally identified as a regulator of HIV-1-Tat mediated transcription. It is an AAA-ATPase component of the 19S regulative subunit of the proteasome and, as other members of this protein family, fulfils different cellular functions including proteolysis and transcriptional regulation. We and others reported that over expression of TBP-1 diminishes cell proliferation in different cellular contexts with mechanisms yet to be defined.

A dominant mutation etiologic for human tricho-dento-osseous syndrome impairs the ability of DLX3 to downregulate ΔNp63α.

The homeodomain transcription factors play crucial roles in many developmental processes ranging from organization of the body plan to differentiation of individual tissues. The homeodomain protein Distal-less-3 (DLX3) has an essential role in epidermal stratification and development of ectodermal appendages, placenta and bones. A four-nucleotide deletion in the human DLX3 gene is etiologic for the human hereditary tricho-dento-osseous (TDO) ectodermal dysplasia, a dominant syndrome characterized by abnormalities in hair, nails, teeth, and bones.

MDM2 and Fbw7 cooperate to induce p63 protein degradation following DNA damage and cell differentiation.

Tight control of p63 protein levels must be achieved under differentiation or apoptotic conditions. Here, we describe a new regulatory pathway for the DeltaNp63alpha protein. We found that MDM2 binds DeltaNp63alpha in the nucleus promoting its translocation to the cytoplasm.

Identification of DeltaNp63alpha protein interactions by mass spectrometry.

p63, a transcription factor related to the p53 tumor suppressor, plays a key role in epidermal differentiation and limb development. The gene has two distinct promoters that allow the formation of proteins that either contain (TA) or lack (DeltaN) a transactivation domain. DeltaNp63alpha is the most widely expressed isoform, at all stages of development and in adult tissues.

Downregulation of DeltaNp63alpha in keratinocytes by p14ARF-mediated SUMO-conjugation and degradation.

The tumor suppressor p14(ARF) inhibits cell growth in response to oncogenic stress in a p53-dependent and independent manner. However, new physiologic roles for ARF activation have been proposed. We have previously demonstrated that ARF interacts with p63, influencing its transcriptional activity.