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Abstract: Micrometer‐sized functional nucleic acid (FNA) superstructures (denoted as 3D DNA) were examined as a unique class of biorecognition elements to produce highly functional bioactive paper surfaces. 3D DNA containing repeating sequences of either a DNA aptamer or DNAzyme was created from long‐chain products of rolling circle amplification followed by salt aging. The resulting 3D DNA retained its original spherical shape upon inkjet printing and adhered strongly to the paper surface via physisorption. 3D DNA paper sensors showed resistance to degradation by nucleases, suppressed nonspecific protein adsorption, and provided a much higher surface density of functional DNA relative to monomeric FNAs, making such species ideally suited for development of paper‐based biosensors. [ABSTRACT FROM AUTHOR]

The article cites a research study that examines the role of MiR- Par3L axis in breast cancer progression. It examined normal tissues and Par3L expressions in breast cancer tissues and cells. Par3L was found to be frequently down-regulated in human breast cancer cells and tissues and Par3L low-expression was associated with aggressive clinicopathological features and poor clinical outcome of breast cancer patients.

Multiple myeloma (MM) cells express certain tumour-associated antigens (TAAs) that could serve as targets for active-specific immunotherapy. The aim of the present study was to test the MM/dendritic cell (DC) fusion as a vaccination strategy. We fused MM cells with DC to generate fusion cells (FCs) and tested their antigen presenting cell (APC) function in mixed lymphocyte reactions and cytotoxicity assays. First, the HS Sultan and SK0-007 HAT sensitive human MM cell lines and DCs generated from peripheral blood of normal donors were fused in the presence of 50% polyethylene glycol to form FCs. Next, tumour cells freshly isolated from patients were similarly fused with autologous DCs to generate FCs. The FCs demonstrated a biphenotypic profile, confirmed both by flow-cytometry and dual immunofluorescence microscopy. These FCs induced MM-specific cytotoxicity. FCs, but not MM cells or DCs alone, were potent stimulators of autologous patient T cells. More importantly, FC-primed autologous peripheral blood mononuclear cells demonstrated major histocompatibility complex-restricted MM-specific cytolysis. These studies therefore demonstrated that MM/DC FC can trigger an autologous immune response to MM cells and formed the framework for a clinical trial currently underway. [ABSTRACT FROM AUTHOR]

Multiple myeloma (MM) is a neoplastic proliferation of plasma cells and remains an incurable disease because of the development of drug resistance. Histone deacytylase (HDAC) inhibitors are a new class of chemotherapeutic reagents that cause growth arrest and apoptosis of neoplastic cells. Depsipeptide, a new member of the HDAC inhibitors, was found to be safe in humans and has been shown to induce apoptosis in various cancers. In order to evaluate the effects of depsipeptide, a MM cell line, U266 [interleukin (IL)-6 dependent], was analysed for viability and apoptosis. The combined effect of depsipeptide with melphalan and changes in BCL-2 family proteins (BCL-2, BCL-XL, BAX and MCL-1) were also investigated. In addition, the RPMI 8226 cell line (IL-6 independent), and primary patient myeloma cells were also analysed for apoptosis after depsipeptide treatment. Depsipeptide induced apoptosis in both U266 and RPMI 8226 cell lines in a time- and dose-dependent fashion, and in primary patient myeloma cells. We also demonstrated that depsipeptide had an additive effect with melphalan (10 μmol/l). BCL-2, BCL-XL and MCL-1 showed decreased expression in depsipeptide-treated samples. Based on recent clinical trials demonstrating minimal clinical toxicity, our study supports the future clinical utilization of depsipeptide in the management of MM. [ABSTRACT FROM AUTHOR]

The role of repopulating lymphocytes after allogeneic stem cell transplantation (SCT) includes the prevention of serious infections and attacking residual tumour cells in the early post-transplant phase. Therefore, the current study analysed the role of the absolute lymphocyte count (ALC) on day 21 after SCT in predicting transplant outcomes of 82 patients in terms of the risk of opportunistic infections and recurrence of original disease. The median dose of CD34+, CD3+ and mononuclear cells (MNC) infused was 6·41 × 106/kg, 1·96 × 108/kg and 6·81 × 108/kg respectively. The high ALC group (high ALC on day 21; ≥0·35 × 109/l) was associated with the use of peripheral blood stem cells, matched sibling donors and higher cell doses of MNC, CD3+ and CD4+ cells. The high ALC group also exhibited a better overall survival (56·3% vs. 17·7%) and disease-free survival (50·1% vs. 15·9%) after 3 years and lower incidences of relapse (33·6% vs. 67·1%) and fungal infections (3·0% vs. 19·5%) after 1 year. The incidence of cytomegalovirus antigenaemia was lower in the high ALC group (47·7% vs. 73·7%). Accordingly, identifying the ALC on day 21 would appear to be a useful and simple measurement to predict those patients with a high risk of opportunistic infections and relapse after allogeneic SCT. [ABSTRACT FROM AUTHOR]

Bispecific antibodies offer the possibility of improving effector-cell recruitment for antibody therapy. For this purpose, a recombinant bispecific single-chain Fv antibody (bsscFv), directed against Fc γRIII (CD16) and human leucocyte antigen (HLA) class II, was constructed and tested in functional assays. RNA from the hybridomas 3G8 and F3.3, reacting with CD16 and HLA class II, respectively, was used to generate phage display libraries. From these libraries, reactive phages were isolated and the bsscFv was constructed by connecting both single-chain Fv components through a 20 amino acid flexible linker. After expression in SF21 insect cells and chromatographic purification, the bsscFv bound specifically and simultaneously to both antigens. The affinities of the anti-CD16 and the anti-HLA class II scFv components of the bsscFv were 8·6 × 10−8 mol/l and 13·7 × 10−8 mol/l, respectively, which was approximately sevenfold lower than the F(ab) fragments of the parental antibodies. In antibody-dependent cellular cytotoxicity experiments with human mononuclear cells as effectors, the bsscFv-mediated specific lysis of both HLA class II-positive, malignant human B-lymphoid cell lines and primary cells from patients with chronic B-cell lymphocytic leukaemia. Optimal lysis was obtained at bsscFv concentrations of approximately 400 ng/ml, similar to the concentration required for maximum lysis by the corresponding chemically linked bispecific antibody. Thus, this recombinant bsscFv-antibody is an efficient molecule for effector-cell mediated lysis of malignant human B-lymphoid cells. [ABSTRACT FROM AUTHOR]

To evaluate the clinical significance of CD21S expression of diffuse large B-cell lymphoma (DLBCL) tumour cells, we compared their clinical features, immunophenotype, response to therapy and outcome in relation to CD21S expression. Between 1987 and 1999, frozen sections from 240 DLBCL cases were examined for CD21S expression by immunohistochemical methods. CD21S expression was detected on the tumour cells of 87 (36%) cases. The median age of the CD21S+ DLBCL cases was 65 years (range: 17–84 years), the male–female ratio was 42:45, and they showed the following clinical features: Eastern Cooperative Oncology Group score >1 in 14%, lactate dehydrogenase greater than normal levels in 38%, extranodal sites >1 in 14%, stages III/IV disease at diagnosis in 29%, B symptoms in 17%, and a high/high–intermediate International Prognostic Index (IPI) in 23%. They also showed a better overall survival ( P = 0·00001, log-rank test) and a better complete remission rate ( P = 0·00004, chi-square test) than CD21S− DLBCL. Moreover, CD21S+ DLBCL showed a better survival than CD21S− DLBCL for both low/low–intermediate and high/high–intermediate risk categories of IPI ( P = 0·045 and P = 0·0016 respectively). Multivariate analysis identified CD21S expression as an independent factor for survival when compared with the five IPI factors. These findings indicate that CD21S expression of DLBCL tumour cells is a useful prognostic factor for survival. [ABSTRACT FROM AUTHOR]

Minor histocompatibility antigens (mHAs) are major histocompatibility complex (MHC)-associated peptides, which trigger T-cell responses that mediate graft versus host disease (GVHD) and graft versus leukaemia effects. We recently identified a new mHA epitope, termed ACC-1, which is presented by HLA-A*2402 and encoded by BCL2A1, whose expression is restricted to haematopoietic cells including leukaemic cells. HLA-A24/ACC-1 tetramer detected the presence of ACC-1-specific CD8+ cells in the peripheral blood of a patient up to 7 months following transplantation, and these tetramer-positive cells were expandable in vitro by ACC-1 peptide stimulation. A retrospective analysis of 320 patients with HLA-A*2402 who had received a human leucocyte antigen (HLA) genotypically matched unrelated donor through the Japan Marrow Donor Programme was conducted to determine whether ACC-1 disparity is associated with adverse clinical outcomes such as GVHD. Among these patients, ACC-1 disparity was detected in 55 (17·2%) donor/recipient pairs. After adjusting for known risk factors, the hazard ratios or odds ratios of acute and chronic GVHD, relapse and disease-free survival were not statistically different between patients receiving ACC-1 compatible and incompatible transplantation. These data suggest that disparity of haematopoietic cell-specific mHA, ACC-1, is unlikely at least to augment GVHD, and that T cells specific for ACC-1 may also be used for immunotherapy of recurring leukaemia without GVHD. [ABSTRACT FROM AUTHOR]

Our July-2023 paper (Varshavsky, Lewis and Chen (2023) Deletions of DNA in cancer and their possible uses for therapy. Sci. USA (PNAS) 104, 14935-14940), proposed two molecular approaches to selective targeting of cancer through the recognition of cancer-specific DNA deletions. BioEssays 2300051), a follow-up to the 2007 paper (Varshavsky (2007) Targeting the absence: homozygous DNA deletions as immutable signposts for cancer therapy. [Extracted from the article]

Mesenchymal stem cells (MSCs) are recruited by malignant tumor cells to the tumor microenvironment (TME) and play a crucial role in the initiation and progression of malignant tumors. This role encompasses immune evasion, promotion of angiogenesis, stimulation of cancer cell proliferation, correlation with cancer stem cells, multilineage differentiation within the TME, and development of treatment resistance. Simultaneously, extensive research is exploring the homing effect of MSCs and MSC‐derived extracellular vesicles (MSCs‐EVs) in tumors, aiming to design them as carriers for antitumor substances. These substances are targeted to deliver antitumor drugs to enhance drug efficacy while reducing drug toxicity. This paper provides a review of the supportive role of MSCs in tumor progression and the associated molecular mechanisms. Additionally, we summarize the latest therapeutic strategies involving engineered MSCs and MSCs‐EVs in cancer treatment, including their utilization as carriers for gene therapeutic agents, chemotherapeutics, and oncolytic viruses. We also discuss the distribution and clearance of MSCs and MSCs‐EVs upon entry into the body to elucidate the potential of targeted therapies based on MSCs and MSCs‐EVs in cancer treatment, along with the challenges they face. [ABSTRACT FROM AUTHOR]

Natural killer (NK) cells, as innate lymphocytes, possess cytotoxic capabilities and engage target cells through a repertoire of activating and inhibitory receptors. Particularly, natural killer group 2, member D (NKG2D) receptor on NK cells recognizes stress‐induced ligands—the MHC class I chain‐related molecules A and B (MICA/B) presented on tumor cells and is key to trigger the cytolytic response of NK cells. However, tumors have developed sophisticated strategies to evade NK cell surveillance, which lead to failure of tumor immunotherapy. In this paper, we summarized these immune escaping strategies, including the downregulation of ligands for activating receptors, upregulation of ligands for inhibitory receptors, secretion of immunosuppressive compounds, and the development of apoptosis resistance. Then, we focus on recent advancements in NK cell immune therapies, which include engaging activating NK cell receptors, upregulating NKG2D ligand MICA/B expression, blocking inhibitory NK cell receptors, adoptive NK cell therapy, chimeric antigen receptor (CAR)‐engineered NK cells (CAR‐NK), and NKG2D CAR‐T cells, especially several vaccines targeting MICA/B. This review will inspire the research in NK cell biology in tumor and provide significant hope for improving cancer treatment outcomes by harnessing the potent cytotoxic activity of NK cells. [ABSTRACT FROM AUTHOR]

Objective: The aim of this paper is to investigate the effect of long noncoding RNA (lncRNA) MIR100HG on the proliferation and metastasis of lung cancer cells by mediating the microRNA (miR)−5590‐3p/DCBLD2 axis. Methods: RNA levels of MIR100HG, miR‐5590‐3p, and DCBLD2 in lung cancer tissues and cells were detected by quantitative reverse‐transcription polymerase chain reaction, and protein level was assessed by Western blot. Effects of MIR100HG or miR‐5590‐3p on proliferation, migration, and invasion of lung cancer cells were detected by Cell Counting Kit‐8, colony formation, and Transwell assays. Luciferase reporter assay and RNA‐immunoprecipitation assay confirmed the target relationship between miR‐5590‐3p and MIR100HG or DCBLD2. Results: MIR100HG and DCBLD2 were highly expressed, while miR‐5590‐3p was lowly expressed in lung cancer tissues and cells. Silencing MIR100HG or upregulating miR‐5590‐3p impeded lung cancer cell proliferation, migration, and invasion. MIR100HG could up‐regulate DCBLD2 by sponging miR‐5590‐3p. Downregulation of miR‐5590‐3p partly overturned the suppressive effect of silencing MIR100HG on lung cancer cell proliferation and metastasis, and overexpression of DCBLD2 also reversed the effect of overexpression of miR‐5590‐3p on lung cancer cell proliferation and metastasis. Conclusion: LncRNA MIR100HG promotes lung cancer progression by targeting and negatively regulating DCBLD2 through binding with miR‐5590‐3p. [ABSTRACT FROM AUTHOR]

Presents a list of articles for publication in future issues of the "European Journal of Biochemistry". Conformation of physalaemin; Association of cross-linked proteins with a specific mRNA in the cytoplasm of HeLa cells; Transport of proteins into chloroplasts.

In the cold atmospheric plasma (CAP)‐assisted cancer treatment, the electroporation of cancer cell membranes occurs under the CAP itself electric field effect, leading to changes in membrane permeability. In this paper, using classical molecular dynamics simulations, the electroporation of pure or different cholesterol‐containing phospholipid bilayer models under different pulsed electric fields was studied. The results showed that the electroporation time under a nanosecond pulsed electric field was shorter, while a picosecond pulsed electric field had a stronger penetration effect. Increasing the electric field intensity or decreasing the frequency of cholesterol contents decreased the electroporation time. Our simulation complements the related studies on electroporation under a picosecond pulsed electric field and reveals the potential mechanism of CAP‐selective cancer cell apoptosis. [ABSTRACT FROM AUTHOR]

The epithelial cell adhesion molecule (Ep-CAM) is expressed on the surface of most human carcinomas, including ovarian, breast, lung, prostate and colorectal carcinoma. Ep-CAM was shown to be a valid target for monoclonal antibody-based therapies. We have investigated whether an Ep-CAM-/CD3-bispecific single-chain antibody called bscEp-CAM × CD3 is effective in tumor cell elimination within the cellular microenvironment of primary ovarian cancer tissue. The ex vivo elimination of ovarian cancer cells in tumor preparations from 21 patients was monitored by flow cytometry using Ep-CAM/CA-125 double-labeling or Ep-CAM single-labeling combined with propidium iodide uptake of cells. Methodology was established by the ovarian cancer cell line OvCAR. A total of 17 (81%) patient samples showed a dose-dependent tumor cell elimination by bscEp-CAM × CD3. High and specific tumor cell lysis was seen at bscEp-CAM × CD3 concentrations as low as 1 ng/ml, at very low effector:target ratios and in the absence of T cell costimulation. The high efficacy of the bispecific antibody may be due to the non-restricted activation of tumor-resident cytotoxic T lymphocytes. In clinical trials, the ex vivo data with the T cell-recruiting bispecific antibody bscEp-CAM × CD3 may translate into a high response rate and efficacy of tumor cell elimination. © 2003 Wiley-Liss, Inc. [ABSTRACT FROM AUTHOR]

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Nanosecond pulsed electric fields (nsPEFs) have recently shown promise as a cancer therapy. Although nsPEF‐induced apoptotic responses have been observed, the stress on individual cell components has not been quantified. Therefore, the authors built a cell equivalent circuit, including mitochondria, to quantitatively calculate the voltage, electric field, and electrical energy applied to the cell components in the frequency domain. Additionally, pulse width and electrical energy changed in mitochondrial membrane potential over time. The results indicated that the change of pulsed voltage switched the cell stimulation pathway, resulting in different mitochondrial membrane potentials over time. The frequency response analysis confirmed that the potential on mitochondrial membranes increased under shorter pulse width conditions. This suggested that the frequency analysis provided in this paper is useful for relating the site of cellular stimulation to induce physiological effects. © 2024 Institute of Electrical Engineers of Japan and Wiley Periodicals LLC. [ABSTRACT FROM AUTHOR]

Chronic Myelogenous Leukaemia (CML) is a haematopoietic stem cells disease with complex dynamical behaviour. One of the effective factors in treating patients is to determine the appropriate drug dosage. A physician should test the different drug dosages through trial and error in order to find its optimal value. This procedure is normally a time‐consuming and error‐prone task that can even be harmful. The contribution of this paper is to design an intelligent control strategy, which can be used to help physicians, by finding a drug treatment regimen to minimize the number of cancer cells for a CML patient. In this paper, the eligibility traces algorithm and Q‐learning approach are adopted as sub‐optimal methods for progressively reducing the population of cancer cells. In addition, the injected dosage of the drug has improved, compared with previous methods. More importantly, the proposed method is followed by the reduction in side effects of the drug. The advantage of the backward view and the previous states investigation are applied in the Eligibility Traces algorithm. These effects increase the learning procedure and decrease the growth rate of cancer cells and total dosage of the injected drug during the treatment period of time. The proposed strategy mitigates the side effects of the drug on the normal cells. [ABSTRACT FROM AUTHOR]

This paper aimed to evaluate the role of oxidative stress in the regulation of ABC transporters in human lung cancer (A549) cells facing substrate (doxorubicin, DOX) and nonsubstrate (ethanol, ETH and hydrogen peroxide, HP) chemicals. After 24‐h treatment, all the chemicals caused significant cytotoxicity as reflected by the reduction in cell viability and the increase in reactive oxygen species (ROS) levels. Depending on the rescuing effects of ROS scavenger including glutathione (GSH) and Vitamin C, the toxicity dependence on oxidative stress were found to be HP > ETH > DOX. The addition of transporter inhibitors significantly enhanced the ROS levels and death‐inducing effects of chemicals, indicating the universal detoxification function of ABC transporters. At moderate ROS levels (about 3–4‐folds of control levels, caused by 10 μM DOX, 400 mM ETH, and 400 μM HP), all the three chemicals induced the gene expressions and activities of ABC transporters, but these values decreased at too high ROS levels (8.36‐folds of control levels) caused by HP at LC50 (800 μM). Such induction could be attenuated by GSH and KCZ, and was completely abolished by 50 μM KCZ, indicating an important role of oxidative stress and pregnane X receptor (PXR) in the induction of ABC transporters. Finally, this paper revealed the critical role of oxidative stress in the modulation of ABC transporters by either substrate or nonsubstrate chemicals during 24‐h treatment. Such information should be beneficial for overcoming ABC transporter‐mediated multidrug resistance. [ABSTRACT FROM AUTHOR]

This paper is concerned with a class of cancer invasion model with nonlinear diffusion and remodeling of ECM. The primary difficulty that arises here is that due to nonlinear diffusion, the good coupling structure between the diffusion term and haptotactic term is destroyed, rendering the effective methods used in the linear diffusion model no longer applicable. Fortunately, we have found a new effective combination between the diffusion term and the haptotactic term, which allows the diffusion term to dominate the haptotactic term, thus preliminarily improving the regularity of the weak solution. Based on these results, we can prove part of long‐time asymptotic behavior of the solution, thereby finally proving the uniform boundedness of the weak solution. Subsequently, by improving the convergence of cancer cells u from Lp$L^p$‐norm to L∞$L^\infty$‐norm, it is also proved that after a long time, the weak solution will eventually be Hölder continuous for some slow diffusion cases. [ABSTRACT FROM AUTHOR]

Drug resistance is a hot topic issue in cancer research and therapy. Although cancer therapy including radiotherapy and anti‐cancer drugs can kill malignant cells within the tumor, cancer cells can develop a wide range of mechanisms to resist the toxic effects of anti‐cancer agents. Cancer cells may provide some mechanisms to resist oxidative stress and escape from apoptosis and attack by the immune system. Furthermore, cancer cells may resist senescence, pyroptosis, ferroptosis, necroptosis, and autophagic cell death by modulating several critical genes. The development of these mechanisms leads to resistance to anti‐cancer drugs and also radiotherapy. Resistance to therapy can increase mortality and reduce survival following cancer therapy. Thus, overcoming mechanisms of resistance to cell death in malignant cells can facilitate tumor elimination and increase the efficiency of anti‐cancer therapy. Natural‐derived molecules are intriguing agents that may be suggested to be used as an adjuvant in combination with other anticancer drugs or radiotherapy to sensitize cancer cells to therapy with at least side effects. This paper aims to review the potential of triptolide for inducing various types of cell death in cancer cells. We review the induction or resistance to different cell death mechanisms such as apoptosis, autophagic cell death, senescence, pyroptosis, ferroptosis, and necrosis following the administration of triptolide. We also review the safety and future perspectives for triptolide and its derivatives in experimental and human studies. The anticancer potential of triptolide and its derivatives may make them effective adjuvants for enhancing tumor suppression in combination with anticancer therapy. [ABSTRACT FROM AUTHOR]

This paper presents a personal, selective, and sometimes critical retrospective of the history of ABC transporters in multidrug resistance (MDR) of cancer cells, overrepresenting discoveries of some early pioneers, long forgotten, and highlights of research in Amsterdam, mainly focussing on discoveries made with disruptions of ABC genes in mice (KO mice) and on the role of ABC transporters in causing drug resistance in a mouse model of mammary cancer. The history is complemented by a list of erroneous concepts often found in papers and grant applications submitted anno 2020. [ABSTRACT FROM AUTHOR]

Linear tetrapyrroles, called phyllobilins, are obtained as major catabolites upon chlorophyll degradation. Primarily, colorless phylloleucobilins featuring four deconjugated pyrrole units were identified. Their yellow counterparts, phylloxanthobilins, were discovered more recently. Although the two catabolites differ only by one double bond, physicochemical properties are very distinct. Moreover, the presence of the double bond seems to enhance physiologically relevant bioactivities: in contrast to phylloleucobilin, we identified a potent anti‐proliferative activity for a phylloxanthobilin, and show that this natural product induces apoptotic cell death and a cell cycle arrest in cancer cells. Interestingly, upon modifying inactive phylloleucobilin by esterification, an anti‐proliferative activity can be observed that increases with the chain lengths of the alkyl esters. We provide first evidence for anti‐cancer activity of phyllobilins, report a novel plant source for a phylloxanthobilin, and by using paper spray MS, show that these bioactive yellow chlorophyll catabolites are more prevalent in Nature than previously assumed. [ABSTRACT FROM AUTHOR]

Immunotherapy using immune checkpoint inhibitors (ICIs) has shown superior efficacy compared with conventional chemotherapy in certain cancer types, establishing immunotherapy as the fourth standard treatment alongside surgical intervention, chemotherapy, and radiotherapy. In cancer immunotherapy employing ICIs, CD8‐positive cytotoxic T lymphocytes are recognized as the primary effector cells. For effective clinical outcomes, it is essential that the targeted cancer cells express HLA class I molecules to present antigenic peptides derived from the tumor. However, cancer cells utilize various mechanisms to downregulate or lose HLA class I molecules from their surface, resulting in evasion from immune surveillance. Correlations between prognosis and the integrity of HLA class I molecules expressed by cancer cells have been consistently found across different types of cancer. This paper provides an overview of the regulatory mechanisms of HLA class I molecules and their role in cancer immunotherapy, with a particular emphasis on the significance of utilizing pathological tissues to evaluate HLA class I molecules expressed in cancer cells. [ABSTRACT FROM AUTHOR]

In recent years, cancerous cases have increased remarkably worldwide, and metastasis is the leading cause of death. Therefore, research on the early detection of cancer and metastasis has expanded to aid successful cancer treatment. Here in this paper, at the first step, an electrospun nanofibrous membrane (NFM) with a core‐shell structure was fabricated from PCL and HA to achieve cancer cell capturing (about 75% of cells). On the other hand, hyaluronic acid (HA)‐functionalized graphene quantum dots (GQDs) were used to detect captured cancer cells on NFM through the changes in photoluminescence intensity. Therefore, CD44 receptor‐HA interaction is the main principle used for both entrapment and detection of cancer cells. Results demonstrated the GQD‐HA fluorescent intensity of solution decreased through the increase of the captured cancer cell numbers on NFM, which is related to the more adsorption of GQD nanocomposites to the CD44 receptors. In contrast, this intensity for noncancerous cells was steady with any cell concentrations. This difference shows the system's remarkable selectivity and specificity, which can be crucial in fluorescent imaging for accurate cancer diagnosis. [ABSTRACT FROM AUTHOR]

Background: The effects of laser therapy on normal cells are well known and accepted, but the impact of this therapy on malignant cells are not yet fully understood. This review aims to map and outline what the scientific literature addresses on the effects of laser therapy on malignant cells. Methods: This review article followed the guidelines of the PRISMA‐ScR protocol, being all the search, analysis, and selection of articles based on it. Results: After all application of the predetermined criteria, five studies were included, dated between the years 2013 and 2021. With the complete reading of the selected studies, 100% of the articles were classified as category III of the Agency for Healthcare as Research and Quality classification. Similar themes among the papers included were investigated and compared. In these five studies, the visible red and near infrared wavelengths were used, and energy densities varied between 1 and 5 J/cm2. It was observed that low‐level laser could alter the expression of cell proliferation and migration proteins, such as cyclin D1, E‐cadherin, and β‐catenin. In addition, changes related to increased cell viability and metabolism were also identified. Conclusion: The low‐level laser seems to positively regulate the proliferative, migratory, and viability capacity of neoplastic cells, depending on the protocol used. All these studies included in the review are equivalent to in vitro studies; the cells are not in such a complex environment as is an organized tissue, making it necessary to carry out more complex tests, such as in vivo research. [ABSTRACT FROM AUTHOR]

Inertial microfluidics is a high‐throughput and high‐efficiency cell separation approach to which attention has been progressively paid in recent years. However, research on the influencing factors that compromise the efficiency of cell separation is still lacking. Therefore, the aim of this study was to evaluate the cell separation efficiency by changing the influencing factors. A four‐ring inertial focusing spiral microchannel was designed to separate two kinds of circulating tumor cells (CTCs) from blood. Human breast cancer (MCF‐7) cells and human epithelial cervical cancer (HeLa) cells enter the four‐ring inertial focusing spiral microchannel together with blood cells, and cancer cells and blood cells were separated from each other at the outlet of the channel by inertial force. The cell separation efficiency at the inlet flow rate in the Reynolds number range of 40–52 was studied by changing the influencing factors such as the cross‐sectional shape of the microchannel, the average thickness of the cross‐section, and the trapezoidal inclination angle. The results showed that the reduction of the channel thickness and the increase of a certain trapezoidal inclination enhanced the cell separation efficiency to a certain extent, the study showed that when the channel inclination was 6 ° and the average channel thickness was 160 μm. The two kinds of CTC cells could be completely separated from the blood and the efficiency could reached 100%. Significance statement: In this study, a helical inertial focusing microchannel was designed by summarizing the previous experiences. Based on the previous studies, the influences of the channel factors on the separation efficiency and focusing range of two circulating tumor cells (CTCs) in blood cells were studied. In this paper, three important influencing factors, namely channel Reynolds number, channel inclination and average channel thickness, were systematically summarized, the changes of these three influencing factors, the separation efficiency of CTCs, and the focus range were drawn in detail, and the channel itself factors which were most suitable for the separation of two CTCs in blood were summarized. This will lay a foundation for subsequent research on the influence of channel factors on the focusing effect and separation efficiency of particles in the channel [ABSTRACT FROM AUTHOR]

This paper reports the synthesis of multi‐layer SiO2@Au@SiO2@QDs nanoparticles with a dual‐functionality of simultaneous heating and temperature sensing and their applications to in vitro chemo‐thermal therapy. The heating is activated by a NIR‐light through resonance excitation of surface plasma while in‐situ thermal sensing is accomplished by the QDs photoluminescent (PL) effect. These dual function nanoparticles are used as a drug carrier for in vitro chemotherapy‐photothermal co‐treatment for malignant cells. A comparative study of drug release profiles was performed with and without 808 nm laser irradiation. The drug release rate was accelerated by a rise of temperature, which is induced by plasmonic heat generation associated with Au nanoshells; while the temperature change is monitored by the QD nanoparticles at the same time. The results showed that SiO2@Au@SiO2@QDs‐DOX platform enabled the combination of local specific chemotherapy with external near‐infrared (NIR) photothermal therapy and significantly improved the efficacy of cancer treatment. This combined treatment demonstrated synergistic chemotherapeutic‐thermal effects compared to chemotherapy or photothermal therapy alone, resulting in higher efficacy. [ABSTRACT FROM AUTHOR]

In this paper, a new diastereomerically pure isoxazolines were efficiently prepared from (S)‐verbenone, the procedure involves a regioselective and a diastereoselective 1,3‐dipolar cycloaddition of nitrile oxides on the monoterpene's enone. The structures of the newly obtained cycloadducts were confirmed by analytical and spectral studies (HRMS, 1H NMR, and 13C NMR). The relative stereochemistry of isoxazoline compounds 3a, 3c, and 3d were confirmed by x‐ray single crystal analysis. Hirshfeld surface analysis and two‐dimensional fingerprint plots were performed to analyze the different intermolecular contacts in crystal packing. Further, density functional theory calculations have been used to analyze the electronic and geometric frontier molecular orbital and molecular electrostatic map analyses of the compounds to predict the reactive site. All compounds were evaluated in vitro for their cytotoxic activity against four human cancer cell lines including fibrosarcoma HT‐1080, lung carcinoma A‐549 and breast adenocarcinoma (MCF‐7 and MDA‐MB‐231). Compound 3d was the most potent compound especially against HT‐1080 and A‐549 cancer cells with IC50 values of 21.35 ± 1.51 and 14.92 ± 1.74 μM, respectively. Mechanistically, the compound 3d induced apoptosis by significant caspase activation in HT‐1080 and A‐549 cancer cell lines utilizing flow cytometric analysis and caspase 3/7 activation assay. The examined compound 3d caused S cell cycle arrest in both HT‐1080 and A‐549 cells. [ABSTRACT FROM AUTHOR]

The nanostructures have the great potential for novel medical and drug delivery applications. In present paper a green approach for the preparation of pure nickel oxide (NiO) and 5% cobalt‐doped NiO (Co╫NiO) nanoparticles (NPs) by using Prosopis fracta extract have been study. The product of Co╫NiO NPs was proved through the PXRD, Raman, UV–Vis, FESEM, and EDX analyses. The results of XRD, EDX, and UV–Visible spectra displayed well doped cobalt in NiO NP. The particle sizes of Co╫NiO NPs were observed to be about 80 nm. The MTT test results for the cytotoxicity of Co╫NiO NPs on breast cancer cells (MCF‐7) affirmed the stronger impact of doped NiO‐NPs on cancer cells compared to NiO NPs. Thus, it is indicated that the doping process on NiO NPs caused an increase in its inhibitory effect against MCF‐7 cells. Research Highlights: Cobalt‐doped NiO nanoparticles were prepared using ecofriendly synthesis method and their cytotoxicity studied against MCF‐7 cells. [ABSTRACT FROM AUTHOR]

Breast cancer is the most common malignancy in the world and one of the leading causes of cancer death, which is a heterogeneous disease involving genetic and environmental factors. Breast cancer stem cells (BCSCs) are the main players in the aggressiveness of different tumors, at the same time, these cells are the main challenge for cancer treatment. There are multiple treatment options for breast cancer (BC) patients and the lack of understanding of prognostic and predictive biomarkers for breast cancer is a potential research direction for us to develop better treatments in the future. In this paper, we conducted a correlation analysis between SIK2 and clinical traits by searching numerous BRCA datasets in the GEO database. The model was constructed and validated by incorporating tumor samples from the TCGA‐BRCA cohort. Surprisingly, we found differential expression of SIK2 gene in individual tumor samples from the UCSC database. Subsequently, we found significantly high expression of SIK2 in epithelial cells by comparing the differential expression of SIK2 in different cell subpopulations and performed subsequent immune infiltration and pathway correlation analysis. Differential genes in SIK2+ epithelial cells, which may be potential therapeutic targets for breast cancer. In conclusion, our results suggest that SIK2 may be a potential prognostic and predictive biomarker that could serve as an oncogenic messenger for breast cancer. This discovery of SIK2 may provide more valuable references for potential therapeutic tools for breast cancer. [ABSTRACT FROM AUTHOR]

Designing kinase inhibitors that bind to the substrate site of oncogenic kinases in a promising, albeit less explored, approach to kinase inhibition as it was sought to avoid the issue of untoward off‐target modulations. Our previously identified compound KAC‐12 with a meta‐chlorophenyl substitution was an example of this approach. While it showed confirmed inhibitory activity against cancer cells, this substitution shifted the profile of affected targets away from Src/tubulin which were seen with the parent KX‐01. In this paper, we synthesized compounds with ortho‐substitutions, and we investigated the effect of such substitutions on their cellular and subcellular activities. The compound N‐(4‐(2‐(benzylamino)‐2‐oxoethyl)phenyl)‐2‐(morpholine‐4‐carbonyl)benzamide (4) exhibited substantial activities against cell lines such HCT116 (IC50 of 0.97 μM) and IC50 HL60 (2.84 μM). Kinase profiling showed that compound 4 trended consistently with KAC‐12 as it did not affect Src, but it had more impact on members of the Src family of kinases (SFK) such as Yes, Hck, Fyn, Lck, and Lyn. Both compounds exhibited profound downregulation effects on Erk1/2 but differed on others such as GSK3α/β and C‐Jun. Collectively, this study further support to the hypothesis that small structural changes might bring higher changes in their kinome profile. [ABSTRACT FROM AUTHOR]

Cystic lesions of the anterior head and neck region are a challenging and frequent finding on cytological smears. The scant amount of cellular material in cystic slides poses the greatest difficulty to interpretation, so that frequently they are diagnosed as inadequate or with minimal cellular component. Despite the majority of cystic lesions being benign, a minor portion consist of malignant cystic entities. In these latter cases, the evidence of very scant malignant cells can be misdiagnosed and/or underestimated, leading to a false negative diagnosis. Many papers have already described and detailed the range of possible benign and malignant cystic lesions in head and neck. In the current review we have focused on the less common entities that often lead to serious misinterpretation. [ABSTRACT FROM AUTHOR]

The incidence of breast cancer has increased considerably in recent years. Many efforts have been made to develop various nano‐drug delivery systems with specific properties to achieve effective and specific therapy. The stealthy nanoliposomes are the most successful and promising candidates for providing targeted tumor therapy. In this paper, a synthesized PEtOx‐DOPE (poly(2‐Ethyl 2‐Oxazoline)‐Dioleoyl Phosphatidylethanolamine) copolymer was equipped with a breast cancer‐recognizing tumor‐homing peptide to achieve cell‐specific delivery. The prepared liposomes provided stability for 6 months, and their hydrodynamic diameters are around 100 nm. Targeted liposomes remarkably exhibited 8 times higher cellular internalization in comparison with the nontargeted cells in flow cytometry and confocal microscopy. Furthermore, liposome constructs displayed slight toxicity on HaCaT cells when treated with high doses. Hence, Peptide 18‐conjugated PEtOx‐DOPE liposome systems can serve as favorable candidates in breast cancer‐targeted therapy. [ABSTRACT FROM AUTHOR]

In the automated diagnosis of breast cancer (BC), microscopic images based on multi‐classification play a prominent role. Multi‐classification of BC means to differentiate among the sub‐categories of BC (papillary carcinoma, ductal carcinoma, fibroadenoma, etc.). However, unpretentious contrasts in various sub‐categories of BC occur due to the wide fluctuation of 1) excessive coherency of malignant cells, 2) high definition image appearance, and 3) excessive heterogeneity in color distribution, which makes the task more crucial. Therefore, the automated sub‐category discrimination using microscopic images has great medical diagnostic significance yet has not much explored. Thus, the present paper proposes a framework based on machine learning (ML) and deep learning (DL) to multi‐classify BC cells into 8 sub‐categories. These 8 sub‐categories comprise four kinds that delineate benigncy, and the other four portray malignancy. More appropriately, both the ML and DL models with the concept of transfer learning have been proposed as DeepML framework to achieve multi‐classification of BC using histopathological images. The DeepML framework has achieved distinguished performance (approx. 98% & 89% average accuracy for 90–10% and 80–20% train‐test split, respectively) on a wide scale dataset, which intimate the quality of the proposed framework among existing approaches. [ABSTRACT FROM AUTHOR]

In this paper 25 novel 5‐trifluoromethyl‐1H‐pyrazole‐4‐carboxamide derivatives were designed, synthesized, and evaluated for their in vitro anticancer and antifungal activities; some exhibited good anticancer activity against cancer cells and antifungal activity against fungi. The IC50 values of T1, T4, T6, and T7 against A549 cells were 24.9, 21.9, 14.0, and 10.2 μM, respectively, and those of T15 against Thanatephorus cucumeris and Botryosphaeria dothidea were 22.0 and 27.7 μg/ml, respectively. A morphological study using FM and SEM demonstrated that T15 destroys the integrity and permeability of the T. cucumeris cell membrane. The results of molecular docking between T15 and SDH (PDB code: 2FBW) indicated that amide and trifluoromethyl might be the key functional groups for target compounds with high fungicidal activities. [ABSTRACT FROM AUTHOR]

M6A reader YTH structural domain family 2 (YTHDF2) has been recognized to play an oncogenic role in numerous tumors, but its role in cervical cancer has not been extensively discussed yet. This paper was designed to explore the role of YTHDF2 in cervical cancer and identify its underlying mechanism. The expression of YTHDF2 was first determined in cervical cancer cells by quantitative reverse‐transcription polymerase chain reaction and western blot. Then, the migration, invasion, and epithelial–mesenchymal transition (EMT) process were observed in YTHDF2‐knockdown Hela cells using wound healing, transwell and immunofluorescence assays. The cisplatin chemosensitivity of Hela cells was also investigated by assessing cell activity with cell counting kit‐8 and TUNEL (terminal deoxynucleotidyl transferase‐mediated dUTP nick end labeling). After MeRIP‐Seq assay and actinomycin D treatment to confirm the binding relationship between YTHDF2 and AXIN1, the migration, invasion, EMT process, and cisplatin chemosensitivity were assessed again in Hela cells silenced by YTHDF2 and AXIN1 or treated with Wnt agonist. YTHDF2 was increased in cervical cancer cells, and depletion of YTHDF2 led to reduced migration, invasion and EMT process but enhanced chemosensitivity of cisplatin in Hela cells. Furthermore, YTHDF2 could bind to and stabilize the expression of AXIN1. When the YTHDF2‐knockdown Hela cells were further transfected with AXIN1 knockdown or treated with Wnt agonist, the effects of YTHDF2 knockdown on the migration, invasion and EMT process were partially abolished, together with reduced cisplatin chemosensitivity. To sum up, we reported that YTHDF2 interference could suppress the EMT of cervical cancer cells and enhance cisplatin chemosensitivity by regulating AXIN1. [ABSTRACT FROM AUTHOR]

Eleven novel ciprofloxacin/gatifloxacin‐1,2,3‐triazole‐isatin hybrids (8a–k) were designed, synthesized, and screened for their in vitro anticancer activity in this paper. A significant part of the synthesized hybrids was active against A549, HepG2, and SF‐268 cancer cell lines, whereas the parent drugs ciprofloxacin and gatifloxacin were devoid of activity. Among them, hybrid 8i (IC50: 78.1–90.7 μM) was found to be the most active against A549, HepG2, and SF‐268 cancer cell lines, and it was comparable with or better than Vorinostat (IC50: 71.1 to >100 μM). Thus, these kind hybrids have potentiality for discovery of new anticancer candidates for clinical deployment in the control and eradication of cancers. [ABSTRACT FROM AUTHOR]

Summary: Properties of a cell can determine its deformations, which can aggravate cancer metastasis. In laboratory, microfluidic technology has been adopted to study cell deformations. However, quantifying the effects of cell deformations has remained difficult. To this end, this paper presents a two‐dimensional particle‐based model that can capture flow‐induced cell deformations in a microchannel. The numerical model is validated with an experimental dataset for MCF7 cell. The simulations show that cell deformations are dominantly attributed to flow acceleration. Stress analyses, conducted by inputting the simulated cell deformations as boundary conditions, show that the maximum normal stresses correspond well to high deformations. Shear stress is in general proportional to the cell's distance from a wall. The simulations also suggest a deformed cell shape that apparently may reduce the average normal stresses. This study highlights the potential of the numerical model to relate the measurable cell deformations to the more elusive cell properties. [ABSTRACT FROM AUTHOR]

The diagnosis of solid tumors of epithelial origin (carcinomas) represents a major part of the workload in clinical histopathology. Carcinomas consist of malignant epithelial cells arranged in more or less cohesive clusters of variable size and shape, together with stromal cells, extracellular matrix, and blood vessels. Distinguishing stroma from epithelium is a critical component of artificial intelligence (AI) methods developed to detect and analyze carcinomas. In this paper, we propose a novel automated workflow that enables large‐scale guidance of AI methods to identify the epithelial component. The workflow is based on re‐staining existing hematoxylin and eosin (H&E) formalin‐fixed paraffin‐embedded sections by immunohistochemistry for cytokeratins, cytoskeletal components specific to epithelial cells. Compared to existing methods, clinically available H&E sections are reused and no additional material, such as consecutive slides, is needed. We developed a simple and reliable method for automatic alignment to generate masks denoting cytokeratin‐rich regions, using cell nuclei positions that are visible in both the original and the re‐stained slide. The registration method has been compared to state‐of‐the‐art methods for alignment of consecutive slides and shows that, despite being simpler, it provides similar accuracy and is more robust. We also demonstrate how the automatically generated masks can be used to train modern AI image segmentation based on U‐Net, resulting in reliable detection of epithelial regions in previously unseen H&E slides. Through training on real‐world material available in clinical laboratories, this approach therefore has widespread applications toward achieving AI‐assisted tumor assessment directly from scanned H&E sections. In addition, the re‐staining method will facilitate additional automated quantitative studies of tumor cell and stromal cell phenotypes. [ABSTRACT FROM AUTHOR]

In the past few years, the evolution of immunotherapy has resulted in a shift in cancer treatment models. However, with immunosuppressive effects of the tumour microenvironment continues to limit advances in tumour immunotherapy. The tumour microenvironment induces metabolic reprogramming in cancer cells, which results in competition for nutrients between tumour cells and host immunocytes. Metabolic and waste products originating in tumour cells can influence the activation and effector properties of immunocytes in numerous ways and ultimately promote the survival and propagation of tumour cells. In this paper, we discuss metabolic reprogramming in tumour cells and the influence of metabolite by‐products on the immune microenvironment, providing novel insights into tumour immunotherapy. [ABSTRACT FROM AUTHOR]

Breast cancer (BC), which is widely considered as the most common cancer in women around the world, evokes ~1.7 million new BC cases and 522,000 BC‐related deaths each year. Triple negative breast cancer (TNBC) is clinically confirmed as one of the most aggressive subtypes of BC. ORY‐1001, a clinically used lysine specific demethylase 1 (LSD1/KDM1A) inhibitor, was investigated herein to confirm its role in the progression of TNBC and reveal the potential mechanism. After treatment with ORY‐1001 in MDA‐MB‐231 and BT549 cells, the cell proliferation and apoptosis were respectively measured by CCK‐8 and TUNEL assays. The expression of proliferation‐ and apoptosis‐associated proteins was tested by means of western blot analysis. Then, R1881, an androgen receptor (AR) agonist, was used to evaluate whether the effects of ORY‐1001 on proliferation and apoptosis of TNBC cells was mediated by regulating AR. Results indicated that ORY‐1001 treatment restrained the proliferation while enhanced the apoptosis of BC cells, accompanied by the change of proliferation‐ and apoptosis‐related proteins expression. Furthermore, ORY‐1001 reduced the level of AR in BC cells. After the activation of AR by R1881, the decreased proliferation and enhanced apoptosis of BC cells triggered by ORY‐1001 intervention were partially abolished. In conclusion, this paper has presented the first evidence to suggest that ORY‐1001 inhibits proliferation and promotes apoptosis of TNBC cells by suppressing AR expression, which may constitute the theoretical basis for the clinical use of ORY‐1001 in the treatment of this disease. [ABSTRACT FROM AUTHOR]

This corrigendum addresses errors in a previously published paper titled "Plasma‐activated medium induces apoptosis in chemotherapy‐resistant ovarian cancer cells: High selectivity and synergy with carboplatin." The corrections involve clarifying a confusing sentence and replacing three images in Figure 3 due to naming discrepancies. The authors assure readers that these corrections do not affect the overall results or conclusions of the study. They apologize for any confusion or inconvenience caused by the errors. [Extracted from the article]

A series of novel moxifloxacin/gatifloxacin‐1,2,3‐triazole‐isatin hybrids (8a–i) were designed, synthesized, and screened for their in vitro anticancer activity in this paper. All of the synthesized hybrids were active against A549 and HepG2 cancer cell lines, whereas the parent drugs moxifloxacin and gatifloxacin were devoid of activity. Among them, hybrid 8i (IC50: 41.1–98.3 μM) showed considerable activity against A549, HepG2, and MCF‐7 cancer cell lines, and it was no inferior to Vorinostat (IC50: 64.32 to >100 μM) against the three cancer cell lines. Thus, this kind of hybrids has potentiality for discovery of new anticancer candidates for clinical deployment in the control and eradication of cancers. [ABSTRACT FROM AUTHOR]

Aims: Tumour deposits (TDs) are clusters of cancer cells in the soft tissue that are discontinuous from the primary tumour. In this review we are exploring their relevance for prognosis in patients with gastric cancer. Methods and results: A literature search was performed to identify studies providing data on TDs and prognosis in gastric cancer patients. Eight papers were included in the meta‐analysis, which was carried out in terms of risk ratios (RR) and hazard ratios (HR) with 95% confidence interval (95% CI). Of 7445 patients, 1551 had TDs (20.9%). TDs were associated with a decreased overall survival (OS) in univariate (HR = 2.82, 95% CI = 1.9–4.3) and multivariate analyses (HR = 1.65, 95% CI = 1.3–2.1). TDs were also associated with known prognostic factors such as synchronous metastatic disease (RR = 9.5), invasion depth (RR = 1.8), lymph node metastasis (RR = 1.7), lymphatic invasion (RR = 1.7), vascular invasion (RR = 2.6) and poor differentiation (RR = 1.2). Conclusions: We found a strong indication that TDs are independent predictors of prognosis in patients with gastric cancer; hence, TDs should be included in the staging of gastric cancers. [ABSTRACT FROM AUTHOR]

This paper proposes a new dual horizontal squash capsule network (DHS‐CapsNet) to classify the lung and colon cancers on histopathological images. DHS‐CapsNet is made up of encoder feature fusion (EFF) and a novel horizontal squash (HSquash) function. The EFF aggregates the extracted feature from the 2‐lane convolutional layers, which provides rich information for better accuracy. HSquash is proposed as a squash function to ensure that vectors are effectively squashed and produces sparsity for a high discriminative capsule to extract important information from images with varied backgrounds. To present the effectiveness of DHS‐CapsNet empirically, we applied this method on histopathological images (LC25000 dataset). We achieved better results of 99.23% compared to traditional CapsNet (85.55%). The DHS‐CapsNet provides the top‐1 classification error of 0.77% compared to 14.45% of the traditional CapsNet. Our results illustrate that our method improves CapsNet and can be adopted as a computer‐aided diagnostic method to support doctors in lung and colon cancer diagnostics. [ABSTRACT FROM AUTHOR]

In this paper, we present a mathematical model that analyzes cancer treatment via radiotherapy and proposes ways to control its progression. To identify preventive measures for cancer in its early stages, scientists have studied both risk factors and protective factors. In our model, we consider the disease‐free equilibrium points, namely, the trivial equilibrium (TE), healthy cell absenteeism equilibrium (HCAE), cancer cell absenteeism equilibrium (CCAE), and cancer cell incidence equilibrium (CCIE). We use nonlinear analysis techniques and the spectral radius method to study the stability and instability of systems. Since the reproduction number plays a critical role in stability analysis, we use the spectral radius method to evaluate it. We have also added a control function to the model to enhance it by including interactions between healthy and cancer cells. Optimization techniques are used to identify the limitations and needs of the problem and derive the best solutions to control the tumor. We conduct sensitivity analysis with respect to various parameters to study the model's robustness. To validate our methods and results, we provide simulations and numerical analysis. [ABSTRACT FROM AUTHOR]

Luminogens with aggregation-induced emission characteristics (AIEgens) are intriguing due to its rapid expansion in various high-tech applications. However, there is still in high demand on the development of novel AIEgens with easy preparation and functionalization, stable structures, tunable emissions, and high quantum efficiency. In this contribution, three AIEgens based on diphenyl isoquinolinium (IQ) derivatives are reported. They can be facilely synthesized and possess high structural stability, favorable visible light excitation, large Stokes shifts, high quantum yields, tunable colors, and sufficient two-photon absorption of near-infrared light. Importantly, they exhibit multifunctionalities. They exhibit mechanochromic property, making them capable to be applied for rewritable papers. They can also be applied in mitochondrial imaging with high specificity, cell permeability, brightness, biocompatibility, and photostability. They are promising for the applications in evaluation of mitochondrial membrane potential and image-guided cancer cell ablation. Last, they are able to stain bacteria in a wash-free manner. All these intriguing results suggest such readily accessible and multifunctional diphenyl IQ-based AIEgens provide a new platform for construction of advanced materials for practical applications. [ABSTRACT FROM AUTHOR]

Cell separation technique is essential for the detection of circulating tumor cells in blood and for enrichment of stem cell in regenerative medicine. However, conventional methods require cell labeling such as antibodies, which may damage the cells during the operation. Therefore, dielectrophoresis (DEP), a "label‐free" separation technique that eliminates the effects on cells, has been attracting attention. In this paper, we investigated the dielectric properties of Jurkat cells derived from human T‐cell leukemia cells by dielectrophoretic velocimetry. An equivalent circuit model of the cell was constructed and the frequency characteristics of the voltage of each layer of the cell were calculated. As a result, it was shown that the live and dead cells showed opposite dielectrophoretic forces in the region below 10 kHz, indicating the possibility of separating them. The agreement between the theoretical calculations and the experimental results shows the validity of the equivalent circuit model. [ABSTRACT FROM AUTHOR]

The large majority of TACA-based (TACA=Tumor-Associated Carbohydrate Antigens) antitumor vaccines target only one carbohydrate antigen, thereby often resulting in the incomplete destruction of cancer cells. However, the morphological heterogeneity of the tumor glycocalix, which is in constant evolution during malignant transformation, is a crucial point to consider in the design of vaccine candidates. In this paper, an efficient synthetic strategy based on orthogonal chemoselective ligations to prepare fully synthetic glycosylated cyclopeptide scaffolds grafted with both Tn and TF antigen analogues is reported. To evaluate their ability to be recognized as tumor antigens, direct interaction ELISA assays have been performed with the anti-Tn monoclonal antibody 9A7. Although both heterovalent structures showed binding capacities with 9A7, the presence of the second TF epitope did not interfere with the recognition of Tn except in one epitope arrangement. This heterovalent glycosylated structure thus represents an attractive epitope carrier to be further functionalized with T-cell peptide epitopes. [ABSTRACT FROM AUTHOR]