Early diagnosis of cancer using circulating microbial DNA.

The study by Chen et al. has advanced research by developing predictive models based on circulating microbial DNA, offering potential for early cancer detection and personalized treatment. However, further validation and simplification of techniques are needed for widespread clinical application.

Psychosocial needs of post-radiotherapy cancer survivors and their direct caregivers - a systematic review.

Radiotherapy is an important modality for cancer treatment. About 50% of cancer patients receive radiotherapy, and one-third of radiotherapy recipients were identified as having unmet psychosocial needs. The unmet psychosocial needs worsen the patient's quality of life and treatment effectiveness. This review aims to identify the psychosocial needs of post-radiotherapy cancer survivors and their direct caregivers. Systematic research of Embase, Scopus and PubMed was done and 17 studies were selected for analysis. The results show that patients encounter distress and fear due to treatment immobilization and unfamiliarity with procedures respectively. Information provision is a common need raised by patients and caregivers. Patients and caregivers report relationship problems due to affected sexual functions. To facilitate future studies, solutions to each identified psychosocial need are proposed in the discussion based on the 17 selected papers and other supporting literature. This review proposes art therapy to alleviate psychological distress, and pre-treatment information sessions to reinforce information delivery. Creative interventions such as a sexual rehabilitation program are recommended. Future studies are warranted to examine the interventions and thus improve the patients' and caregivers' well-being.

Proteomic Profiling of Chemotherapy Responses in FOLFOX-Resistant Colorectal Cancer Cells.

Chemoresistance mechanisms of colorectal cancer remain largely elusive. We aim to compare the difference of chemotherapy responses between FOLFOX-resistant and wild-type colorectal cancer cells by proteomic profiling to suggest novel treatment targets. FOLFOX-resistant colorectal cancer cells DLD1-R and HCT116-R were developed by chronic exposure to progressive FOLFOX doses. Proteomic profiling of FOLFOX-resistant and wild-type cells under FOLFOX exposure were conducted by mass-spectrometry-based protein-analysis technology. Verification of selected KEGG pathways was conducted by Western blot. DLD1-R had significantly higher FOLFOX-chemoresistance (10.81 times) than its wild-type counterpart. A total of 309 and 90 differentially expressed proteins were identified in DLD1-R and HCT116-R, respectively. In terms of gene ontology molecular function, RNA binding and cadherin binding ranked first for DLD1 and HCT116 groups, respectively. For gene set enrichment analysis, ribosome pathway and DNA replication were significantly up-regulated and down-regulated in DLD1-R, respectively. The most significantly up-regulated pathway in HCT116-R was regulation of the actin cytoskeleton. Up-regulations in the ribosome pathway (DLD1-R) and actin cytoskeleton (HCT116-R) were verified by Western blot. There were several significantly altered signaling pathways in FOLFOX-resistant colorectal cancer cells under FOLFOX with notable up-regulations in the ribosomal process and actin cytoskeleton.

In Vivo Reversal of P-Glycoprotein-Mediated Drug Resistance in a Breast Cancer Xenograft and in Leukemia Models Using a Novel, Potent, and Nontoxic Epicatechin EC31.

The modulation of P-glycoprotein (P-gp, ABCB1) can reverse multidrug resistance (MDR) and potentiate the efficacy of anticancer drugs. Tea polyphenols, such as epigallocatechin gallate (EGCG), have low P-gp-modulating activity, with an EC50 over 10 µM. In this study, we optimized a series of tea polyphenol derivatives and demonstrated that epicatechin EC31 was a potent and nontoxic P-gp inhibitor. Its EC50 for reversing paclitaxel, doxorubicin, and vincristine resistance in three P-gp-overexpressing cell lines ranged from 37 to 249 nM. Mechanistic studies revealed that EC31 restored intracellular drug accumulation by inhibiting P-gp-mediated drug efflux. It did not downregulate the plasma membrane P-gp level nor inhibit P-gp ATPase. It was not a transport substrate of P-gp. A pharmacokinetic study revealed that the intraperitoneal administration of 30 mg/kg of EC31 could achieve a plasma concentration above its in vitro EC50 (94 nM) for more than 18 h. It did not affect the pharmacokinetic profile of coadministered paclitaxel. In the xenograft model of the P-gp-overexpressing LCC6MDR cell line, EC31 reversed P-gp-mediated paclitaxel resistance and inhibited tumor growth by 27.4 to 36.1% (p < 0.001). Moreover, it also increased the intratumor paclitaxel level in the LCC6MDR xenograft by 6 fold (p < 0.001). In both murine leukemia P388ADR and human leukemia K562/P-gp mice models, the cotreatment of EC31 and doxorubicin significantly prolonged the survival of the mice (p < 0.001 and p < 0.01) as compared to the doxorubicin alone group, respectively. Our results suggested that EC31 was a promising candidate for further investigation on combination therapy for treating P-gp-overexpressing cancers.

Suppression of small nucleolar RNA host gene 8 (SNHG8) inhibits the progression of colorectal cancer cells.

Colorectal cancer (CRC) is one of the most common gastrointestinal malignancies around the world with high mortality. Accumulating evidences demonstrate that long non-coding RNAs (lncRNAs) play critical roles in CRC tumorigenesis by regulating different pathways of carcinogenesis. SNHG8 (small nucleolar RNA host gene 8), a lncRNA, is highly expressed in several cancers and acts as an oncogene that promotes cancer progression. However, the oncogenic role of SNHG8 in CRC carcinogenesis and the underlying molecular mechanisms remain unknown. In this study, we explored the role of SNHG8 in CRC cell lines by performing a series of functional experiments. Similar to the data reported in the Encyclopedia of RNA Interactome, our RT-qPCR results showed that SNHG8 expression was significantly upregulated in CRC cell lines (DLD-1, HT-29, HCT-116, and SW480) compared to the normal colon cell line (CCD-112CoN). We performed dicer-substrate siRNA transfection to knockdown the expression of SNHG8 in HCT-116 and SW480 cell lines which were expressing high levels of SNHG8. SNHG8 knockdown significantly reduced CRC cell growth and proliferation by inducing autophagy and apoptosis pathways through the AKT/AMPK/mTOR axis. We performed wound healing migration assay and demonstrated that SNHG8 knockdown significantly increased migration index in both cell lines, indicating reduced migration abilities of cells. Further investigation showed that SNHG8 knockdown suppresses epithelial to mesenchymal transition and reduces cellular migratory properties of CRC cells. Taken together, our study suggests that SNHG8 acts as an oncogene in CRC through the mTOR-dependent autophagy, apoptosis, and EMT pathways. Our study provides a better understanding the role of SNHG8 in CRC at molecular level and SNHG8 might be used as novel therapeutic target for CRC management.

Autophagy in gastrointestinal cancers.

Gastrointestinal cancers are a group of cancers occurred in gastrointestinal tissues with high morbidity and mortality rate. Although numerous studies were conducted on the investigation of gastrointestinal cancers, the real mechanisms haven't been discovered, and no effective methods of prevention and treatment of gastrointestinal cancers have been developed. Autophagy, a vital catabolic process in organisms, have been proven to participate in various mechanisms and signaling pathways, thus producing a regulatory effect on various diseases. The role of autophagy in gastrointestinal cancers remains unclear due to its high complexity. In this review, firstly, the biological features of autophagy will be introduced. Secondly, the role of autophagy in three popular gastrointestinal cancers, namely esophageal cancer, gastric cancer, and colorectal cancer will be described and discussed by reviewing the related literature. We aimed to bring novel insights in exploring the real mechanisms for gastrointestinal cancers and developing effective and efficient therapeutic methods to treat gastrointestinal cancers.

Proteomic profiling of metabolic proteins as potential biomarkers of radioresponsiveness for colorectal cancer.

Surgery, radiation therapy (RT), and chemotherapy are commonly used treatment modalities for CRC management. The locally advanced CRC is managed with preoperative RT or in combination of chemoradiotherapy whereas palliative RT is recommended for metastatic CRC patients to enhance overall survival and reduce distressing symptoms. There are many biomarkers established based on tumour staging, grading and molecular characteristics of patients (e.g., mutation, DNA methylation, and gene expression profiling). Interestingly, none of these markers are adequately validated for RT scheme. In order to establish the radioresponsive biomarker in CRC, we established a mouse xenograft tumour model and applied radiation to the tumours. We identified 9 metabolic proteins, namely PGK1, PGAM1, ENO1, PKM, TKT, GLUD1, LDHA, GAPDH, and MDH2, which are differentially expressed in tumours with different radioresponsiveness. Furthermore, we validated their expression in tumours from the unirradiated, poorly responded and highly responded tumour groups. In addition, we analysed their expressions in clinical samples from the public database. Extensive literature studies shown that these metabolic proteins are associated with key biochemical pathways including, glycolysis, ammonia detoxification, carcinogenesis, and drug responses. Further studies are needed to translate our findings into clinical use. SIGNIFICANCE: With the increasing incidence of colorectal cancer (CRC) globally, it is crucial to establish strategic treatment protocol by personalizing cancer treatment. Despite the well-established treatment protocols for CRC in the past decades, the mortality remains high. There is a trend of applying personalized treatment to improve patient survival. It has been reported that biomarkers may be used to predict treatment outcomes or to adjust individual treatment protocols. This project aims to identify specific metabolic proteins as biomarkers for CRC radioresponsiveness. Using bioinformatical analysis, we have identified 9 metabolic proteins which could be used as potential biomarkers for radiation therapy in CRC tumours.

Advances in High Throughput Proteomics Profiling in Establishing Potential Biomarkers for Gastrointestinal Cancer.

Gastrointestinal cancers (GICs) remain the most diagnosed cancers and accounted for the highest cancer-related death globally. The prognosis and treatment outcomes of many GICs are poor because most of the cases are diagnosed in advanced metastatic stages. This is primarily attributed to the deficiency of effective and reliable early diagnostic biomarkers. The existing biomarkers for GICs diagnosis exhibited inadequate specificity and sensitivity. To improve the early diagnosis of GICs, biomarkers with higher specificity and sensitivity are warranted. Proteomics study and its functional analysis focus on elucidating physiological and biological functions of unknown or annotated proteins and deciphering cellular mechanisms at molecular levels. In addition, quantitative analysis of translational proteomics is a promising approach in enhancing the early identification and proper management of GICs. In this review, we focus on the advances in mass spectrometry along with the quantitative and functional analysis of proteomics data that contributes to the establishment of biomarkers for GICs including, colorectal, gastric, hepatocellular, pancreatic, and esophageal cancer. We also discuss the future challenges in the validation of proteomics-based biomarkers for their translation into clinics.

Ultrasensitive Detection of Ribonucleic Acid Biomarkers Using Portable Sensing Platforms Based on Organic Electrochemical Transistors.

The analysis of ribonucleic acid (RNA) plays an important role in the early diagnosis of diseases and will greatly benefit patients with a higher cure rate. However, the low abundance of RNA in physiological environments requires ultrahigh sensitivity of a detection technology. Here, we construct a portable and smart-phone-controlled biosensing platform based on disposable organic electrochemical transistors for ultrasensitive analysis of microRNA (miRNA) biomarkers within 1 h. Due to their inherent amplification function, the devices can detect miRNA cancer biomarkers from little-volume solutions with concentrations down to 10-14 M. The devices can distinguish blood miRNA expression levels at different cancer stages using a 4T1 mouse tumor model. The technique for ultrasensitive and fast detection of RNA biomarkers with high selectivity opens a window for mobile diagnosis of various diseases with low cost.

RAMS11 promotes CRC through mTOR-dependent inhibition of autophagy, suppression of apoptosis, and promotion of epithelial-mesenchymal transition.

BACKGROUND: Long non-coding RNAs (lncRNAs), a class of non-coding RNAs (ncRNAs) associated with diverse biological processes of cells. Over the past decades, cumulating research evidences revealed that abnormal expressions of lncRNAs are associated with colorectal cancer (CRC) initiation, progression, metastasis, and resistance to therapies. Moreover, their usefulness as candidate biomarkers for CRC diagnosis and prognosis are well evident throughout previous literature. In the current study, we examined the role and molecular mechanisms of newly identified lncRNA named RNA associated with metastasis-11 (RAMS11) in CRC development. METHODS: The expression of RAMS11 in CRC cell lines DLD-1, HT-29, HCT-116, and SW480 and colon normal cells CCD-112-CoN were evaluated by quantitative RT-qPCR. The results showed that the RAMS11 is significantly upregulated in CRC cell lines compared to the normal cells. The CCK-8 proliferation assay, colony formation assay, and migration assay were performed to evaluate the biological and physiological functions of RAMS11 in vitro. To decipher the molecular mechanisms of RAMS11 medicated CRC progression, we further performed western blot analysis of the key pathway proteins (e.g., AMPK, AKT, and mTOR). RESULTS: Our results revealed that higher expression of RAMS11 is associated with increased CRC proliferation, migration, and development of metastasis. Knockdown of RAMS11 induced autophagy, apoptosis along with reduction of epithelial-mesenchymal transition (EMT) suggesting that RAMS11 is involved in CRC progression. The molecular mechanisms of RAMS11 indicated that knockdown of RAMS11 significantly inhibited CRC carcinogenesis through mTOR-dependent autophagy induction. CONCLUSIONS: In sum, our results suggested that RAMS11 is an important oncogene in CRC pathogenesis. Targeting RAMS11 could be a potential therapeutic strategy for CRC management.

JNK in Tumor Microenvironment: Present Findings and Challenges in Clinical Translation.

The c-Jun N-terminal kinases (JNKs) are a group of mitogen-activated protein kinases (MAPKs). JNK is mainly activated under stressful conditions or by inflammatory cytokines and has multiple downstream targets for mediating cell proliferation, differentiation, survival, apoptosis, and immune responses. JNK has been demonstrated to have both tumor promoting and tumor suppressing roles in different cancers depending on the focused pathway in each study. JNK also plays complex roles in the heterogeneous tumor microenvironment (TME). JNK is involved in different tumorigenesis pathways. TME closely relates with tumor development and consists of various stressful and chronic inflammatory conditions along with different cell populations, in which the JNK pathway may have various mediating roles. In this review, we aim to summarize the present knowledge of JNK-mediated processes in TME, including hypoxia, reactive oxygen species, inflammation, immune responses, angiogenesis, as well as the regulation of various cell populations within TME. This review also suggests future research directions for translating JNK modulation in pre-clinical findings to clinical benefits.

Computer-assisted ultrasound assessment of plaque characteristics in radiation-induced and non-radiation-induced carotid atherosclerosis.

BACKGROUND: This study investigated the feasibility of using a computer-assisted method to evaluate and differentiate the carotid plaque characteristics in radiation-induced and non-radiation-induced carotid atherosclerosis. METHODS: This study included 107 post-radiotherapy (post-RT) nasopharyngeal carcinoma (NPC) patients and 110 subjects with cardiovascular risk factors (CVRFs). Each participant had a carotid ultrasound examination, and carotid plaques and carotid intima-media thickness (CIMT) were evaluated with grey scale ultrasound. The carotid plaque characteristics were evaluated for grey-scale median (GSM) and detailed plaque texture analysis (DPTA) using specific computer software. In DPTA, five different intra-plaque components were colour-coded according to different grey scale ranges. A multivariate linear regression model was used to evaluate the correlation of risk factors and carotid plaque characteristics. RESULTS: Post-RT NPC patients have significantly higher CIMT (748±15.1 µm, P=0.001), more patients had a plaque formation (80.4%, P<0.001) and more plaque locations (2.3±0.2, P<0.001) than CVRF subjects (680.4±10.0 µm, 38.2% and 0.5±0.1 respectively). Among the five intra-plaque components, radiation-induced carotid plaques had significantly larger area of calcification (4.8%±7.7%, P=0.012), but lesser area of lipid (42.1%±16.9%, P=0.034) when compared to non-radiation-induced carotid plaques (3.0%±5.7% and 46.3%±17.9% respectively). Age, radiation and number of CVRF were significantly associated with the carotid atherosclerosis burden (P<0.001). Besides, age was significantly associated with the amount of lipid and calcification within carotid plaques (P<0.001). CONCLUSIONS: Radiation caused more severe carotid artery disease than CVRF with larger CIMT and more prevalent of carotid plaque. Radiation-induced carotid plaques tended to have more intra-plaque calcifications, whereas non-radiation-induced carotid plaques had more lipids. Ultrasound aided by computer-assisted image analysis has potential for more accurate assessment of carotid atherosclerosis.

Cancer Susceptibility Candidate 9 (CASC9) Promotes Colorectal Cancer Carcinogenesis via mTOR-Dependent Autophagy and Epithelial-Mesenchymal Transition Pathways.

BACKGROUND: Colorectal cancer (CRC) is the third most common cancer worldwide. Many recent studies have demonstrated that different long non-coding RNAs (lncRNAs) are involved in the initiation, advancement, and metastasis of many cancers including CRC. Cancer susceptibility candidate 9 (CASC9) is an lncRNA that has been reported in many cancers, but its role in CRC is poorly understood. In this study, we aimed to examine the expression of CASC9 in CRC cell lines and to determine the mechanism of action of CASC9 in CRC carcinogenesis. METHODS: The expression of CASC9 in CRC tissues was compared with normal samples from publicly available datasets in The Cancer Genome Atlas (TCGA) and The Encyclopedia of RNA Interactomes (ENCORI). CASC9 expression was further verified in four CRC cell lines (DLD1, HT-29, SW480, and HCT-116) and normal colorectal cell line (CCD-112CoN) by real-time quantitative polymerase chain reaction (RT-qPCR). After gene silencing in HCT-116 and SW480, Cell Counting Kit-8 assay, clonogenic assay, and wound healing assay were performed to evaluate cell proliferation, viability, and migration index of cells. Western blotting was used to explore the key pathways involved. RESULTS: CASC9 was significantly upregulated as analyzed from both public datasets TCGA and ENCORI where its overexpression was associated with poor survival of CRC patients. Similarly, CASC9 was significantly overexpressed in the CRC cell lines compared with normal cells studied. The silencing of CASC9 in HCT-116 and SW480 attenuated cell proliferation and migration significantly. Furthermore, pathways investigations showed that silencing of CASC9 significantly induced autophagy, promoted AMP-activated protein kinase (AMPK) phosphorylation, inhibited mTOR and AKT signaling pathways, and altered epithelial-mesenchymal transition (EMT) marker protein expression. CONCLUSION: We demonstrated that silencing of CASC9 contributes to the reduced CRC cell proliferation and migration by regulating autophagy and AKT/mTOR/EMT signaling. Therefore, CASC9 plays an important role in carcinogenesis, and its expression may act as a prognostic biomarker and a potential therapeutic target of CRC management.

Immune Complexes Impaired Glomerular Endothelial Cell Functions in Lupus Nephritis.

Lupus nephritis (LN) is one of the most common and severe complications of lupus. However, the mechanisms for renal damage have not been well elucidated. There are evidences show that glomerular endothelial cells (GECs) are damaged in LN. Immune complexes can deposit in subendothelial area and could affect GEC functions. In the present study, we used heat-aggregated gamma globulin (HAGG) to simulate immune complexes and investigated their effects on GEC functions. Our results revealed that HAGG impaired different aspect of the GEC functions. HAGG changed cell morphology, upregulated the expression of active caspase-3, inhibited angiogenesis, and increased NO production in GECs. These results provide new clues for the mechanisms of renal damage and the pathology of LN.

Role of Regulatory T Cells in Noninherited Maternal Antigen-Related Tolerance in Cord Blood: An in Vitro Study.

Cord blood (CB) is an alternative stem cell source for allogeneic hematopoietic stem cell transplantation (HSCT). The unique advantages of using CB as a stem cell source are a degree of permissibility for HLA mismatch, rapid availability, and relatively risk-free cell collection. Because HLA is highly polymorphic and population-specific, optimal HLA-matched unrelated donors or cord blood units (CBUs) might not be available. In view of the possibility that matched CBUs that include noninherited maternal antigens (NIMAs) might contain acceptable HLA mismatches, we attempted to determine the degree of alloreactivity of CB mononuclear cells (MNCs) on stimulation by the maternal, paternal, and unrelated stimulator cells. Suppression of T cell proliferation, cytotoxicity, and a cytokine profile indicating suppressed Th1 and elevated IL-10 and TGF-ß1 responses were observed in the mixed lymphocyte reaction in response to NIMAs. The increases in IL-10 and TGF-ß1 production may be due to the Th2 response and/or regulatory T cells (Tregs). The reduced IL-10 and TGF-ß1 production after CD25 depletion could have been due to removal of Tregs from the CB cells. Thus, Tregs appear to play an important role in the CB MNC response to NIMAs, possibly due to the induction of IL-10 and TGF-ß1. We hope that our work can provide some evidence of the beneficial effect of NIMAs.

Immune complexes suppressed autophagy in glomerular endothelial cells.

Lupus nephritis is an immune-complexes mediated glomerulonephritis. Vascular lesions and endothelial cell injuries are common in lupus nephritis and important for renal damage. However, the precise mechanisms by which immune complexes lead to endothelial cell injuries are still unclear. Autophagy is a conserved metabolic process and shows protective roles in many cell types and diseases. In present study, we investigated whether immune complexes could affect autophagy and participate in endothelial dysfunctions. Heat-aggregated gamma globulin (HAGG) was used to substitute immune complexes. Glomerular endothelial cells (GECs) were incubated with HAGG and autophagy-related markers were evaluated. Results showed that HAGG suppressed autophagy in GECs, through Akt/mTOR-dependent pathway. The combination of HAGG and tumor necrosis factor-alpha suppressed autophagy in GECs and further decreased cell viabilities. The suppressed effects of HAGG on GECs autophagy and viability, especially under inflammatory microenvironment, may provide new views for explaining the mechanisms of renal impairments in lupus nephritis.

Autophagy-Modulating Long Non-coding RNAs (LncRNAs) and Their Molecular Events in Cancer.

Cancer is a global threat of health. Cancer incidence and death is also increasing continuously because of poor understanding of diseases. Although, traditional treatments (surgery, radiotherapy, and chemotherapy) are effective against primary tumors, death rate is increasing because of metastasis development where traditional treatments have failed. Autophagy is a conserved regulatory process of eliminating proteins and damaged organelles. Numerous research revealed that autophagy has dual sword mechanisms including cancer progressions and suppressions. In most of the cases, it maintains homeostasis of cancer microenvironment by providing nutritional supplement under starvation and hypoxic conditions. Over the past few decades, stunning research evidence disclosed significant roles of long non-coding RNAs (lncRNAs) in the regulation of autophagy. LncRNAs are RNA containing more than 200 nucleotides, which have no protein-coding ability but they are found to be expressed in most of the cancers. It is also proved that, autophagy-modulating lncRNAs have significant impacts on pro-survival or pro-death roles in cancers. In this review, we highlighted the recently identified autophagy-modulating lncRNAs, their signaling transduction in cancer and mechanism in cancer. This review will explore newly emerging knowledge of cancer genetics and it may provide novel targets for cancer therapy.

Highly Sensitive Detection of Protein Biomarkers with Organic Electrochemical Transistors.

The analysis of protein biomarkers is of great importance in the diagnosis of diseases. Although many convenient and low-cost electrochemical approaches have been extensively investigated, they are not sensitive enough in the detection of protein biomarkers with low concentrations in physiological environments. Here, this study reports a novel organic-electrochemical-transistor-based biosensor that can successfully detect cancer protein biomarkers with ultrahigh sensitivity. The devices are operated by detecting electrochemical activity on gate electrodes, which is dependent on the concentrations of proteins labeled with catalytic nanoprobes. The protein sensors can specifically detect a cancer biomarker, human epidermal growth factor receptor 2, down to the concentration of 10-14 g mL-1 , which is several orders of magnitude lower than the detection limits of previously reported electrochemical approaches. Moreover, the devices can successfully differentiate breast cancer cells from normal cells at various concentrations. The ultrahigh sensitivity of the protein sensors is attributed to the inherent amplification function of the organic electrochemical transistors. This work paves a way for developing highly sensitive and low-cost biosensors for the detection of various protein biomarkers in clinical analysis in the future.

Conjugated Polymer for Voltage-Controlled Release of Molecules.

Conjugated polymers are attractive in numerous biological applications because they are flexible, biocompatible, cost-effective, solution-processable, and electronic/ionic conductive. One interesting application is for controllable drug release, and this has been realized previously using organic electronic ion pumps. However, organic electronic ion pumps show high operating voltages and limited transportation efficiency. Here, the first report of low-voltage-controlled molecular release with a novel organic device based on a conjugated polymer poly(3-hexylthiophene) is presented. The releasing rate of molecules can be accurately controlled by the duration of the voltage applied on the device. The use of a handy mobile phone to remotely control the releasing process and its application in delivering an anticancer drug to treat cancer cells are also successfully demonstrated. The working mechanism of the device is attributed to the unique switchable permeability of poly(3-hexylthiophene) in aqueous solutions under a bias voltage that can tune the wettability of poly(3-hexylthiophene) via oxidation or reduction processes. The organic devices are expected to find many promising applications for controllable drug delivery in biological systems.

Influence of autophagy on the efficacy of radiotherapy.

Autophagy is an important catabolic process in which cells digest and recycle their own cytoplasmic contents for maintaining cellular homeostasis. Interestingly, autophagy could play both pro-death and pro-survival roles in influencing the development of cancer via various signal pathways. As radiotherapy is one of the main treatment modalities for cancer, we reviewed the effect of autophagy modulations on radiosensitivity and radiotherapy efficacy in various cancer types. The future development of autophagy modifications for improving radiotherapy efficacy and cancer prognosis will also be discussed.