Serum taurine affects lung cancer progression by regulating tumor immune escape mediated by the immune microenvironment.

INTRODUCTION: Taurine is a naturally occurring sulfonic acid involved in various physiological and pathological processes, such as the regulation of calcium signaling, immune function, inflammatory response, and cellular aging. It has the potential to predict tumor malignant transformation and formation. Our previous work discovered the elevated taurine in lung cancer patients. However, the precise impact and mechanism of elevated serum taurine levels on lung cancer progression and the suitability of taurine or taurine-containing drinks for lung cancer patients remain unclear. OBJECTIVES: Our study aimed to systematically investigate the role of taurine in lung cancer, with the ultimate goal of contributing novel strategies for lung cancer treatment. METHODS: Lung cancer C57 and nude mice models, RNA sequencing, and stable transfection were applied to explored the effects and mechanisms of taurine on lung cancer. Tissues of 129 non-small cell lung cancer (NSCLC) patients derived from 2014 to 2017 for immunohistochemistry were collected in Taihe Hospital. RESULTS: Low doses of taurine, as well as taurine-infused beverages at equivalent doses, significantly enhanced lung tumor growth. Equally intriguing is that the promoting effect of taurine on lung cancer progression wanes as the dosage increases. The Nuclear factor erythroid 2-like 1 (Nfe2l1 or Nrf1)-reactive oxygen species (ROS)-PD-1 axis may be a potential mechanism for dual role of taurine in lung cancer progression. However, taurine's impacts on lung cancer progression and the anti-tumor function of Nfe2l1 were mainly determined by the immune competence. Taurine inhitited lung tumor growth probably by inhibiting NF-κB-mediated inflammatory responses in nude mice rather than by affecting Nfe2l1 function. As patients age increased, Nfe2l1 gene and protein gradually returned to the levels observed in healthy individuals, but lost its anti-lung cancer effects. CONCLUSIONS: Taurine emerges as a potential biomarker for lung cancer progression, predicting poor prognosis and unsuitability for specific patients. Lung cancer patients, especially young patients, should be conscious of potential effects of taurine-containing drinks. Conversely, taurine or its drinks may be more suitable for older or immune-deficient patients.

Finding the optimal balance: father-athlete challenges facing elite Nordic skiers.

Background: In the last decade, a growing body of research has focused on the many aspects and challenges of combining parenthood with elite sport. Although the number of father-athletes is significantly higher than the number of mother-athletes, few studies to date have focused on male athletes' experiences in a parenting context. Aim: The aims of the present study were to explore how father-athlete challenges manifest among elite Nordic skiers in Norway, and to better understand how male athletes balance their priorities as they initiate, maintain, and/or discontinue their athletic career as a father-athlete. Methods: Qualitative data were collected through semi-structured interviews with 10 world-class male Nordic skiers in Norway (3 athletes without a child, 4 current father-athletes and 3 former father-athletes) and the content was analyzed using thematic analysis. Results: Four main stages were identified in the father-athlete transition: (a) Expecting incompatibility (b) Taking the step, (c), The first blow, and (d) Finding the optimal balance. Through these stages the informants expected/had experienced challenges such as performance decline, disturbed sleeping patterns, fear of sickness and role conflicts. To manage these challenges, the father-athletes had developed various strategies to balance their dual roles (e.g., adapting training and competition seasons). Among the benefits, the father-athletes mentioned that they had become more structured, time efficient and ruthless with their priorities, enhanced motivation to train and a better work-life balance. Conclusion: This study offers valuable insights into father-athlete challenges that can be used to support career longevity and work-life balance among male athletes.

The dual role of SUSD2 in cancer development.

Sushi domain-containing protein 2 (SUSD2, also known as the complement control protein domain) is a representative and vital protein in the SUSD protein family involved in many physiological and pathological processes beyond complement regulation. Cancer is one of the leading causes of death worldwide. The complex role of SUSD2 in tumorigenesis and cancer progression has raised increasing concerns. Studies suggest that SUSD2 has different regulatory tendencies among different tumors and exerts its biological effects in a cancer type-specific manner; for instance, it has oncogenic effects on breast cancer, gastric cancer, and glioma and has tumor-suppression effects on lung cancer, bladder cancer, and colon cancer. Moreover, SUSD2 can be regulated by noncoding RNAs, its promoter methylation and other molecules, such as Galectin-1 (Gal-1), tropomyosin alpha-4 chain (TPM4), and p63. The therapeutic implications of targeting SUSD2 have already been preliminarily revealed in some malignancies, including melanoma, colon cancer, and breast cancer. This article reviews the role and regulatory mechanisms of SUSD2 in cancer development, as well as its structure and distribution. We hope that this review will advance the understanding of SUSD2 as a diagnostic and/or prognostic biomarker and provide new avenues for the development of novel cancer therapies.

A breakthrough in macro-scale circularity and eco-efficiency assessment: A case study of OECD countries.

Countries' circularity performance and CO2 emissions should be addressed as a part of the UN net-zero Sustainable Development Goals (SDGs) 2030. Macro-scale circularity assessment is regarded as a helpful tool for tracking and adjusting nations' progress toward the sustainable Circular Economy (CE) and SDGs. However, practical frameworks are required to address the shortage of real-world circularity assessments at the macro level. The establishment of CE benchmarks is also essential to enhance circularity in less sustainable nations. Further, monitoring the extent to which nations' circularity activities are sustainable and in line with the SDGs is an area that lacks sufficient practical research. The current research aims to develop a macro-level framework and benchmarks for national sustainable circularity assessments. Methodologically, we develop a dynamic network data envelopment analysis (DN-DEA) framework for multi-period circularity and eco-efficiency assessment of OECD countries. To do so, we incorporate dual-role and bidirectional carryovers in our macro-scale framework. From a managerial perspective, we conduct a novel comparative analysis of the circularity and eco-efficiency of the nations to monitor macro-scale sustainable CE trends. Research results reveal a significant performance disparity in circularity, eco-efficiency, and benchmarking patterns. Accordingly, circularly efficient nations cannot necessarily be considered eco-friendly and sustainable. Although Germany (as a superior circular nation) can be regarded as a circularity benchmark, it cannot serve as an eco-efficiency benchmark for less eco-efficient nations. Hence, the new method allows decision-makers not only to identify the nations' circularity outcome but also to distinguish sustainable nations from less sustainable ones. This, on the one hand, provides policymakers with a multi-faceted sustainability analysis, beyond the previous unidimensional analysis. On the other, it proposes improvement benchmarks for planning and regulating nations' future circularity in line with real sustainability goals. The capabilities of our innovative approach are demonstrated in the case study.

Thioredoxin Domain Containing 5 (TXNDC5): Friend or Foe?

This review focuses on the thioredoxin domain containing 5 (TXNDC5), also known as endoplasmic reticulum protein 46 (ERp46), a member of the protein disulfide isomerase (PDI) family with a dual role in multiple diseases. TXNDC5 is highly expressed in endothelial cells, fibroblasts, pancreatic ß-cells, liver cells, and hypoxic tissues, such as cancer endothelial cells and atherosclerotic plaques. TXNDC5 plays a crucial role in regulating cell proliferation, apoptosis, migration, and antioxidative stress. Its potential significance in cancer warrants further investigation, given the altered and highly adaptable metabolism of tumor cells. It has been reported that both high and low levels of TXNDC5 expression are associated with multiple diseases, such as arthritis, cancer, diabetes, brain diseases, and infections, as well as worse prognoses. TXNDC5 has been attributed to both oncogenic and tumor-suppressive features. It has been concluded that in cancer, TXNDC5 acts as a foe and responds to metabolic and cellular stress signals to promote the survival of tumor cells against apoptosis. Conversely, in normal cells, TXNDC5 acts as a friend to safeguard cells against oxidative and endoplasmic reticulum stress. Therefore, TXNDC5 could serve as a viable biomarker or even a potential pharmacological target.

Discovery of a Novel Antiviral Effect of the Restriction Factor SPOC1 against Human Cytomegalovirus.

The chromatin-remodeler SPOC1 (PHF13) is a transcriptional co-regulator and has been identified as a restriction factor against various viruses, including human cytomegalovirus (HCMV). For HCMV, SPOC1 was shown to block the onset of immediate-early (IE) gene expression under low multiplicities of infection (MOI). Here, we demonstrate that SPOC1-mediated restriction of IE expression is neutralized by increasing viral titers. Interestingly, our study reveals that SPOC1 exerts an additional antiviral function beyond the IE phase of HCMV replication. Expression of SPOC1 under conditions of high MOI resulted in severely impaired viral DNA replication and viral particle release, which may be attributed to inefficient viral transcription. With the use of click chemistry, the localization of viral DNA was investigated at late time points after infection. Intriguingly, we detected a co-localization of SPOC1, RNA polymerase II S5P and polycomb repressor complex 2 (PRC2) components in close proximity to viral DNA in areas that are hypothesized to harbor viral transcription sites. We further identified the N-terminal domain of SPOC1 to be responsible for interaction with EZH2, a subunit of the PRC2 complex. With this study, we report a novel and potent antiviral function of SPOC1 against HCMV that is efficient even with unrestricted IE gene expression.

The dual role of autophagy in the regulation of cancer treatment.

As a catabolic process, autophagy through lysosomes degrades defective and damaged cellular materials to support homeostasis in stressful conditions. Therefore, autophagy dysregulation is associated with the induction of several human pathologies, including cancer. Although the role of autophagy in cancer progression has been extensively studied, many issues need to be addressed. The available evidence suggest that autophagy shows both cytoprotective and cytotoxic mechanisms. This dual role of autophagy in cancer has supplied a renewed interest in the development of novel and effective cancer therapies. Considering this, a deeper understanding of the molecular mechanisms of autophagy in cancer treatment is crucial. This article provides a summary of the recent advances regarding the dual and different mechanisms of autophagy-mediated therapeutic efficacy in cancer.

Investigating the Influence of Gut Microbiota-related Metabolites in Gastrointestinal Cancer.

Gastrointestinal (GI) cancer is a major health concern due to its prevalence, impact on well-being, high mortality rate, economic burden, and potential for prevention and early detection. GI cancer research has made remarkable strides in understanding biology, risk factors, and treatment options. An emerging area of research is the gut microbiome's role in GI cancer development and treatment response. The gut microbiome, vital for digestion, metabolism, and immune function, is increasingly linked to GI cancers. Dysbiosis and alterations in gut microbe composition may contribute to cancer development. Scientists study how specific bacteria or microbial metabolites influence cancer progression and treatment response. Modulating the gut microbiota shows promise in enhancing treatment efficacy and preventing GI cancers. Gut microbiota dysbiosis can impact GI cancer through inflammation, metabolite production, genotoxicity, and immune modulation. Microbes produce metabolites like short-chain fatty acids, bile acids, and secondary metabolites. These affect host cells, influencing processes like cell proliferation, apoptosis, DNA damage, and immune regulation, all implicated in cancer development. This review explores the latest research on gut microbiota metabolites and their molecular mechanisms in GI cancers. The hope is that this attempt will help in conducting other relevant research to unravel the precise mechanism involved, identify microbial signatures associated with GI cancer, and develop targets.

The ethics of induction of labor at 39 weeks in low-risk nulliparas in research and clinical practice.

The "A Randomized Trial of Induction Versus Expectant Management" trial (ARRIVE trial) published in 2018 suggested that induction of labor can be considered a "reasonable option" for low-risk nulliparous women at ≥39 weeks of gestation. The study results led some professional societies to endorse the option for elective induction of labor at 39 weeks of gestation in low-risk nulliparas, and this has begun to change obstetrical practice. The ARRIVE trial provided valuable information supporting the benefits of induction of labor; however, the trial is insufficient to serve as the primary justification for widespread elective induction of labor at 39 weeks of gestation in low-risk nulliparas because of concerns about external validity. Thus, the French ARRIVE trial was designed to test the hypothesis in a different setting that elective induction of labor at 39 weeks of gestation in low-risk nulliparas leads to a lower cesarean delivery rate than expectant management. This ongoing trial has been criticized as "pseudoscientific" and telling "women where, when, and how to give birth." We reject these allegations and extensively examine the ethical framework that should govern clinical and research interventions, including elective induction of labor at 39 weeks of gestation in low-risk nulliparas. This study aimed to discuss the ethical issues that emerge from randomized trials of elective induction of labor at 39 weeks of gestation in low-risk nulliparas and the ethics of the clinical practice itself. The analysis of existing evidence shows the importance of further research on induction of labor at 39 weeks of gestation in low-risk women. Certain aspects of research ethics in this area, particularly the consent of pregnant women in a context where autonomy remains fragile, call for vigilance. In addition, we emphasize that childbirth is not only a medical object but also a social phenomenon that cannot be regarded only from the perspective of a health risk to be managed by clinical research. Further research on this issue is needed to allow pregnant women to make informed decisions, and the results should be integrated with social issues. The perspective of women is required in constructing, evaluating, and implementing medical interventions in childbirth, such as induction of labor at 39 weeks of gestation.

Role of epithelial splicing regulatory protein 1 in cancer progression.

As aberrant alternative splicing by either dysregulation or mutations of splicing factors contributes to cancer initiation and progression, splicing factors are emerging as potential therapeutic targets for cancer therapy. Therefore, pharmacological modulators targeting splicing factors have been under development. Epithelial splicing regulatory protein 1 (ESRP1) is an epithelial cell-specific splicing factor, whose downregulation is associated with epithelial-mesenchymal transition (EMT) by regulating alternative splicing of multiple genes, such as CD44, CTNND1, ENAH, and FGFR2. Consistent with the downregulation of ESRP1 during EMT, it has been initially revealed that high ESRP1 expression is associated with favorable prognosis and ESRP1 plays a tumor-suppressive role in cancer progression. However, ESRP1 has been found to promote cancer progression in some cancers, such as breast and ovarian cancers, indicating that it plays a dual role in cancer progression depending on the type of cancer. Furthermore, recent studies have reported that ESRP1 affects tumor growth by regulating the metabolism of tumor cells or immune cell infiltration in the tumor microenvironment, suggesting the novel roles of ESRP1 in addition to EMT. ESRP1 expression was also associated with response to anticancer drugs. This review describes current understanding of the roles and mechanisms of ESRP1 in cancer progression, and further discusses the emerging novel roles of ESRP1 in cancer and recent attempts to target splicing factors for cancer therapy.

The dual and multifaceted role of relaxin-2 in cancer

The continuous increase in cancer-associated deaths despite the substantial improvement in diagnosis and treatment has sparked discussions on the need for novel biomarkers and therapeutic strategies for cancer. Although increasing evidence has demonstrated the pivotal role of relaxin-2 in multiple cancers, their role is a double-edged sword with both protumor and antitumor having been reported in various malignant tumors. Considering this dual role, it appears the biological mechanism underpinning the action of relaxin-2 in cancer is not clear and further studies to elucidate their potential as a preventive factor for cancers are of prime importance. Herein, a summarized up-to-date report on the role of relaxin-2 in human cancer including detailed clinical and experimental evidence supporting their tumor-promoting and inhibitory functions in cancer development and progression has been elucidated. Also, signaling pathways and other factors orchestrating the activities of relaxin-2 in the tumor microenvironment has been discussed. Collectively, the evidence from this review has demonstrated the need for further evaluation of the role of relaxin-2 as a diagnostic and or prognostic biomarker for cancer (AU)

Dual Role of TiO(acac)2 as a Reagent and an Activator/Catalyst: A Study on the Solvent Dependent Product Formation.

The dual operation of a chemical species in synthetic chemistry is an intriguing and relatively unexplored phenomenon. The application of such a species is expected to reduce the use of multiple reaction partners and catalysts/activators. Herein, we report a simple and easy-to-use protocol for the twin application of TiO(acac)2 , as a reagent and an activator to synthesize ß-enamino ketones with amines in acetonitrile. The same early transition metal precursor when employed in N,N-dimethylformamide with the amines, resulted in the formation of the substituted amides. Both reactions were explored with various substrates to check the viability of the present protocol. Moreover, experimental studies were conducted to understand the mechanism of both reactions.

"Juggle the different hats we wear": enacted strategies for negotiating boundaries in overlapping relationships.

Despite agreement that teaching on professional boundaries is needed, the design of health profession curricula is challenged by a lack of research on how boundaries are maintained and disagreement on where boundaries should be drawn. Curricula constrained by these challenges can leave graduates without formal preparation for practice conditions. Dual role or overlapping relationships are an example: they continue to be taught as boundary crossings amidst mounting evidence that they must be routinely navigated in small, interconnected communities. In this study, we examined how physicians are navigating overlapping personal (non-sexual) and professional relationships with the goal to inform teaching and curricula on professional boundaries. Following constructivist grounded theory methodology, 22 physicians who had returned to their rural, northern and/or remote hometown in British Columbia, Canada or who had lived and practised in a such a community for decades were interviewed in iterative cycles informed by analysis. We identified four strategies described by physicians for regulating multiple roles within overlapping relationships: (a) signalling the appropriate role for the current context; (b) separating roles by redirecting an interaction to an appropriate context; (c) switching roles by pushing the appropriate role forward into the context and pulling other roles into the background; and (d) suspending an interfering role by ending a relationship. Negotiating boundaries within overlapping relationships may involve monitoring role clarity and role alignment, while avoiding role conflict. The enacted role regulation strategies could be critically assessed within teaching discussions on professional boundaries and also analyzed through further ethics research.

Metal-Catalyst-Free One-Pot Aqueous Synthesis of trans-1,2-Diols from Electron-Deficient α,ß-Unsaturated Amides via Epoxidation Using Oxone as a Dual Role Reagent.

In organic synthesis, incorporating two functional groups into the carbon-carbon double bond of α,ß-unsaturated amides is challenging due to the electron-deficient nature of the olefin moiety. Although a few examples of dihydroxylation of α,ß-unsaturated amides have been demonstrated, producing cis-1,2-diols using either highly toxic OsO4 or other specialized metal reagents in organic solvents, they are limited to several specific amides. We describe herein a general and one-pot direct synthesis of trans-1,2-diols from electron-deficient α,ß-unsaturated amides through dihydroxylation using oxone as a dual-role reagent in water. This reaction does not require any metal catalyst and produces non-hazardous and nontoxic K2 SO4 as the sole byproduct. Moreover, epoxidation products could also be selectively formed by adjusting the reaction conditions. By the strategy, the intermediates of Mcl-1 inhibitor and antiallergic bioactive molecule can be synthesized in one pot. The gram-scale synthesis of trans-1,2-diol which is isolated and purified by recrystallization further shows the potential applications of this new reaction in organic synthesis.

Regulation Mechanism of Nicotine Catabolism in Sphingomonas melonis TY by a Dual Role Transcriptional Regulator NdpR.

A gene cluster ndp, responsible for nicotine degradation via a variant of the pyridine and pyrrolidine pathways, was previously identified in Sphingomonas melonis TY, but the regulation mechanism remains unknown. The gene ndpR within the cluster was predicted to encode a TetR family transcriptional regulator. Deletion of ndpR resulted in a notably shorter lag phase, higher maximum turbidity, and faster substrate degradation when cultivated in the presence of nicotine. Real-time quantitative PCR and promoter activity analysis in wild-type TY and TYΔndpR strains revealed that genes in the ndp cluster were negatively regulated by NdpR. However, complementation of ndpR to TYΔndpR did not restore transcription repression, but, instead, the complemented strain showed better growth than TYΔndpR. Promoter activity analysis indicates that NdpR also functions as an activator in the transcription regulation of ndpHFEGD. Further analysis through electrophoretic mobility shift assay and DNase I footprinting assay revealed that NdpR binds five DNA sequences within ndp and that NdpR has no autoregulation. These binding motifs overlap with the -35 or -10 box or are located distal upstream of the corresponding transcriptional start site. Multiple sequence alignment of these five NdpR-binding DNA sequences found a conserved motif, with two of the binding sequences being partially palindromic. 2,5-Dihydroxypyridine acted as a ligand of NdpR, preventing NdpR from binding to the promoter region of ndpASAL, ndpTB, and ndpHFEGD. This study revealed that NdpR binds to three promoters in the ndp cluster and is a dual-role transcriptional regulator in nicotine metabolism. IMPORTANCE Gene regulation is critical for microorganisms in the environment in which they may encounter various kinds of organic pollutants. Our study revealed that transcription of ndpASAL, ndpTB, and ndpHFEGD is negatively regulated by NdpR, and NdpR also exhibits a positive regulatory effect on PndpHFEGD. Furthermore, 2,5-dihydroxypyridine was identified as the effector molecular for NdpR and can both prevent the binding of free NdpR to the promoter and release NdpR from the promoters, which is different from previously reported NicR2. Additionally, NdpR was found to have both negative and positive transcription regulatory effects on the same target, PndpHFEGD, while only one binding site was identified, which is notably different from the previously reported TetR family regulators. Moreover, NdpR was revealed to be a global transcriptional regulator. This study provides new insight into the complex gene expression regulation of the TetR family.

Dual-role nurse interpreter perceptions of language barriers and Spanish-speaking patients: A qualitative study.

AIM: As the United States population is ever changing and is growing in diverse population patterns, the health care system is called to initiate responsive health care practices that are based on the public's changing and diverse cultural patterns. This study sought to explore the perceptions of certified medical interpreter dual-role nurses and their experiences with Spanish-speaking patients from admission to discharge in hospital stays. DESIGN: A qualitative descriptive case study was applied in this study. METHODS: Data was collected from nurses working at a United States Southwest Borderland hospital using purposive sampling and semi-structured in-depth interviews. A total of four dual-role nurses participated, and thematic narrative analysis was applied. RESULTS: Four major themes emerged. The main themes were "being a dual-role nurse interpreter," "patient experience," "culture and competence, "and "nursing and caring," With each major theme multiple sub themes emerged. Two sub themes emerged with "being a dual-role nurse interpreter," and two sub themes emerged with "patient experiences." The major themes that emerged from the interviews indicated that the language barrier greatly affects Spanish-speaking patients in their hospital stay. Participants reported having at least one encounter with a Spanish-speaking patient that was not afforded interpretation services or had interpretation from someone other than a qualified interpreter. Patients experienced confusion, apprehension and anger associated with not being able to communicate their needs to the healthcare system. CONCLUSIONS: According to the experiences of the certified dual-role nurse interpreters, having a language barrier makes a tremendous impact on the care of Spanish-speaking patients. Nurse participants describe how patients and their family members experience dissatisfaction, anger and confusion when there is a language barrier and most importantly how language barriers have detrimental effects on patients with wrong medication prescriptions and wrong diagnosis. CLINICAL RELEVANCE: When hospital administration recognize and support nurses as certified medical interpreters as a key component for patient care when assisting persons with limited English proficiency, patients are empowered to become active members of their healthcare regimen. The role of dual-role nurses enables brokering between the healthcare system and serves as a tool to bridge health disparities based on linguistic inequities existing in healthcare. Recruitment and retention of certified medical interpreter trained Spanish-speaking nurses deter errors in healthcare and makes a positive impact on the healthcare regimen of Spanish-speaking patients enabling patient empowerment through education and advocacy.

The dual and multifaceted role of relaxin-2 in cancer.

The continuous increase in cancer-associated deaths despite the substantial improvement in diagnosis and treatment has sparked discussions on the need for novel biomarkers and therapeutic strategies for cancer. Although increasing evidence has demonstrated the pivotal role of relaxin-2 in multiple cancers, their role is a double-edged sword with both protumor and antitumor having been reported in various malignant tumors. Considering this dual role, it appears the biological mechanism underpinning the action of relaxin-2 in cancer is not clear and further studies to elucidate their potential as a preventive factor for cancers are of prime importance. Herein, a summarized up-to-date report on the role of relaxin-2 in human cancer including detailed clinical and experimental evidence supporting their tumor-promoting and inhibitory functions in cancer development and progression has been elucidated. Also, signaling pathways and other factors orchestrating the activities of relaxin-2 in the tumor microenvironment has been discussed. Collectively, the evidence from this review has demonstrated the need for further evaluation of the role of relaxin-2 as a diagnostic and or prognostic biomarker for cancer.

The dual role of DNA repair protein MGMT in cancer prevention and treatment.

Alkylating agents are genotoxic chemicals that can induce and treat various types of cancer. This occurs through covalent bonding with cellular macromolecules, in particular DNA, leading to the loss of functional integrity under the persistence of modifications upon replication. O6-alkylguanine (O6-AlkylG) adducts are proposed to be the most potent DNA lesions induced by alkylating agents. If not repaired correctly, these adducts can result, at the molecular level, in DNA point mutations, chromosome aberrations, recombination, crosslinking, and single- and double-strand breaks (SSB/DSBs). At the cellular level, these lesions can result in malignant transformation, senescence, or cell death. O6-methylguanine-DNA methyltransferase (MGMT) is a DNA repair protein capable of removing the alkyl groups from O6-AlkylG adducts in a damage reversal process that can prevent the adverse biological effects of DNA damage caused by guanine O6-alkylation. MGMT can thereby defend normal cells against tumor initiation, however it can also protect tumor cells against the beneficial effects of chemotherapy. Hence, MGMT can play an important role in both the prevention and treatment of cancer; thus, it can be considered as a double-edged sword. From a clinical perspective, MGMT is a therapeutic target, and it is important to explore the rational development of its clinical exploitation.

A Reflection on the Tensions of Acting in Dual Roles of Doctoral Researcher and Practitioner when Evaluating a Lifestyle Intervention for Breast Cancer Patients.

This reflection was completed as part of a doctoral project to develop and trial a lifestyle intervention for people following the completion of their treatment for breast cancer. In this study the graduate student acted in the dual roles of nutrition practitioner and researcher. This article uses the experience, reflection, action (ERA) cycle of reflection to consider some of the tensions faced due to the divergent priorities and requirements of these two roles. One challenge occurred during study recruitment when a few potential participants did not meet the inclusion criteria for the study but still wished to attend the intervention sessions. It was also a challenge to mitigate the risks of distress of potentially vulnerable participants during group intervention sessions. In both instances there was a potential conflict between the needs of patients and research requirements. This reflection concluded that the obligations of both roles should be adhered to where possible, but if in doubt, the needs of the participants were paramount.