BACKGROUND/OBJECTIVES:Rectal cancer radiotherapy often causes long-term adverse effects impacting patients and caregivers. Psychosocial needs specific to this population, particularly within Hong Kong's unique context, remain understudied. This study aims to investigate the psychosocial needs of rectal cancer patients and caregivers before and after radiotherapy. METHODS:This study was a prospective observational study. Rectal cancer patients with radiotherapy and their direct caregivers were recruited from [Princess Margaret Hospital], Hong Kong from 2022 to 2023. Psychosocial needs and quality of life were assessed using validated questionnaires: the European Organization for Research and Treatment of Cancer core and colorectal modules for patients, and the CareGiver Oncology Quality of Life questionnaire for caregivers, administered at baseline, 3 months, and 6 months post-radiotherapy. RESULTS:Twenty-four subjects including 13 patients and 11 caregivers were recruited. The mean age of patients and caregivers were 66.3 ± 12.7 years old and 49.8 ± 14.8 years old respectively. Majority of patients worried about their future health before the radiotherapy. Fatigue and sleeping difficulties were commonly reported by the survivors. An improvement in the patients' overall health and quality of life was discerned as the treatment progressed. Caregivers reported receiving support from friends and healthcare providers. Their emotional and intimate lives were less affected with a positive self-image identified. CONCLUSIONS:Rectal cancer radiotherapy survivors faced substantial psychological distress, fatigue and sleeping difficulties. Exercise programs are suggested to address fatigue and distress in survivors. Future large-scale studies should further explore caregiver quality of life and self-image dynamics across the caregiving trajectory.

Background Photobiomodulation therapy (PBMT) has been shown to reduce fibrosis, yet evidence regarding its effect on radiation-induced fibrosis (RIF) is scarce. This study established a mouse model of mild joint RIF to investigate the effects of prophylactic and post-irradiation PBMT on radiation-induced joint fibrosis. Methods Knee joint fibrosis was induced by irradiating a single X-ray dose of 15 Gy to both legs and pelvis. Mice with RIF were treated with PBMT once a day, three times per week, for 7 weeks, using light-emitting diodes (660 nm and 850 nm) and a laser (810 nm). Eighteen mice were divided into three groups: post-irradiation PBMT, prophylactic PBMT, and positive control groups (n = 6 for each group). Results The established mouse RIF model presented with acute radiation dermatitis, leg contracture, and histological changes of mild RIF, including cartilage fibrillation and pannus formation. No significant differences in outcomes between the post-irradiation PBMT, prophylactic PBMT, and positive control groups, potentially attributed to the small sample size. Conclusion Despite the insignificant results, the study established a stable joint RIF model to evaluate the effects of PBMT and other emerging therapies. Future large-scale studies incorporating biochemical analysis of inflammation, as well as functional and behavioural assessments, are warranted to extend our understanding regarding the effectiveness of PBMT in modulating RIF.

Tumor hypoxia involves limited oxygen supply within the tumor microenvironment and is closely associated with aggressiveness, metastasis, and resistance to common cancer treatment modalities such as chemotherapy and radiotherapy. Traditional methodologies for hypoxia assessment, such as the use of invasive probes and clinical biomarkers, are generally not very suitable for routine clinical applications. Radiomics provides a non-invasive approach to hypoxia assessment by extracting quantitative features from medical images. Thus, radiomics is important in diagnosis and the formulation of a treatment strategy for tumor hypoxia. This article discusses the various imaging techniques used for the assessment of tumor hypoxia including magnetic resonance imaging (MRI), positron emission tomography (PET), and computed tomography (CT). It introduces the use of radiomics with machine learning and deep learning for extracting quantitative features, along with its possible clinical use in hypoxic tumors. This article further summarizes the key challenges hindering the clinical translation of radiomics, including the lack of imaging standardization and the limited availability of hypoxia-labeled datasets. It also highlights the potential of integrating radiomics with multi-omics to enhance hypoxia visualization and guide personalized cancer treatment.

Radiomics has shown remarkable potential in predicting cancer prognosis by noninvasive and quantitative analysis of tumors through medical imaging. This review summarizes recent advances in the use of radiomics across various cancer types and imaging modalities, including computed tomography (CT), magnetic resonance imaging (MRI), ultrasound, positron emission tomography (PET), and interventional radiology. Innovative sampling methods, including deep learning-based segmentation, multiregional analysis, and adaptive region of interest (ROI) methods, have contributed to improved model performance. The review examines various feature selection approaches, including least absolute shrinkage and selection operator (LASSO), minimum redundancy maximum relevance (mRMR), and ensemble methods, highlighting their roles in enhancing model robustness. The integration of radiomics with multi-omics data has further boosted predictive accuracy and enriched biological interpretability. Despite these advancements, challenges remain in terms of reproducibility, workflow standardization, clinical validation and acceptance. Future research should prioritize multicenter collaborations, methodological coordination, and clinical translation to fully unlock the prognostic potential of radiomics in oncology.

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.

Background/Objectives: Colorectal cancer (CRC) is the third most diagnosed cancer globally. Radiotherapy is a common treatment strategy for patients but factors such as gene expressions and molecular mechanism effects may affect tumor radioresponse. The aim of this review is to systematically identify genes suggested to have molecular mechanism effects on the radioresponsiveness of CRC patients. Methods: By following the PRISMA guidelines, a comprehensive literature search was conducted on Pubmed, EMBASE and Cochrane Library. After exclusion and inclusion criteria sorting and critical appraisal for study quality, data were extracted from seven studies. A gene set analysis was conducted on reported genes. Results: From the seven studies, 56 genes were found to have an effect on CRC radioresponsiveness. Gene set analysis show that out of these 56 genes, 24 genes have roles in pathways which could affect cancer radioresponse. These are AKT1, APC, ATM, BRAF, CDKN2A, CTNNB1, EGFR, ERBB2, FLT3, KRAS, MET, mTOR, MYC, NFKB1, KRAS, PDGFRA, PIK3CA, PTEN, PTGS1, PTGS2, RAF1, RET, SMAD4 and TP53. The current project was conducted between the period May 2024 to August 2024. Conclusions: The current review systematically presented 56 genes which have been reported to be related to RT or CRT treatment effectiveness in rectal cancer patients. Gene set analysis shows that nearly half of the genes were involved in apoptosis, DNA damage response and repair, inflammation and cancer metabolism molecular pathways that could affect cancer radioresponse. The gene cohort identified in this study may be used as a foundation for future works focusing on the molecular mechanism of specific pathways contributing to the radioresponse of CRC.

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.

Abstract Background Inflammatory bowel disease (IBD) is a collective term for chronic inflammatory diseases resulting from complex genetic susceptibility, microbial flora, and immune abnormality. Due to the complicated pathogenesis, therapies for IBD are largely limited to the treatment of symptoms. However, these existing drugs sometimes fail or lead to adverse effects in long-term therapies. The development of new drugs and new therapies for IBD are still the top priorities. Trehalose (TRE) is an autophagy inducer through an mTOR-independent pathway. Given its safe and protective nature, TRE has gained significant attention for the potential application in disease treatment. It is a natural product that may be used as a harmless autophagy regulator. In our research, we use the Dextran Sulfate Sodium (DSS)-induced IBD model to explore the therapeutic effects of trehalose on autophagy and inflammation in mice. Methods 6-8 weeks old C57BL/6J male mice were used for experiments. Mice were given 2% DSS (MP Biomedicals) in autoclaved drinking water for 4 days to induce colitis, Then TRE (2 g/kg body weight, Sigma-Aldrich), rapamycin (1.25mg/kg body weight, MedChemExpress) or normal saline were intraperitoneally injected for 5 days. Mice were weighed daily, and stool consistency, diarrhea, or blood in the stools were monitored to calculate the disease activity index (DAI). At the end of the experiment, the colons were measured, opened longitudinally, and handled according to standard procedures. The tissue samples were collected for RNA, protein extraction, histology, and macrophage isolation respectively. Western Blot was used for autophagy analysis and flow cytometry was used for macrophage subtype and apoptosis analysis. Besides, Real-time quantitative PCR assay was used for examining the cytokine expression. Results In TRE-treated mice, the cessation of diarrhea and anal bleeding occurred earlier and hence the DAI scores decreased more rapidly when compared to the other groups. Correspondingly, the colons in TRE-treated mice shortened less than the saline treated control suggesting recovery from DSS-induced colitis. Even though no significant difference was observed in H&E staining and tissue scores for mice in different groups, significant difference in macrophage polarization and cytokine production was observed. DSS-induced intestinal CD86+ macrophages, whereas TRE treatment increased CD206+ macrophages and decreased the expression of pro-inflammatory cytokines, such as IL-6 and TNF-alpha. Conclusion Our results demonstrate that TRE decreases the symptoms of experimental colitis by regulating macrophage polarization, probably mediated by macrophage autophagy. These findings indicate the potential of TRE to be an adjuvant therapy for IBD.

Electrochemical transistors (ECTs) have shown broad applications in bioelectronics and neuromorphic devices due to their high transconductance, low working voltage, and versatile device design. To further improve the device performance, semiconductor materials with both high carrier mobilities and large capacitances in electrolytes are needed. Here, we demonstrate ECTs based on highly oriented two-dimensional conjugated metal-organic frameworks (2D c-MOFs). The ion-conductive vertical nanopores formed within the 2D c-MOFs films lead to the most convenient ion transfer in the bulk and high volumetric capacitance, endowing the devices with fast speeds and ultrahigh transconductance. Ultraflexible device arrays are successfully used for wearable on-skin recording of electrocardiogram (ECG) signals along different directions, which can provide various waveforms comparable with those of multilead ECG measurement systems for monitoring heart conditions. These results indicate that 2D c-MOFs are excellent semiconductor materials for high-performance ECTs with promising applications in flexible and wearable electronics.

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.

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.

504 Background: Colorectal cancer is the second most common cancer in Hong Kong. Radiotherapy has been established as an indispensable component during treatment of rectal cancer. Radiation-induced adverse effects are common for radiotherapy patients, severely affecting the quality of life of both the patients and their caregivers. Although previous studies have demonstrated the impacts of radiation-induced adverse effects on the quality of life of rectal radiotherapy patients, little were studied about the impacts on the patients’ and their direct caregivers’ psychosocial health. As there was no previous similar study done in local context, this research serves as a pilot study for improving the understanding of psychosocial needs and quality of life of rectal radiotherapy patients and their direct caregivers in Hong Kong. Methods: This study was a prospective and observational research. Rectal radiotherapy patients and their direct caregivers were recruited from Princess Margaret Hospital, Hong Kong from 2022 to 2023. The primary endpoint was the questionnaire assessment of psychosocial needs and quality of life of rectal radiotherapy patients and their direct caregivers before and after radiotherapy treatment. Questionnaires in different versions for the patients and their direct caregivers before radiotherapy treatment, 3-month and 6-month post-radiotherapy courses were distributed. Results: Twenty-four subjects were recruited, including 13 patients and 11 caregivers. The results show that rectal radiotherapy patients worried about their health in the future. Their direct caregivers’ emotional and intimate lives were affected. Nevertheless, the patients’ health and quality of life improved throughout the post-treatment period. For the caregivers, their feelings of anxiety and depression improved throughout the follow-up period. Conclusions: Most of the results are consistent with previous studies. This study provides a knowledge foundation and research direction for future studies. More future studies with a larger subject number are highly encouraged to solidify the knowledge on psychosocial needs and to improve the care of the patients and caregivers.

e15588 Background: Chemoresistance is a major cause of colorectal cancer (CRC) mortality. Although multidrug regimen has been established as the backbone of CRC chemotherapy for better treatment efficacy, chemoresistance is common among late-stage CRC. Proteomic profiling of both the chemoresistant and wild-type CRC cells may provide hints for the mechanisms of chemoresistance and suggest targets for improving chemotherapy efficacy. Methods: Human CRC cell lines (DLD-1 and HCT-116) were treated with progressively increased dosage of FOLFOX (5-flurouracil (5-FU), folinic acid (LEU) and oxaliplatin (OXA)) to develop chemoresistance as DLD-1-R and HCT-116-R respectively. After confirmation of the successful development of chemoresistance by Cell Counting Kit-8 test (CCK-8), the comparison of cell samples between chemoresistant and wild-type cell lines were conducted by proteomic profiling using quantitative mass spectrometry (MS)-based techniques. MS and MS/ MS peptides spectra were analysed by Progenesis QI for proteomics software compared with Swiss-Prot dataset. Differentially expressed proteins (DEP) are defined as -1 > log2FC > 1, p < 0.05. Gene-list enrichment by Enrichr (https://maayanlab.cloud/Enrichr/) was employed for identifying the hallmark gene sets of the significantly enriched molecular processes and pathways of each group. All experiments were performed with at least 3 replications. Results: The development of FOLFOX-resistance took one year. The highest drug concentrations achieved were 0.5mM 5-FU, 50µM LEU, and 50µM OXA for DLD-1-R, and 5µM 5-FU, 0.5µM LEU, and 0.5µM OXA for HCT-116-R. The chemoresistance was found to be 14.73 (DLD-1-R) and 1.61 (HCT-116-R) times of the wild-type DLD-1 and HCT-116 respectively from CCK-8 tests. A total of 345 DEP with 154 up-regulated and 191 down-regulated proteins were found in DLD-1-R. While a total of 95 DEP with 66 up-regulated and 29 down-regulated proteins were found in HCT-116-R. Gene ontology molecular process (2021) analyses found that cadherin binding were significantly enriched in both DLD-1-R and HCT-116-R (Adjusted p-value < 0.05). KEGG pathway (2021) analysis found that oxidative phosphorylation, regulation of actin cytoskeleton and HIF-1 signalling pathway are among the significantly enriched pathways in DLD-1-R (Adjusted p value < 0.05). There was no significantly enriched pathway found in HCT-116-R in the same analysis. Conclusions: Our study has successfully established CRC cells with chemoresistance to the FOLFOX regimen. Proteomic profiling has found the cadherin binding as the significantly altered molecular process along with several important signalling pathways in chemoresistant CRC cells. These findings could suggest new directions in the development of anti-chemoresistance strategies of CRC.

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.

Inflammatory bowel disease (IBD) is a typical immune-mediated chronic inflammatory disorder. Following the industrialization and changes in lifestyle, the incidence of IBD in the world is rising, which makes health concerns and heavy burdens all over the world. However, the pathogenesis of IBD remains unclear, and the current understanding of the pathogenesis involves dysregulation of mucosal immunity, gut microbiome dysbiosis, and gut barrier defect based on genetic susceptibility and environmental triggers. In recent years, autophagy has emerged as a key mechanism in IBD development and progression because Genome-Wide Association Study revealed the complex interactions of autophagy in IBD, especially immunopathogenesis. Besides, autophagy markers are also suggested to be potential biomarkers and target treatment in IBD. This review summarizes the autophagy-related genes regulating immune response in IBD. Furthermore, we explore the evolving evidence that autophagy interacts with intestinal epithelial and immune cells to contribute to the inflammatory changes in IBD. Finally, we discuss how novel discovery could further advance our understanding of the role of autophagy and inform novel therapeutic strategies in IBD.

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.

Sepsis is a life-threatening syndrome with disturbed host responses to severe infections, accounting for the majority of death in hospitalized patients. However, effective medicines are currently scant in clinics due to the poor understanding of the exact underlying mechanism. We previously found that blocking caspase-11 pathway (human orthologs caspase-4/5) is effective to rescue coagulation-induced organ dysfunction and lethality in sepsis models. Herein, we screened our existing chemical pools established in our lab using bacterial outer membrane vesicle (OMV)-challenged macrophages, and found 7-(diethylamino)-1-hydroxy-phenothiazin-3-ylidene-diethylazanium chloride (PHZ-OH), a novel phenothiazinium-based derivative, was capable of robustly dampening caspase-11-dependent pyroptosis. The in-vitro study both in physics and physiology showed that PHZ-OH targeted AP2-associated protein kinase 1 (AAK1) and thus prevented AAK1-mediated LPS internalization for caspase-11 activation. By using a series of gene-modified mice, our in-vivo study further demonstrated that administration of PHZ-OH significantly protected mice against sepsis-associated coagulation, multiple organ dysfunction, and death. Besides, PHZ-OH showed additional protection on Nlrp3 −/− and Casp1 − / − mice but not on Casp11 −/− , Casp1/11 −/− , Msr1 −/− , and AAK1 inhibitor-treated mice. These results suggest the critical role of AAK1 on caspase-11 signaling and may provide a new avenue that targeting AAK1-mediated LPS internalization would be a promising therapeutic strategy for sepsis. In particular, PHZ-OH may serve as a favorable molecule and an attractive scaffold in future medicine development for efficient treatment of bacterial sepsis.

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.

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.