The incidence of rectal carcinoids is rising because of the widespread use of screening colonoscopy. Rectal carcinoids detected incidentally are usually in earlier stages at diagnosis. Rectal carcinoids estimated endo...The incidence of rectal carcinoids is rising because of the widespread use of screening colonoscopy. Rectal carcinoids detected incidentally are usually in earlier stages at diagnosis. Rectal carcinoids estimated endoscopically as < 10 mm in diameter without atypical features and confined to the submucosal layer can be removed endoscopically. Here, we review the efficacy and safety of various endoscopic treatments for small rectal carcinoid tumors, including conventional polypectomy, endoscopic mucosal resection(EMR),cap-assisted EMR(or aspiration lumpectomy),endoscopic submucosal resection with ligating device,endoscopic submucosal dissection, and transanal endoscopic microsurgery. It is necessary to carefully choose an effective and safe primary resection method for complete histological resection.展开更多
Background:Type Ⅱ diabetes mellitus(DM2)is a significant risk factor for cancers,including breast cancer.However,a proper diabetic breast cancer mouse model is notwell-established for treatment strategy design.Additi...Background:Type Ⅱ diabetes mellitus(DM2)is a significant risk factor for cancers,including breast cancer.However,a proper diabetic breast cancer mouse model is notwell-established for treatment strategy design.Additionally,the precise diabetic signaling pathways that regulate cancer growth remain unresolved.In the present study,we established a suitable mouse model and demonstrated the pathogenic role of diabetes on breast cancer progression.Methods:We successfully generated a transgenic mouse model of human epidermal growth factor receptor 2 positive(Her2^(+) or ERBB2)breast cancer with DM2 by crossing leptin receptor mutant(Lepr^(db/+))mice with (MMTV-ErbB2/neu)mice.Themousemodelswere administrated with antidiabetic drugs to assess the impacts of controlling DM2 in affecting tumor growth.Magnetic resonance spectroscopic imaging was employed to analyze the tumor metabolism.Results:Treatment with metformin/rosiglitazone in MMTV-ErbB2/Lepr^(db/db) mousemodel reduced serum insulin levels,prolonged overall survival,decreased cumulative tumor incidence,and inhibited tumor progression.Anti-insulin resistance medications also inhibited glycolytic metabolism in tumors in vivo as indicated by the reduced metabolic flux of hyperpolarized ^(13)C pyruvate-to-lactate reaction.The tumor cells from MMTV-ErbB2/Lepr^(db/db) transgenic mice treated with metformin had reprogrammed metabolism by reducing levels of both oxygen consumption and lactate production.Metformin decreased the expression of Myc and pyruvate kinase isozyme 2(PKM2),leading to metabolism reprogramming.Moreover,metformin attenuated the mTOR/AKT signaling pathway and altered adipokine profiles.Conclusions:MMTV-ErbB2/Lepr^(db/db) mouse model was able to recapitulate diabetic HER2^(+) human breast cancer.Additionally,our results defined the signaling pathways deregulated in HER2^(+) breast cancer under diabetic condition,which can be intervened by anti-insulin resistance therapy.展开更多
Human gut microbiota,containing at least 100 trillion bacteria,resides in the mucosal surface of the human intestine.Each individual is host to a distinct set of at least 160 species in the gut.The collective microbia...Human gut microbiota,containing at least 100 trillion bacteria,resides in the mucosal surface of the human intestine.Each individual is host to a distinct set of at least 160 species in the gut.The collective microbial genome encodes 500 times more genes than the human genome,and so it is tempting to consider human genes as noise in the storm of microbial signals[1].Recent data suggest that,while microbial signals modulate crucial functions of the healthy human body,there are also accumulating data suggesting that many human diseases have their origin in distorted gut microbiota composition[2].展开更多
Many microorganisms reside in the gastrointestinal tract and the dysbiosis of microorganisms can affect our health.Fungi have a relatively low level of presence(about 0.1%of the totalmicroorganisms)compared with bacte...Many microorganisms reside in the gastrointestinal tract and the dysbiosis of microorganisms can affect our health.Fungi have a relatively low level of presence(about 0.1%of the totalmicroorganisms)compared with bacteria,which makes it easier to underestimate their potential threat to health.However,fungal infections indeed participate in the onset and progression of many intestinal diseases,so they are crucially affecting our health[1,2].Recently,Li et al.described that C-type lectin receptors(CLRs)on myeloid cells,including Dectin-1,Dectin-2,Dectin-3,and Mincle,play an important role in the immune function induced by fungal pathogens of the intestinal microbiota[3].展开更多
基金Supported by Grant funded by the Catholic Cancer Center madein the program of 2010the National Research Foundation ofKorea grant funded by the Korea government,No.2010-0023295
文摘The incidence of rectal carcinoids is rising because of the widespread use of screening colonoscopy. Rectal carcinoids detected incidentally are usually in earlier stages at diagnosis. Rectal carcinoids estimated endoscopically as < 10 mm in diameter without atypical features and confined to the submucosal layer can be removed endoscopically. Here, we review the efficacy and safety of various endoscopic treatments for small rectal carcinoid tumors, including conventional polypectomy, endoscopic mucosal resection(EMR),cap-assisted EMR(or aspiration lumpectomy),endoscopic submucosal resection with ligating device,endoscopic submucosal dissection, and transanal endoscopic microsurgery. It is necessary to carefully choose an effective and safe primary resection method for complete histological resection.
基金Fidelity Foundation,Grant/Award Number:2020YFA0803300Shenzhen Municipal GovernmentNationalNatural Science Foundation of China,Grant/Award Numbers:81702749,81630072,81773098,81803568,8160242.
文摘Background:Type Ⅱ diabetes mellitus(DM2)is a significant risk factor for cancers,including breast cancer.However,a proper diabetic breast cancer mouse model is notwell-established for treatment strategy design.Additionally,the precise diabetic signaling pathways that regulate cancer growth remain unresolved.In the present study,we established a suitable mouse model and demonstrated the pathogenic role of diabetes on breast cancer progression.Methods:We successfully generated a transgenic mouse model of human epidermal growth factor receptor 2 positive(Her2^(+) or ERBB2)breast cancer with DM2 by crossing leptin receptor mutant(Lepr^(db/+))mice with (MMTV-ErbB2/neu)mice.Themousemodelswere administrated with antidiabetic drugs to assess the impacts of controlling DM2 in affecting tumor growth.Magnetic resonance spectroscopic imaging was employed to analyze the tumor metabolism.Results:Treatment with metformin/rosiglitazone in MMTV-ErbB2/Lepr^(db/db) mousemodel reduced serum insulin levels,prolonged overall survival,decreased cumulative tumor incidence,and inhibited tumor progression.Anti-insulin resistance medications also inhibited glycolytic metabolism in tumors in vivo as indicated by the reduced metabolic flux of hyperpolarized ^(13)C pyruvate-to-lactate reaction.The tumor cells from MMTV-ErbB2/Lepr^(db/db) transgenic mice treated with metformin had reprogrammed metabolism by reducing levels of both oxygen consumption and lactate production.Metformin decreased the expression of Myc and pyruvate kinase isozyme 2(PKM2),leading to metabolism reprogramming.Moreover,metformin attenuated the mTOR/AKT signaling pathway and altered adipokine profiles.Conclusions:MMTV-ErbB2/Lepr^(db/db) mouse model was able to recapitulate diabetic HER2^(+) human breast cancer.Additionally,our results defined the signaling pathways deregulated in HER2^(+) breast cancer under diabetic condition,which can be intervened by anti-insulin resistance therapy.
基金supported in part by the National Key R&D Program of China[2018YFC0910303]Foundation,Fidelity Foundation,the National Natural Science Foundation of China[81630072]National Key Clinical Discipline.
文摘Human gut microbiota,containing at least 100 trillion bacteria,resides in the mucosal surface of the human intestine.Each individual is host to a distinct set of at least 160 species in the gut.The collective microbial genome encodes 500 times more genes than the human genome,and so it is tempting to consider human genes as noise in the storm of microbial signals[1].Recent data suggest that,while microbial signals modulate crucial functions of the healthy human body,there are also accumulating data suggesting that many human diseases have their origin in distorted gut microbiota composition[2].
文摘Many microorganisms reside in the gastrointestinal tract and the dysbiosis of microorganisms can affect our health.Fungi have a relatively low level of presence(about 0.1%of the totalmicroorganisms)compared with bacteria,which makes it easier to underestimate their potential threat to health.However,fungal infections indeed participate in the onset and progression of many intestinal diseases,so they are crucially affecting our health[1,2].Recently,Li et al.described that C-type lectin receptors(CLRs)on myeloid cells,including Dectin-1,Dectin-2,Dectin-3,and Mincle,play an important role in the immune function induced by fungal pathogens of the intestinal microbiota[3].