Fever is prevalent in hospitalized patients. In hematology-oncology patients, it is related with infection, a disease manifestation or a consequence of immunological dysfunction. This single-center retrospective study...Fever is prevalent in hospitalized patients. In hematology-oncology patients, it is related with infection, a disease manifestation or a consequence of immunological dysfunction. This single-center retrospective study aims to determine fever prevalence, describe its causes and evaluate the impact of infection on mortality. We reviewed clinical records of 222 patients admitted to the hospital in three random months of 2015. Around 35% of all hospitalizations were complicated by fever, 42.5% of unknown origin. 90.4% were under treatment. Around 81% did antibiotics, most commonly piperacillin/tazobactam, for around 11 days. 41% changed antibiotics due to fever persistence or microbiological results. The diagnostic yield of microbiological tests was 25%;in 66.7%, a Gram-negative microorganism was isolated. We didn’t find an association between infection and mortality. We conclude that fever is common in our hematology-oncology clinic and that the team is trained to assume infection;empirical treatment is in accordance with international recommendations.展开更多
AIM To identify chromosomal copy number aberrations(CNAs) in early-stage hepatocellular carcinoma(HCC) and analyze whether they are correlated with patient prognosis.METHODS One hundred and twenty patients with early-...AIM To identify chromosomal copy number aberrations(CNAs) in early-stage hepatocellular carcinoma(HCC) and analyze whether they are correlated with patient prognosis.METHODS One hundred and twenty patients with early-stage HCC were enrolled in our study, with the collection of formalin fixed, paraffin-embedded(FFPE) specimens and clinicopathological data. Tumor areas were marked by certified pathologists on a hematoxylin and eosinstained slide, and cancer and adjacent non-cancerous tissues underwent extraction of DNA, which was analyzed with the Affymetrix Onco Scan platform to assess CNAs and loss of heterozygosity(LOH). Ten individuals with nonmalignant disease were used as the control group. Another cohort consisting of 40 patients with stage Ⅰ/Ⅱ HCC were enrolled to analyze gene expression and to correlate findings with the Onco Scan data.RESULTS Copy number amplifications occurred at chromosomes 1 q21.1-q44 and 8 q12.3-24.3 and deletions were found at 4 q13.1-q35.2, 8 p 23.2-21.1, 16 q23.3-24.3, and 17 p13.3-12, while LOH commonly occurred at 1 p32.3, 3 p21.31, 8 p23.2-21.1, 16 q22.1-24.3, and 17 p 13.3-11 in early-stage HCC. Using Cox regression analysis, we also found that a higher percentage of genome change(≥ 60%) was an independent factor for worse prognosis in early-stage HCC(P = 0.031). Among the 875 genes in the Onco Scan Gene Chip, six were independent predictors of worse disease-free survival, of which three were amplified(MYC, ELAC2, and SYK) and three were deleted(GAK, MECOM, and WRN). Further, patients with HCC who exhibited ≥ 3 CNAs involving these six genes have worse outcomes compared to those who had < 3 CNAs(P < 0.001). Similarly, Asian patients with stage I HCC from The Cancer Genome Atlas harboring CNAs with these genes were also predicted to have poorer outcomes.CONCLUSION Patients with early-stage HCC and increased genome change or CNAs involving MYC, ELAC2, SYK, GAK, MECOM, or WRN are at risk for poorer outcome after resection.展开更多
Three genetic mechanisms activate oncogenes in human neoplasms: 1) mutations, 2) gene amplification, and 3) chromosome rearrangements. These mechanisms result in either an alteration of protooncogene structure or an i...Three genetic mechanisms activate oncogenes in human neoplasms: 1) mutations, 2) gene amplification, and 3) chromosome rearrangements. These mechanisms result in either an alteration of protooncogene structure or an increase in protooncogene expression. The role of epigenetic aberrancies in carcinogenesis has been described earlier however to clinicians, the biological implications of epigenetic therapies to prevent cancer and the mechanisms involved have been a mystery. Furthermore, there is no biomarker suggested to track the carcinogenesis steps long before cancer develops, and this has caused a significant lack of proactive and preventive measures to be taken as all recommendations in preventive oncology are either deficiently and blindly made or through screening methods which are too late in the game. Here we explored a very different approach by applying our deepest understanding of epigenetics and carcinogenesis and even further we developed a framework where our clinical findings could translate to the research and vice versa by generating advanced and novel hypotheses on “how we get cancer”, by exploring the relation between the host and the tumor cells in a way no one had perceived before. The role of specific cancer stem cell pathways is dissected and how to inhibit each of these initiators using multitargeted epigenetic therapies and off-label medications are explained. We should admit that without considering this sophisticated amazing biological network, cancer will remain an unsolved challenge. Further, we were able to solve this unsolved puzzle by bridging the gap from a hypothetical point of view/hypothesis to possibilities that explain the clinical findings we had observed, and conclude that such an approach can completely change the way practitioners are treating cancer.展开更多
目的探讨C-C趋化因子受体9(CCR9)/C-C基序趋化因子配体25(CCL25)轴对阿霉素(DOX)诱导的心脏毒性的影响.方法将60只野生型C57BL/6J小鼠随机分为四组:对照组(CTL组,n=15)、腹腔注射阿霉素组(DOX组,n=15)、腹腔注射阿霉素+尾静脉注射生理...目的探讨C-C趋化因子受体9(CCR9)/C-C基序趋化因子配体25(CCL25)轴对阿霉素(DOX)诱导的心脏毒性的影响.方法将60只野生型C57BL/6J小鼠随机分为四组:对照组(CTL组,n=15)、腹腔注射阿霉素组(DOX组,n=15)、腹腔注射阿霉素+尾静脉注射生理盐水组(DOX+NS组,n=15)、腹腔注射阿霉素+尾静脉注射抗CCL25中和抗体组(DOX+anti-CCL25组,n=15);造模7天后,超声心动图评估小鼠心功能;使用程序化电刺激记录小鼠在体心脏的单向动作电位时程(MAPD)、有效不应期(ERP)、电交替(ALT)阈值和室性心律失常的诱发率.结果与CTL组相比,DOX组左室射血分数(LVEF)和短轴缩短分数(FS)显著降低,左心室舒张末期内径(LVIDd)和左心室收缩末期内径(LVIDs)显著增加(P均<0.05);30%单向动作电位时程(MAPD30)、MAPD50、MAPD70、MAPD90和动作电位复极化时限三角测量值(triangulation)均延长,ERP延长,ALT阈值降低(P均<0.05);10 V和20 V Burst刺激下室性心律失常的诱发率和S1S1程序化刺激下室性心律失常的诱发率均显著升高(P均<0.008);与DOX组相比,DOX+anti-CCL25组LVEF和FS显著升高,LVIDd和LVIDs减小(P均<0.05);MAPD70、MAPD90、Triangulation和ERP缩短(P均<0.05).结论DOX导致小鼠心脏结构重构和电重构,发生室性心律失常的易感性增加,抗CCL25中和抗体可以明显改善DOX小鼠心脏的结构重构和电重构,CCR9/CCL25通路在阿霉素诱导的心脏毒性中有重要作用.展开更多
Diffusion weighted imaging(DWI) is a method of signal contrast generation based on the differences in Brownian motion. DWI is a method to evaluate the molecular function and micro-architecture of the human body. DWI s...Diffusion weighted imaging(DWI) is a method of signal contrast generation based on the differences in Brownian motion. DWI is a method to evaluate the molecular function and micro-architecture of the human body. DWI signal contrast can be quantified by apparent diffusion coefficient maps and it acts as a tool for treatment respon-se evaluation and assessment of disease progression. Ability to detect and quantify the anisotropy of diffusion leads to a new paradigm called diffusion tensor imaging(DTI). DTI is a tool for assessment of the organs with highly organised fibre structure. DWI forms an integral part of modern state-of-art magnetic resonance imaging and is indispensable in neuroimaging and oncology. DWI is a field that has been undergoing rapid technical evolution and its applications are increasing every day. This review article provides insights in to the evolution of DWI as a new imaging paradigm and provides a summary of current role of DWI in various disease processes.展开更多
文摘Fever is prevalent in hospitalized patients. In hematology-oncology patients, it is related with infection, a disease manifestation or a consequence of immunological dysfunction. This single-center retrospective study aims to determine fever prevalence, describe its causes and evaluate the impact of infection on mortality. We reviewed clinical records of 222 patients admitted to the hospital in three random months of 2015. Around 35% of all hospitalizations were complicated by fever, 42.5% of unknown origin. 90.4% were under treatment. Around 81% did antibiotics, most commonly piperacillin/tazobactam, for around 11 days. 41% changed antibiotics due to fever persistence or microbiological results. The diagnostic yield of microbiological tests was 25%;in 66.7%, a Gram-negative microorganism was isolated. We didn’t find an association between infection and mortality. We conclude that fever is common in our hematology-oncology clinic and that the team is trained to assume infection;empirical treatment is in accordance with international recommendations.
基金Supported by the Chang Gung Memorial Hospital in Taiwan,No.CMRPG 3C0951-3 and No.CMRPG 3A0671 to Yu MC,and No.CMRPD3F0011 to Tsai CN
文摘AIM To identify chromosomal copy number aberrations(CNAs) in early-stage hepatocellular carcinoma(HCC) and analyze whether they are correlated with patient prognosis.METHODS One hundred and twenty patients with early-stage HCC were enrolled in our study, with the collection of formalin fixed, paraffin-embedded(FFPE) specimens and clinicopathological data. Tumor areas were marked by certified pathologists on a hematoxylin and eosinstained slide, and cancer and adjacent non-cancerous tissues underwent extraction of DNA, which was analyzed with the Affymetrix Onco Scan platform to assess CNAs and loss of heterozygosity(LOH). Ten individuals with nonmalignant disease were used as the control group. Another cohort consisting of 40 patients with stage Ⅰ/Ⅱ HCC were enrolled to analyze gene expression and to correlate findings with the Onco Scan data.RESULTS Copy number amplifications occurred at chromosomes 1 q21.1-q44 and 8 q12.3-24.3 and deletions were found at 4 q13.1-q35.2, 8 p 23.2-21.1, 16 q23.3-24.3, and 17 p13.3-12, while LOH commonly occurred at 1 p32.3, 3 p21.31, 8 p23.2-21.1, 16 q22.1-24.3, and 17 p 13.3-11 in early-stage HCC. Using Cox regression analysis, we also found that a higher percentage of genome change(≥ 60%) was an independent factor for worse prognosis in early-stage HCC(P = 0.031). Among the 875 genes in the Onco Scan Gene Chip, six were independent predictors of worse disease-free survival, of which three were amplified(MYC, ELAC2, and SYK) and three were deleted(GAK, MECOM, and WRN). Further, patients with HCC who exhibited ≥ 3 CNAs involving these six genes have worse outcomes compared to those who had < 3 CNAs(P < 0.001). Similarly, Asian patients with stage I HCC from The Cancer Genome Atlas harboring CNAs with these genes were also predicted to have poorer outcomes.CONCLUSION Patients with early-stage HCC and increased genome change or CNAs involving MYC, ELAC2, SYK, GAK, MECOM, or WRN are at risk for poorer outcome after resection.
文摘Three genetic mechanisms activate oncogenes in human neoplasms: 1) mutations, 2) gene amplification, and 3) chromosome rearrangements. These mechanisms result in either an alteration of protooncogene structure or an increase in protooncogene expression. The role of epigenetic aberrancies in carcinogenesis has been described earlier however to clinicians, the biological implications of epigenetic therapies to prevent cancer and the mechanisms involved have been a mystery. Furthermore, there is no biomarker suggested to track the carcinogenesis steps long before cancer develops, and this has caused a significant lack of proactive and preventive measures to be taken as all recommendations in preventive oncology are either deficiently and blindly made or through screening methods which are too late in the game. Here we explored a very different approach by applying our deepest understanding of epigenetics and carcinogenesis and even further we developed a framework where our clinical findings could translate to the research and vice versa by generating advanced and novel hypotheses on “how we get cancer”, by exploring the relation between the host and the tumor cells in a way no one had perceived before. The role of specific cancer stem cell pathways is dissected and how to inhibit each of these initiators using multitargeted epigenetic therapies and off-label medications are explained. We should admit that without considering this sophisticated amazing biological network, cancer will remain an unsolved challenge. Further, we were able to solve this unsolved puzzle by bridging the gap from a hypothetical point of view/hypothesis to possibilities that explain the clinical findings we had observed, and conclude that such an approach can completely change the way practitioners are treating cancer.
文摘目的探讨C-C趋化因子受体9(CCR9)/C-C基序趋化因子配体25(CCL25)轴对阿霉素(DOX)诱导的心脏毒性的影响.方法将60只野生型C57BL/6J小鼠随机分为四组:对照组(CTL组,n=15)、腹腔注射阿霉素组(DOX组,n=15)、腹腔注射阿霉素+尾静脉注射生理盐水组(DOX+NS组,n=15)、腹腔注射阿霉素+尾静脉注射抗CCL25中和抗体组(DOX+anti-CCL25组,n=15);造模7天后,超声心动图评估小鼠心功能;使用程序化电刺激记录小鼠在体心脏的单向动作电位时程(MAPD)、有效不应期(ERP)、电交替(ALT)阈值和室性心律失常的诱发率.结果与CTL组相比,DOX组左室射血分数(LVEF)和短轴缩短分数(FS)显著降低,左心室舒张末期内径(LVIDd)和左心室收缩末期内径(LVIDs)显著增加(P均<0.05);30%单向动作电位时程(MAPD30)、MAPD50、MAPD70、MAPD90和动作电位复极化时限三角测量值(triangulation)均延长,ERP延长,ALT阈值降低(P均<0.05);10 V和20 V Burst刺激下室性心律失常的诱发率和S1S1程序化刺激下室性心律失常的诱发率均显著升高(P均<0.008);与DOX组相比,DOX+anti-CCL25组LVEF和FS显著升高,LVIDd和LVIDs减小(P均<0.05);MAPD70、MAPD90、Triangulation和ERP缩短(P均<0.05).结论DOX导致小鼠心脏结构重构和电重构,发生室性心律失常的易感性增加,抗CCL25中和抗体可以明显改善DOX小鼠心脏的结构重构和电重构,CCR9/CCL25通路在阿霉素诱导的心脏毒性中有重要作用.
文摘Diffusion weighted imaging(DWI) is a method of signal contrast generation based on the differences in Brownian motion. DWI is a method to evaluate the molecular function and micro-architecture of the human body. DWI signal contrast can be quantified by apparent diffusion coefficient maps and it acts as a tool for treatment respon-se evaluation and assessment of disease progression. Ability to detect and quantify the anisotropy of diffusion leads to a new paradigm called diffusion tensor imaging(DTI). DTI is a tool for assessment of the organs with highly organised fibre structure. DWI forms an integral part of modern state-of-art magnetic resonance imaging and is indispensable in neuroimaging and oncology. DWI is a field that has been undergoing rapid technical evolution and its applications are increasing every day. This review article provides insights in to the evolution of DWI as a new imaging paradigm and provides a summary of current role of DWI in various disease processes.
