In December 2019,multiple cases of corona virus disease 2019 were first reported and caused by the coronavirus corona virus disease 2019,which are characterized by strong infectivity,high susceptibility to the population,and long latency periods in Wuhan city,Hubei province.The rapid response of the Central Epidemic Leading Group,the China Centers for Disease Control and Prevention,and the National Health and Medical Commission has made a good tendency in the current epidemic prevention and control,and it is believed that the epidemic will be controlled in the near future.This sudden outbreak for prevention and control has brought a lot of difficulty on diagnosis and treatments to patients with tumors.After the epidemic,cancer patients may return to the hospital for treatment or a peak may occur,especially in the medical oncology patients with severe illness,poor physical condition,urgency to seek medical treatment,and anxiety all bring new challenges to the diagnosis and treatment.This article will combine the understanding of corona virus disease 2019,the specificity of cancer patients,the protection of patients after the epidemic,the orderly diagnosis and treatment to give a thinking for management of oncology patients.This will hope that the medical service of oncology will be helped in the post-epidemic period.

During the outbreak of corona virus disease 2019,various clinics and hospitals across the country have actively participated in the work of preventing and controlling the development of the epidemic.The doctors and nurses in the department of oncology during this period,on the one hand,organized medical support in forefront of the prevention and control for the corona virus disease 2019 epidemic;on the other hand,they insisted on completing its daily diagnosis and treatment of cancer patients.The staffs of doctor and nurse in the department of oncology have faced huge challenges in diagnosis and treatment,clinical medication,and patient management.Through unremitting efforts,they have overcome various difficulties and ensured routine diagnosis and treatment.At the same time,the experience accumulated in clinical practice during the epidemic is worth summing up.At present,the epidemic situation has been effectively controlled.After the epidemic,it is necessary for the medical department of oncology to reflect on the early warning of major public health events,the role of cancer patients in the life-long treatment,patient diagnosis and treatment models,and new drug development.

Since December 2019,the number of corona virus disease 2019 cases has continued to increase.With the spread of the epidemic,clinical trials of anticancer drugs are facing great challenge.Cancer patients are suffering from the tumor itself,surgery,radiotherapy and chemotherapy under special immune status,they are susceptible to the new coronavirus,and are more susceptible to infection with the coronavirus than the normal population.Therefore,this article will elaborate on the particularity of subjects in clinical trials of anticancer drugs in the context of the corona virus disease 2019,management of clinical trials,existing problems and countermeasures to expect optimizing processes and reasonable arrangements,and to ensure the safety of patients so that the smooth progress of the clinical trial is guaranteed.

Since the end of December 2019,corona virus disease 2019(COVID-19)has been spreading globally,bringing great threat to human health.The patients with malignant tumors have low immune function and belong to the high risk susceptible population.Once infected,the disease progresses rapidly.Hepatocellular and pancreatic system tumors are highly invasive,progress rapidly,poor prognosis and high mortality.In the severe epidemic situation,it brings double challenges to both doctor and patient.How to rationally control the patients with hepatobiliary and pancreatic malignancies is particularly important.For patients with severe disease,jaundice or biliary tract infection should take active treatment measures,and patients with stable condition and good physical conditions or postoperative adjuvant treatment can reduce the treatment intensity and time,and delay or even postponed the treatment.The clinicians should choose the individual treatment decision based on the specific situation.

Since December 2019,corona virus disease 2019 epidemic is severe,contagious,concealed,and spreads rapidly,so prevention and control are extremely difficult in China.As a cancer specialist hospital,patients need to travel to and from the hospital multiple times for chemoradiation,reexamination and maintenance,and repeated treatments lead to low immunity.Cancer patients become susceptible to the new type of COVID-19.Improper protection can easily cause nosocomial infections.In this regard,our hospital's catheter clinic established a new set of coronavirus protection measures and optimized the maintenance process.From February 3 to February 28,2020,a total of 758 patients with tumors were maintained,including 159 patients returning from overseas(except for Hubei)and 8 patients returning from Hubei.There was no case of cross-infection for the coronavirus in the hospital.The experience is described as below.

Objective The aim of this study was to understand the epidemic situation of malignant tumors in Tianjin during 2015.Methods According to the stratification by region and gender,the crude incidence,standardization rate,cumulative rate(0~74 years),the incidence and death order and composition of the top 10 malignant tumors in Tianjin were calculated.Results In 2015,the incidence of malignant tumors in Tianjin was 319.17/100,000(314.55/100,000 for males and 323.80/100,000 for females),the bid winning rate was 181.17/100,000,and the world standard trte was 175.15/100,000.The incidence of malignant tumors in urban areas was 383.27/100,000,and in rural areas was 252.50/100,000.The top five cancers were lung cancer,colorectal cancer,breast cancer,thyroid cancer and liver cancer.The city's mortality rate for malignant tumors was 185.73/100,000(214.16/100,000 for males,157.14/100,000 for females),ASRC was 92.22/100,000,and ASRW was 90.78/100,000.The mortality of malignant tumors in urban areas was 229.02/100,000,and that in rural areas was 140.71/100,000.The top five deaths from malignant tumors were lung cancer,liver cancer,colorectal cancer,gastric cancer and pancreatic cancer.Conclusion The incidence of malignant tumors in Tianjin was lower than the national average,but the incidence of malignant tumors in women is higher than the national average.The mortality of malignant tumors is higher in urban areas than in rural areas,and higher in men than in women.

Objective The aim of this study was to investigate,To investigate the effects of propofol on the proliferation,apoptosis and invasion of SCC-74 cells via HIF-1 α signal pathway.Methods SCC-74 cells were cultured in vitro.The final concentrations of propofol were 2.5,10 and 20 μg/mL in low-dose propofol groups,medium-dose propofol group and high-dose propofol groups,respectively.The control group was given the same amount of DMEM culture medium,and the cells were harvested after treatment for 48h.The proliferation,apoptosis and invasion of SCC-74 cells were detected.At the same time,the levels of Akt,p-Akt,HIF-1 α,Fas,FasL,Bcl-2 and Bax protein and mRNA were detected.Results Compared with the control group,the proliferation rate and invasion number of SCC-74 cells in all propofol dose groups was significantly decreased,the apoptosis rate of SCC-74 cells increased(P＜0.05),and the levels of p-Akt and bcl-2 protein in SCC-74 cells was significantly decreased,the levels of HIF-1 α,Bcl-2,Fas,FasL and Bax protein increased in a dose-dependent manner(P＜0.05).There was no significant change in the expression of Akt in SCC-74 cells(P＞0.05).Conclusion Propofol can inhibit the proliferation and invasion of SCC-74 cells and promote the apoptosis of SCC-74 cells by activating HIF-1 α signal pathway.

Objective The Objective of this study was to explore the role of tetrandrine in lung cancer and its molecular mechanism.Methods The MTS method was used to detect the proliferation of lung cancer H1299 cells and A549 cells treated with tetrandrine at 10,15,20,30,40 and 60 μM/L,and then the activities of Caspase3,Caspase8 and Caspase9 were detected by kits,and apoptosis was examined by TUNEL kit.In order to study the mechanism of tetrandrine,Western blot was used to detect the expression of MAPK signaling pathways(p-Akt,PI3K,mTOR and Akt proteins),proliferation and metastasis(MMP-2,MMP-9,PCNA,Cyclin D1 and P21 proteins),cell cycle and apoptosis related proteins(Cyclin D2,Bcl-2,MCL-1,Bax and p53 proteins).Finally,Real-time PCR was used to detect the mRNA expression of PI3k,mTOR,MMP-2,MMP-9,PCNA,Cyclin D1,Cyclin D2,MCL-1,Bax,Bcl-2 and TP53.Results Tetrandrine could inhibit the proliferation of lung cancer H1299 and A549 cells,induce apoptosis,and increase the activities of Caspase3,Caspase8 and Caspase9 in H1299 cells and A549 cells.After treatment with tetrandrine,the expression of PI3K,p-Akt,mTOR,MMP-2,MMP-9,PCNA,Cyclin D1,Cyclin D2and Bcl-2 proteins were reduced,and the expression of P21,MCL-1,Bax and p53 proteins were increased,showing a dose-dependent manner,but no effect on the expression of Akt protein.The mRNA expression of PI3K,mTOR,MMP-2,MMP-9,PCNA,Cyclin D1,Cyclin D2 and Bcl-2 was decreased,and the mRNA expression of TP53,MCL-1 and Bax was increased in H1299 cells and A549 cells.Conclusion Tetrandrine inhibits cell proliferation and induces apoptosis by regulating the MAPK signaling pathway,proliferation and metastasis,cell cycle and apoptosis related proteins and genes expression.

Objective The aims of this study were to analyze the expression of zinc finger protein 12(ZCCHC12)containing CCHC domain in thyroid cancer tissues and cells,and to explore its effect and mechanism on malignant transformation of thyroid cells.Methods The expression of ZCCHC12 in tumor tissues from 30 thyroid cancer patients,10 benign thyroid tissues and cancer cell lines were detected by qRT-PCR and Western blot.ZCCHC12 adenovirus vector or siRNA was used to transfect thyroid cancer cells,and the cell proliferation,invasion ability and expression of corresponding molecules were detected.Results Compared with benign thyroid tissues,the expression of ZCCHC12 in thyroid cancer tissues increased(P＜0.05).At the same time,compared with thyroid follicular epithelial HUM-CELL-0097 cells,the expression of ZCCHC12 at levels of mRNA and protein in thyroid cancer cells also significantly increased(P＜0.05).After ZCCHC12 overexpression,the proliferation and invasive ability of thyroid cancer cells increased significantly(P＜0.05).On the contrary,the proliferation and invasion ability of ZCCHC12 was inhibited after ZCCHC12 silencing(P＜0.05).Compared with the control group,the expression of cyclin D,matrix metalloproteinase 2(MMP-2)and MMP-9 increased after ZCCHC12 overexpression and their expression decreased after ZCCHC12 silencing(P＜0.05).Conclusion ZCCHC12 is highly expressed in thyroid cancer tissues and thyroid cancer cells,and its proliferative activity and invasion ability increase after overexpression ZCCHC12.The abnormal expression of ZCCHC12 can activate the expression of cell cycle related proteins and extracellular matrix related enzymes,and aggravate the malignant transformation of thyroid cells.

Objective The Objective of this study was to investigate the inhibitory effect of ¹³¹I combined with angiogenesis inhibitor apatinib on refractory thyroid cancer cells and its mechanism.Methods The refractory thyroid cancer cells were divided into the control group,¹³¹I group,apatinib group,and ¹³¹I combined with apatinib group(combined group).After treatment for 24 and 48 h,the proliferation of thyroid cancer cells was determined by thiazolyl blue(MTT)assay.The expression of Caspase-3 and VEGF proteins was determined by immunofluorescence and Western blot.Results The proliferative rate of refractory thyroid cancer cells in the combined group was significantly lower than that in the other groups,and the difference was statistically significant(P＜0.01).The expression of Caspase-3 protein in the combined group was significantly higher than that in the other groups(P＜0.01),and the expression of VEGF protein in the combined group was significantly lower than that in the other groups(P＜0.01).Conclusion ¹³¹I combined with apatinib has synergistic effect on refractory thyroid cancer cells.This combination can up-regulate the pro-apoptotic protein Caspase-3 and down-regulate the expression of VEGF protein to inhibit the proliferation of refractory thyroid cancer cells.Thus,this will provide a better strategy for clinical treatment of refractory thyroid cancer.

Objective The aim of this study was to investigate the effect and mechanism of cyclin B1(CCNB1)gene on the proliferation,invasion and migration of oral squamous cell carcinoma.Methods Quantitative real-time fluorescent PCR(qRT-PCR)was used to detect the expression of CCNB1 gene in human normal oral epithelial HOK cell line and human oral squamous cell carcinoma SCC-15,SCC-4 and Gal-27 cell lines.CCNB1 siRNA(si-CCNB1)and negative control(si-NC)were transfected into SCC-15 cells.At the same time,blank control(Control)was set.qRT-PCR and Western blot were used to detect the expression of CCNB1 in each group of SCC-15 cells.MTT,Transwell and Scratch assays were used to detect the effects of silencing CCNB1 on the proliferation,invasion and migration of SCC-15 cells.Western blot was used to detect the expression of MMP-2,MMP-9,PI3K,Akt and p-Akt in SCC-15 cells.Results The expression of CCNB1 in oral squamous carcinoma cells was significantly higher than that in normal oral epithelial cells(P＜0.05).The expression of CCNB1 mRNA and protein in SCC-15 cells in the si-NC group was not different from that of the control group(P＞0.05),The expression of CCNB1 mRNA and protein in the si-CCNB1 group was significantly lower than that in the si-NC group and control group(P＜0.05),The proliferation,invasion and migration ability of SCC-15 cells in the si-NC group and the expression of MMP-2,MMP-9,PI3K,Akt and p-Akt in the si-NC group were not significantly different from those in the control group(P＞0.05).The cell proliferation,invasive and migratory abilities,and the expressions of MMP-2,MMP-9,PI3K and p-Akt in the si-CCNB1 group were significantly lower than those in the si-NC group and control group(P＜0.05).There was no difference in the expression of Akt protein between the si-CCNB1 and si-NC groups(P＞0.05).Conclusion CCNB1 is highly expressed in oral squamous carcinoma cells.Silencing CCNB1 gene can inhibit the proliferation,invasion and migration of human oral squamous carcinoma SCC-15 cells.The mechanism may be related to the inhibitory activation of PI3K/Akt signaling pathway.

Objective The objectives of this study were to investigate the expression of cell division cycle 7 protein(CDC7)in hepatocellular carcinoma(HCC)tissues,and to explore the effect of CDC7 overexpressing on proliferation and invasion of hepatocellular carcinoma cells.Methods Quantitative real-time polymerase chain reaction(qRT-PCR)was used to detect the expression of CDC7 mRNA in liver cancer tissues and adjacent tissues,and the expression of CDC7 mRNA in liver tumor cell lines and normal liver cells.Western blot was used to detect the expression of CDC7 protein in liver cancer tissues and adjacent tissues,and to detect the expression of CDC7 protein in liver tumor cell lines and normal liver cells.Lentivirus vectors were used to construct stable overexpressing CDC7 hepatocellular carcinoma HCCLM3 and SMMC 7721 cell lines.Cell clone and cell counting kit-8(CCK-8)experiments were used to detect the effect of CDC7 overexpression on the proliferation of HCC cells.Scratch and Transwell assays were used to detect the effect of CDC7 overexpression on the invasion and migration of HCC cells.Results Compared with adjacent tissues,the expression of CDC7 at the levels of mRNA and protein was significantly increased in HCC tissues(P＜0.001);compared with normal liver cells,the expression levels of CDC7 at the levels of mRNA and protein were significantly increased in liver cancer cell lines(P＜0.001);CCK-8 experiments and cell cloning experiments showed that overexpression CDC7 significantly enhanced the proliferative ability of HCC cells;Scratch and Transwell experiments showed that overexpression CDC7 significantly improved the invasion ability of HCC cells.Conclusion CDC7 protein is highly expressed in human HCC tissues,and its overexpression promotes the proliferative and invasive capability of HCC cells.

Objective The aims of this study were to investigate the expression and methylation of WNT4 in glioma tissues and malignant glioma cell lines,and its effect and mechanism on the proliferation of glioma U87 cell line.Methods qRT-PCR and Western blot were used to analyze the expression and methylation of WNT4 in human glioma tissues and the expression of WNT4 in U87 cells.MSP was used to analysis the methylation of Wnt4 in glioma tissues.U87 cells were used as experimental cells transfected with lentiviral vectors pLVX-Gfp-WNT4(experimental group)and pLVX-Gfp-NC(control group).Cell proliferation and clone formation experiments were performed to analyze the effect of WNT4A gene on cell proliferation.Western blot was used to verify the effect of WNT4 on the WNT/β-catenin signal pathway.Results Compared with normal human astrocytes,WNT4 mRNA and protein were significantly down-regulated in glioma tissues and cells(P＜0.001).WNT4 methylation was significantly increased in gliomas tissues.The expression of WNT4 was related to the grade of glioma,and the good prognosis of patients with the high expression of WNT4 mRNA;the degree of methylation of WNT4 in glioma tissues was significantly higher than that of normal brain tissues.The Re-expression of WNT4 in significantly decreased in cell viability and proliferation of U87 cells(P＜0.001);The WNT/β-catenin signaling pathway and its downstream cytokines were significantly suppressed after WNT4 expression was restored in U87 cells.Conclusion The expression of WNT4 is down-regulated in human glioma tissues and participates in the progression of gliomas by inhibiting the Wnt/β-catenin signaling pathway.

Objective The aim of this study was to investigate the effect of decitabine combined with cisplatin in the treatment of colorectal cancer and its effect on the structure of intestinal flora.Methods In the study,a mouse colorectal cancer xenograft model was established,and the changes in tumor volume and overall survival of mice after the treatment with decitabine,cisplatin,and decitabine combined with cisplatin were measured;the changes of ABCB1 and MYC gene expression in transplanted tumor tissue from mice treated with decitabine,cisplatin,and decitabine combined with cisplatin were detected;fecal samples of mice were collected,the changes of intestinal flora structure were compared in mouse models by Miseq sequencing.Results The combined use of decitabine and cisplatin could reduce the tumor growth rate and prolong the overall survival time of mouse transplanted tumor models;the combined use could reduce the expression of ABCB1 and MYC genes in a model model.The result of Miseq sequencing showed that the intestinal flora of mice changed significantly after different treatments.The detection rates of Escherichia coli,Enterococcus faecalis and other pathogenic bacteria were significantly higher in the stool of colorectal cancer xenograft mouse models.Conclusion Decitabine combined with cisplatin in the treatment of colorectal cancer can effectively inhibit the growth of tumor and prolong the overall survival time.The larger proportion of pathogenic bacteria in the intestinal track of mouse models may be the important reason for the development of colorectal diseases.When using cisplatin to treat colorectal cancer,it also needs to be combined with intestinal flora conditioning drugs for combined treatment.

Objective The aim of this study was to investigate the effect of perioperative infection on cancer specific survival(CSS)after renal cell carcinoma resection.Methods A total of 1 800 patients with renal cell carcinoma from January 2006 to January 2013 in the Affiliated Hospital of Qingdao University were used as the research subjects,and the infection situation within 30 days after nephrectomy for renal cancer was analyzed.The CSS of infected and uninfected patients was analyzed by Kaplan-Meier curve,and Cox proportional hazard model was established to evaluate CSS.The factors such as sex,age,AJCC stage and classification,tumor size,pathological type,complications,surgical methods and systematic treatment were also controlled.Results The median age of 1 800 patients was 74 years(69~79 months),and the median follow-up time was 42 months(22~67 months).There were 141 cases of severe infection,296 cases of non-severe infection and 1 363 cases of non-infection.Kaplan-Meier analysis showed that severe infection had a tendency to improve CSS in patients with renal cancer(tumor diameter 7.0~9.9)(P=0.048),but severe infected patients with tumor diameter ≥10 cm or ＜7 cm had no effect on CSS(0.1~3.9 cm,P=0.120;4.0~6.9 cm,P=0.768;＞10 cm,P=0.412).Multivariate Cox regression analysis showed that severe infection could improve CSS in patients with renal cancer(HR=0.752,P=0.032).This effect was more obvious in patients with a tumor diameter(＞7 cm)(P=0.041),but it was not in patients with tumor diameter ＜ 7 cm(P=0.268).Conclusion Severe perioperative infection can improve CSS in patients with renal cancer with a tumor diameter of 7~10 cm,but it has no effect on CSS in patients with tumors ≥10 cm or ＜7 cm in diameter.

Objective The Objective of this study was to investigate the effect of ketorolac tromethamine on preventive analgesia in the immune function of patients with lung cancer surgery.Methods A total of 172 patients with lung cancer surgery in our hospital from September 2017 to September 2019 were selected and divided into the prevention group and general anesthesia group according to the random number table.Each group had 86 cases.The general anesthesia group was given general anesthesia intervention.The prevention group was given ketorolac tromethamine as the preventive analgesia.On the basis,the mean arterial pressure(MAP),heart rate(HR),visual analogue scale(VAS),immune globulin(IgA,IgG,and IgM)and T lymphocyte subsets(CD3⁺,CD4⁺,and CD4⁺/CD8⁺)and adverse reaction were compared between the prevention and general anesthesia groups.Results The MAP and HR in the prevention group at 15 min after anesthesia(T₁),tissue incision(T₂),tumor resection(T₃)were significantly lower than those in the general anesthesia group,the difference was statistically significant(P＜ 0.001).The levels of IgA,IgG,IgM,CD3⁺,CD4⁺,and CD4⁺/CD8⁺ in the prevention group after operation were significantly higher than those in the general anesthesia group,the difference was statistically significant(P＜ 0.001).The VAS scores in the prevention group at 4 h,24 h,48 h and 72 h were significantly lower than that in the general anesthesia group,the difference was statistically significant(P＜ 0.001).There was no significant difference in the incidence of adverse reactions between the prevention and general anesthesia groups(P＞0.05).Conclusion Preventive analgesia with ketorolac tromethamine can effectively improve the hemodynamic fluctuations and analgesic effect on patients with lung cancer surgery,and it is beneficial to improve the immune function of patients.It has good safety and worth for further clinical application.

Objective The aim of this study was investigate the dosimetric difference between VMAT and IMRT by VARIAN IX linear accelerator using 6 MV X-ray in flatting-filter-free mode.Methods A retrospective study was conducted on 53 patients with rectal cancer treated by preoperative radiotherapy in Liaoning Cancer Hispital from September 2016 to September 2018.Each patient in flatting-filter-free mode was used the same optimization conditions to perform VMAT and IMRT plans.The dosimetric differences were compared between target areas and organs in two modes of plans.Results In terms of target dose,there were statistically significant of differences in D2%,D98%,D_mean,CI and HI of the two plans.FFF-IMRT compared to FFF-VMAT,D2% increased by 3.1%(P=0.001),D98% decreased by 4.5%(P=0.001),D_mean decreased by 2.4%(P=0.026),CI decreased(P＜0.001),and HI increased(P=0.005).In terms of organ at risk,there were statistically significant of differences in D2%,D_mean of bladder,D2%,D_mean of double femoral heads and D_mean of pelvis between the two plans.FFF-IMRT compared to FFF-VMAT,D2% of bladder increased by 2.7%(P＜0.001)and D_mean decreased by 20.4%(P＜0.001),D2% of double femoral head decreased by 4.2%(P＜0.001),D_mean decreased by 11.2%(P＜0.001),and D_mean of pelvis decreased by 8.9%(P＜0.001).However,there was no significant of differences between D2% and D_mean of intestines(P＞0.05).The planned machine hops of FFF-IMRT were(978±127)MU,which was 1.86 times of the planned machine hops of FFF-VMAT(527±63)MU(P＜0.001).The planned execution time of FFF-IMRT was(510±252.2)s,which was 2.21 times that of FFF-VMAT(232±52.5)s(P＜0.001).Conclusion In the flatting-filter-free mode,the conformity and uniformity of VMAT in target area are better than those of IMRT,the treatment time of VMAT was shorter and the execution efficiency of the plan was higher.However,IMRT could better protect the organs of patients.

SAM pointed domain cintaining Ets transcription factor(SPDEF)is a member of the Ets transcription factor family.SPDEF is also known as prostate-derived Ets factor(PDEF).It was originally found in prostate cancer and plays an important role in the progression of prostate cancer,acting as a prostate-specific antigen(PSA)promoter for a non-androgen-dependent transcriptional activator.Current many studies have found that SPDEF plays a role in inhibiting tumors or promoting tumors in different tissues such as prostate cancer,breast cancer and lung cancer,but the specific mechanism has not been fully elucidated.This article mainly introduces the structure of SPDEF and the regulatory mechanism of SPDEF in different tumors.The important role of SPDEF in tumors is expected to provide new ideas for the prevention and treatment of related tumors.

Follicular lymphoma(FL)is a common B-cell lymphoma with an incidence of non-Hodgkin's lymphoma(NHL)that is second only to diffuse large B lymphoma.FL is an indolent lymphoma.Although the disease progresses slowly,it cannot be cured,and due to recurrence and progression,it seriously affects the survival of patients.In recent years,the“no-chemotherapy”regimen for FL has exact curative effect and low toxicity;the new immunotherapy and targeted drugs also show good curative effect,which has attracted widespread attention from researchers.In order to further deepen the clinician's understanding of the new progress of FL treatment,this article reviews the stratification and treatment progress of FL.