最新刊期

    31 12 2021
    • 2021 Issue 12 Cover

      Vol. 31, Issue 12, (2021)
        
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    • 2021年第12期中文目录

      Vol. 31, Issue 12, (2021)
        
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    • Contents of Issue 12, 2021

      Vol. 31, Issue 12, (2021)
        
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    • 《中 国 癌 症 杂 志》2021 年第 31 卷总目次

      Vol. 31, Issue 12, (2021)
        
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    • Advances in the treatment ofBRAFV600-mutant non-small cell lung cancer

      赵媛媛, 周建英, 范 云, 王佳蕾, 黄鼎智, 李峻岭, 史美祺, 刘基巍, 姚 煜, 邬 麟, 姚文秀, 张 力
      Vol. 31, Issue 12, Pages: 1145-1152(2021) DOI: 10.19401/j.cnki.1007-3639.2021.12.001
      摘要:Lung cancer has the highest morbidity and mortality among malignant tumors in China. Non-small cell lung cancer (NSCLC) represents approximately 85% of all new lung cancer diagnoses. V-Raf murine sarcoma viral oncogene homolog B1 (BRAF) mutations emerge in about 1.5%-3.5% of the NSCLC cases. BRAF V600 accounts for about 50% of all BRAF mutations, among which V600E mutation is the most common. It has been reported that the proportion of men and women and smoking status in patients with BRAF-mutant NSCLC are still disputed. Pathological characteristics show that patients with BRAF-mutant NSCLC (especially BRAF V600E mutation) mainly have adenocarcinoma. Patients with BRAF V600-mutant NSCLC have poor prognosis and short overall survival (OS). The clinical benefits of chemotherapy or immunotherapy for BRAF-mutant NSCLC are not ideal as reported in the current studies. The progression-free survival (PFS) of patients with BRAF-mutant NSCLC treated with chemotherapy is only 1.5-4.2 months, while the PFS of those treated with immune checkpoint inhibitors is 2.5-5.3 months. In recent years, the application of targeted therapy has brought new breakthroughs to the treatment of BRAF V600-mutant NSCLC patients. VE-BASKET was a phase Ⅱ clinical trial, in which the BRAF inhibitor vemurafenib was used to treat BRAF V600E-mutant NSCLC. The final analysis results showed that the median PFS and OS of those patients were 6.5 months and 15.4 months respectively, which preliminarily proved the effectiveness of vemurafenib. However, about 77% of all patients had grade 3/4 adverse events (AEs) which need to be paid more attention. Dabrafenib, another BRAF inhibitor, has achieved significant efficacy in patients with BRAF V600E-mutant NSCLC in the phase Ⅱ clinical trial BRF113928. All patients were divided into three cohorts with dabrafenib monotherapy (cohort A), treated patients with combination therapy of dabrafenib plus mitogen-activated protein kinase (MAPK) kinase (MEK) inhibitor trametinib (cohort B) and untreated patients with combination therapy of dabrafenib plus trametinib (cohort C). The objective response rate (ORR) was 33%, 63.2% and 64%, and PFS was 5.5, 9.7 and 14.6 months in cohort A, B and C, respectively. Recently, the 5-year overall survival (OS) data of this study have also shown that 5-year OS rates of patients in cohort B and C were 19% and 22%, respectively. BRF113928 suggested that dabrafenib plus trametinib had good efficacy in both naive- treatment and treated patients with BRAF V600-mutant NSCLC, which was better than single-agent BRAF inhibition. The safety outcomes showed that the common AEs were fever and gastrointestinal reaction. And most of them were grade 1-2, while the incidence of grade 3/4 AEs or interruption of treatment due to AEs were relatively low. Dabrafenib is generally safe and controllable. Based on the development of existing therapeutic drugs, many research subjects of BRAF V600E-mutant NSCLC is worthy to be explored, including using BRAF inhibitors for adjuvant/neoadjuvant therapy, combination with immunotherapy or antiangiogenic drugs, exploring the drug resistance mechanism to develop new targeted drugs or new combined treatment modes, developing new BRAF inhibitors and exploring the BRAF inhibitors "re-challenge" after dual-target drug resistance. Some related case reports or exploratory studies in recent years have provided clues to these directions. At present, dabrafenib plus trametinib has been preferably recommended for the treatment of BRAF V600E/V600-mutant NSCLC by some guidelines, such as National Comprehensive Cancer Network (NCCN) guidelines of the United States and European Society for Medical Oncology (ESMO) guidelines. This article focused on patients with BRAF V600-mutant NSCLC, and summarized their clinical or pathological characteristics and the treatment progress.  
      关键词:Non-small cell lung cancer;V-Raf murine sarcoma viral oncogene homolog B1;Mutation;Inhibitor;Mitogen-activated protein kinase kinase inhibitor   
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    • 吴绮楠, 童南伟
      Vol. 31, Issue 12, Pages: 1153-1161(2021) DOI: 10.19401/j.cnki.1007-3639.2021.12.002
      摘要:Malignant tumors and diabetes mellitus have gradually become the most common chronic non-communicable diseases in China. They are closely related. The risk, mortality and adverse prognosis of various malignant tumors in diabetic patients are significantly increased. Hyperglycemia in cancer patients is very common. From the aspect of etiology, some malignant tumors lead to hyperglycemia and/or diabetes, and hyperglycemia and/or diabetes can occur during the treatment of malignant tumors, including surgical stress, chemotherapeutic drugs, radiotherapy, glucocorticoids, a variety of targeted drugs and the application of immune checkpoint inhibitors, which is collectively referred to as tumor-associated hyperglycemia. Tumor-associated hyperglycemia is difficult to manage in clinical practice, and the quality of blood glucose control is closely related to the risk and adverse prognosis of patients with malignant tumor. However, there is currently no relevant guideline for the clinical diagnosis and management. Therefore, standardized management of malignant tumor-associated hyperglycemia is necessary. In view of this, the Onco- endocrinology Society of Chinese Anti-Cancer Association and Onco-endocrinology Society of Chong Qing Integrative Medicine Association have drafted Guidelines for the Management of Tumor-associated Hyperglycemia (2021 Edition), a comprehensive report based on the opinions of many domestic experts in oncology and endocrinology. In addition to summarizing the relationship between diabetes and multiple malignant tumors, the guidelines include the etiology of tumor-associated hyperglycemia/diabetes, the epidemiology of tumor-associated hyperglycemia, the concept of tumor-associated hyperglycemia, the diagnostic and differential diagnostic criteria and the standardized management of tumor-associated hyperglycemia, including the overall assessment methods and principles of tumor-associated hyperglycemia, individualized control objectives, management during clinical hospitalization (preadmission preparation, blood glucose management during hospitalization, insulin therapy, intensive care unit and non-intensive care unit management, ketoacidosis and hyperosmolar hyperglycemia, hypoglycemia treatment, perioperative blood glucose management, blood glucose management during enteral/parenteral nutrition, pregnancy with hyperglycemia or diabetes management, glucocorticoid application management, hospice care, transition from inpatient to outpatient, medication precautions, predischarge treatment, etc.), the impact of a variety of hypoglycemic drugs on malignant tumors, the impact of tumor therapeutic drugs on blood glucose and outpatient management, including the establishment of archives of patients with malignant tumors, health examination of blood glucose and complications, long-term follow-up and evaluation. In addition, combined with the actual medical situation in China, the guidelines provide two-way referral and graded diagnosis and treatment for patients with tumor-associated hyperglycemia and put forward relevant suggestions and standards to facilitate the convenient implementation of medical institutions and medical personnel at all levels. The guidelines put forward the corresponding classification of recommendations according to the principle of evidence-based medical evidence classification, which will help clinicians to rationalize and standardize the management of patients with tumor-associated hyperglycemia, so as to improve their clinical outcome and prognosis. Here, we made an interpretation of the contents and recommendations.  
      关键词:Tumor-associated hyperglycemia;Management;Interpretation of guidelines   
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    • 尤 超, 郑惠中, 姜婷婷, 简嘉豪, 范 明, 厉力华, 吴 炅, 顾雅佳, 彭卫军
      Vol. 31, Issue 12, Pages: 1162-1167(2021) DOI: 10.19401/j.cnki.1007-3639.2021.12.003
      摘要:Background and purpose: Digital breast tomosynthesis (DBT) has been applied to breast cancer screening and diagnosis population, which can improve the breast cancer detection. The purpose of this study was to evaluate the differential diagnosis of breast mass lesions based on DBT images. Methods: In the retrospective study, we analyzed the patients undergoing DBT examination in Fudan University Shanghai Cancer Center between April 2019 and August 2020, who were confirmed by surgery and pathology. Finally, a total of 143 female patients showing mass signs were enrolled in this study. Radiomics features were extracted from 3D images of DBT based on mass lesions, and Lasso logistic regression model was used for feature dimension reduction and screening to establish radiomics labels. The model was built by logistic regression (LR), support vector machine (SVM) and gradient boosting decision tree (GBDT) algorithms. Receiver operating characteristic (ROC) was used to evaluate the diagnostic efficacy of radiomic labels for benign and malignant breast tumors. Results: Among 144 lesions confirmed by pathology, 65 were benign and 79 were malignant. It was divided into training set and test set according to the ratio of 8∶2. Based on the classifier algorithm with different number features, the optimal numbers of features of LR, SVM and GBDT were 20, 24 and 32 respectively. The GBDT model achieved an area under curve (AUC) value of 0.91 on the test set. Conclusion: Due to the advantages of integrated learning, GBDT model based on radiomics could effectively distinguish benign from malignant breast lesions in DBT.  
      关键词:Digital breast tomosynthesis;Mass;Radiomics;Diagnosis   
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    • 侯 净, 程纪淦, 王 华, 魏 娜, 倪 青
      Vol. 31, Issue 12, Pages: 1168-1173(2021) DOI: 10.19401/j.cnki.1007-3639.2021.12.004
      摘要:Background and purpose: Nifuroxazide is an oral nitrouracil antibiotic commonly used to treat colitis and diarrhea. Studies have also shown anti-tumor effects of nifuroxazide by inhibiting STAT3 phosphorylation. In the study, through drug screening, nifuroxazide was found to affect homologous recombination (HR) repair of cells. Therefore, the possibility of nifuroxazide combined with poly (ADP-ribose) polymerase (PARP) inhibitor olaparib controlling breast cell growth was further explored. Methods: The SEE-SAW system was used to screen the drugs that had obvious effect on HR repair. Then, the effect of the drug screened on HR was further verified by HR/non-homologous end joining (NHEJ) fluorescence reporting system. DNA damage marker γH2AX foci after drug treatment was detected by immunofluorescence staining. Finally, MTS and clone formation assay were used to detect the effect of drug on cell proliferation. Results: Among 240 small molecule inhibitors screened, a STAT3 inhibitor, nifuroxazide, was found to significantly reduce the level of HR repair. Meanwhile, the combination of nifuroxazide and olaparib aggravated DNA damage and attenuated the ability of DNA damage repair in breast cancer cells. In addition, the combination of nifuroxazide and olaparib further enhanced the killing effect of olaparib on cancer cells. Conclusion: Nifuroxazide can increase the sensitivity of olaparib to breast cancer cells, and can be used as a potential sensitization drug for further study.  
      关键词:Breast cancer;Nifuroxazide;Olaparib;Homologous recombination repair   
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    • 贺国洋, 陈庆庆, 邓美静, 王高翔, 王贝玺, 王永霞, 李 巍, 千新来, 朱会芳
      Vol. 31, Issue 12, Pages: 1174-1184(2021) DOI: 10.19401/j.cnki.1007-3639.2021.12.005
      摘要:Background and purpose: Gastric cancer is one of the common malignant tumors in the digestive system, but its pathogenesis is not clear. Diaphanous-related formin 3 (DIAPH3) plays an important role in the occurrence and development of a variety of tumors, however, its role in gastric cancer has not been reported. This study was to investigate the expression of DIAPH3 in gastric cancer and its effect on the proliferation, migration and invasion of gastric cancer cells. Methods: Gene expression profiling interactive analysis (GEPIA) database was used to analyze the expression of DIAPH3 in gastric cancer. Paraffin embedded tissues and paired adjacent tissues from 62 patients with gastric cancer were collected. The expression of DIAPH3 in gastric cancer was detected by immunohistochemistry, and the clinicopathological correlation was analyzed. Western blot was performed to detect the effects of knockdown or over-expression of DIAPH3 on the protein levels of DIAPH3, cyclin D1, E-cadherin, vimentin and N-cadherin. Real- time fluorescence quantitative polymerase chain reaction (RTFQ-PCR) was used to detect the effect of knockdown or over-expression of DIAPH3 mRNA. Cell proliferation was detected by cell counting kit-8 (CCK-8). Cell migration was detected by the wound healing assay, and cell invasion was detected by transwell chamber experiment. Results: GEPIA database online predicted that the expression of DIAPH3 mRNA was higher in gastric cancer than in adjacent non-cancer tissues (P<0.05). The positive expression rate of DIAPH3 in gastric cancer was 70.97% (44/62), which was higher than that in adjacent non-cancer tissues (16.13%, 10/62, P<0.01). Compared with the high differentiation group, the expression of DIAPH3 in the low differentiation group was higher (P<0.05). Compared with the group without lymph node metastasis, the expression of DIAPH3 in the group with lymph node metastasis was higher (P<0.05). The cell proliferation activity, cell migration rate and cell invasion were lower in the interference DIAPH3 group than in the negative control group (P<0.05). The cell proliferation activity, cell migration rate and cell invasion number were higher in the over-expression of DIAPH3 group than in the over-expression control group (P<0.05). Following over- expression of DIAPH3 and interference of cyclin D1, the proliferation activity of gastric cancer cell line was lower compared with over-expression of DIAPH3 group and higher compared with over-expression control group (P<0.05). Following over-expression of DIAPH3 and interference of vimentin, the cell migration rate and cell invasion number of gastric cancer cell line were lower compared with over-expression DIAPH3 group and higher compared with over-expression control group (P<0.05). Compared with the interference control group, the expression of E-cadherin protein increased, and the expressions of DIAPH3, cyclin D1, vimentin and N-cadherin decreased in the interference DIAPH3 group (P<0.05). Compared with the control group, the expression of E-cadherin protein decreased, and the protein expressions of DIAPH3, cyclin D1, vimentin and N-cadherin increased in the over-expression group. In knockdown or over-expression of DIAPH3 gastric cancer cell lines, the mRNA level of DIAPH3 decreased or increased significantly (P<0.05). Conclusion: DIAPH3 promotes the proliferation, migration and invasion of gastric cancer cells. The role of DIAPH3 is associated with up-regulation of cyclin D1 and epithelial-mesenchymal transition.  
      关键词:Gastric cancer;DIAPH3;Proliferation;Migration;Invasion   
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    • 张进忠, 李悦淇, 石 科, 杨 亮, 郭 丹
      Vol. 31, Issue 12, Pages: 1185-1193(2021) DOI: 10.19401/j.cnki.1007-3639.2021.12.006
      摘要:Background and purpose: As a protein kinase that regulates the cell cycle, polo-like kinase 4 (PLK4) is involved in mitosis initiation, centrosome maturation, cytokinesis, DNA damage detection, etc., which is highly expressed in a variety of tumors. Whether it is involved in the proliferation, invasion and migration of esophageal squamous cell carcinoma (ESCC), and the specific molecular mechanism still remain unclear. This study examined the expression of PLK4 in ESCC cell lines and clinical tissue specimens, and its effect on cancer cell proliferation, invasion and migration. Methods: Total cell RNA was extracted with TRIzol, and cDNA was synthesized with reverse transcription kit for real-time fluorescence quantitative polymerase chain reaction (RTFQ- PCR) to detect the mRNA expression level of PLK4 gene in normal esophageal epithelial cells Het-1A and ESCC cell lines TE-1, TE-8 and TE-13. After the cells were collected by centrifugation, total cell protein was extracted with RIPA lysate. Western blot was used to detect the expression level of PLK4 protein in normal esophageal epithelial cells Het-1A and ESCC cell lines TE-1, TE-8 and TE-13. A total of 93 cases of ESCC tissues and paired adjacent tissues (more than 5 cm from the edge of the primary tumor) confirmed by histopathology were collected at the Affiliated Hospital of Henan Medical College from January 2017 to December 2019. The clinical tissues were quick-frozen by liquid nitrogen followed by total tissue protein extraction by RIPA lysate. Western blot was used to detect the expression level of PLK4 protein in ESCC tissues. We constructed a receiver operating characteristic curve and analyzed the relationship between PLK4 expression and clinicopathological parameters. The expression of PLK4 in TE-13 cells was inhibited by siRNA interference technology. The siRNA interference fragments of PLK4 were designed and synthesized, followed by transfection with Lipofectamine TM 2000 to inhibit the expression of PLK4 in TE-13 cells. The effect of siRNA interference fragments on PLK expression was detected by RTFQ- PCR experiments and Western blot. After the expression of PLK4 was down-regulated in TE-13 cells, cell counting kit-8 (CCK-8) experiment and clone formation experiment were used to detect cell proliferation ability, and transwell chamber experiment and scratch healing experiment were conducted to detect cell invasion and migration abilities. The effects of down-regulation of PLK4 on the expressions of key proteins mTOR, p70S6K, p-mTOR Ser2448 and p-p70S6K Thr421/Ser424 in the mTOR/p70S6K signaling pathway were detected by Western blot experiments. Results: The results of RTFQ-PCR and Western blot experiments showed that the mRNA and protein expression levels of PLK4 gene in ESCC cell lines were significantly higher than those in normal esophageal epithelial cells (P<0.05). Compared with normal tissues adjacent to cancer, the protein expression level of PLK4 in ESCC tissue specimens was abnormally increased (P<0.05). The receiver operating characteristic curve exhibited an area under curve (AUC) of 0.841, a 95% CI of 0.786-0.895 with 74.2% (69/93) sensitivity and 89.2% (83/93) specificity (P<0.0001). There was no relationship between expression level of PLK4 protein and gender, age and tumor size (all P > 0.05) in ESCC tissues. However, expression level of PLK4 protein was related to the degree of differentiation, clinical stage and lymph node metastasis (all P<0.05). The lower degree of ESCC differentiation had higher expression rate of PLK4. The high expression rate of PLK4 in ESCC tissues of poorly differentiated degree was 86.7%, and the high expression rate of PLK4 protein in ESCC tissues of patients with stage Ⅲ-Ⅳ was 92.3%. The high expression of PLK4 was positively correlated with clinical stage (P<0.05). The results of CCK- 8 and clone formation experiments showed that down-regulating the expression of PLK4 significantly inhibited the proliferation of TE-13 cells (P<0.05). The results of the transwell chamber experiment and the scratch experiment showed that down-regulating the expression of PLK4 significantly inhibited the invasion and migration abilities of TE-13 cells (P<0.05). Inhibiting the expression of PLK4 decreased the protein expressions of mTOR and p70S6K in TE-13 cells (P<0.05), and the expressions of p-mTOR Ser2448 and p-p70S6K Thr421/Ser424 decreased (P<0.05). Conclusion: PLK4 is highly expressed in ESCC cells and tissues. Inhibition of PLK4 expression inhibited the proliferation, invasion and migration of ESCC cells. PLK4 may promote the malignant process of ESCC cells through the mTOR/p70S6K signaling pathway.  
      关键词:Polo-like kinase 4;Esophageal squamous cell carcinoma;Clinicopathological characteristics;Proliferation;Invasion and migration   
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    • 李盼盼, 张 卓
      Vol. 31, Issue 12, Pages: 1194-1201(2021)
      摘要:Background and purpose: Primary central nervous system lymphoma (PCNSL) is a rare aggressive type of non-Hodgkin's lymphoma that occurs in the brain, spinal cord, meninges or eyes, without parts outside of central nervous system (CNS) involvement. Compared with other types of lymphoma, PCNSL has shorter survival time, poor prognosis and high recurrence rate. The median survival time of untreated patients is only 3 months. In recent years, studies have found that C-MYC, BCL-2, BCL-6, Ki-67 and other indicators affect the prognosis of PCNSL patients to a certain extent. Therefore, this study analyzed the effects of PCNSL-related protein expression, treatment methods and other clinical factors on the prognosis of patients, hoping to accumulate data for the clinical treatment and prognosis evaluation of the disease. Methods: In this study, we performed a retrospective analysis of the clinical data of 42 patients with primary central nervous system diffuse large B-cell lymphoma treated in the Second Affiliated Hospital of Dalian Medical University from June 2013 to May 2021, including gender, age, number of lesions, Eastern Cooperative Oncology Group (ECOG) score, serum lactate dehydrogenase (LDH), whether the lesion involves deep brain tissue, treatment plan, pathological Hans classification and C-MYC, BCL-2, BCL-6, Ki-67 and other biomarkers, combined with follow- up investigation, to understand the survival time and survival status of patients. Kaplan-Meier method and log-rank test were used to analyze the prognostic factors affecting progression-free survival (PFS) and overall survival (OS). COX regression model was used in multivariate analysis. Results: The median age of onset in 42 patients with PCNSL was 61 years, and the male to female ratio was 1.33:1.00. Most of the brain-enhanced magnetic resonance imaging (MRI) lesions showed homogeneous and obvious enhancement. All patients received chemotherapy with high-dose methotrexate (HD-MTX) regimen. After treatment, there were 20 cases of complete response (CR), 5 cases of partial remission (PR), 11 cases of stable disease (SD) and 6 cases of progressive disease (PD). The median PFS was 21 months, the median OS was 34 months, the 1-year PFS rate was 63.7%, the 2-year PFS rate was 47.0%, the 1-year OS rate was 70.8%, and the 2-year OS rate was 55.6%. Univariate analysis showed that the factors affecting PFS were HD-MTX multidrug combination chemotherapy, intrathecal chemotherapy and combined rituximab. The factors affecting OS were ECOG score ≥2, C-MYC (+), BCL-2 and C-MYC double expression, HD-MTX multidrug combination chemotherapy, intrathecal chemotherapy and combined rituximab. Multivariate analysis showed that rituximab treatment was an independent prognostic factor for PFS (P=0.020), while ECOG score and rituximab were independent prognostic factors for OS (P=0.007, P=0.046). The median PFS and OS of patients receiving consolidation therapy were higher than those of patients without consolidation therapy, and further subgroup analysis showed that the median PFS and OS of autologous stem cell transplantation (ASCT) group were higher than those of whole brain radiotherapy (WBRT) group, however there was no significant statistical difference. Conclusion: PCNSL occurs mostly in middle-aged and elderly people, more men than women without specific imaging characteristics. ECOG score ≥2 is associated with poorer OS in PCNSL patients. C-MYC (+) and dual expression of BCL-2 and C-MYC can be used as prognostic markers to guide risk stratification. HD-MTX-based multidrug combination chemotherapy has become the first choice for the treatment of PCNSL, and the application of rituximab can prolong survival. Systemic chemotherapy combined with local intrathecal chemotherapy can improve the prognosis. Further consolidation treatments mainly include ASCT and WBRT, which can prolong PFS and OS. ASCT can achieve similar curative effects as WBRT and avoid the late neurotoxicity of WBRT. However, due to the limitations of sample size and follow-up time, no clear statistical results have been obtained in this study.  
      关键词:Primary central nervous system lymphoma/PCNSL;Diffuse large B-cell lymphoma;Chemotherapy;Prognosis   
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    • 卢大松, 冯勇军, 王武峰, 牟忠林, 赵 娜
      Vol. 31, Issue 12, Pages: 1202-1208(2021) DOI: 10.19401/j.cnki.1007-3639.2021.12.008
      摘要:Background and purpose: Concurrent chemoradiotherapy is the preferred treatment for locally advanced nasopharyngeal carcinoma. However, concurrent chemoradiotherapy will worsen the nutritional status of patients, thus affecting the quality of life and survival prognosis of patients. This study aimed to investigate the effect of individualized nutritional intervention based on nutritional risk assessment on quality of life and survival prognosis of patients with locally advanced nasopharyngeal carcinoma undergoing concurrent chemoradiotherapy. Methods: A total of 116 patients with locally advanced nasopharyngeal carcinoma treated in the Second Affiliated Hospital of Hainan Medical College from January 2017 to March 2019 were enrolled and randomly divided into the intervention group (58 cases) and the control group (58 cases). The patients in both groups were treated with the same concurrent chemoradiotherapy. The control group received routine dietary guidance, and the intervention group received individualized nutritional intervention based on nutritional risk assessment during concurrent chemoradiotherapy. The nutritional status and life quality of the two groups were compared, and the 2-year and 3-year overall survival (OS), local recurrence-free survival (LRFS) and distant metastasis-free survival (DMFS) of the two groups were analyzed. Results: The incidence of malnutrition in the intervention group at 2 weeks, 4 weeks and the end of radiotherapy was 27.59%, 46.55% and 51.72% respectively, which were lower than 48.28%, 75.86% and 81.03% of the control group (P < 0.05). After treatment, scores of life quality including psychological function, role function, cognitive function, emotional function, social function were significantly higher in the intervention group than in the control group (P < 0.05). The 2-year and 3-year OS, LRFS and DMFS were higher in the intervention group than in the control group (P < 0.05). Conclusion: Individualized nutrition intervention can effectively improve the nutritional status, life quality and the survival prognosis of locally advanced nasopharyngeal carcinoma patients during concurrent chemoradiotherapy.  
      关键词:Nasopharyngeal carcinoma;Locally advanced;Nutrition intervention;Concurrent chemoradiotherapy;Life quality;Survival prognosis   
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    • 卞晓洁, 叶定伟
      Vol. 31, Issue 12, Pages: 1209-1214(2021) DOI: 10.19401/j.cnki.1007-3639.2021.12.009
      摘要:Prostate cancer is the most common male malignant tumor, ranking second among male malignant tumors. The incidence rate of prostate cancer is the highest in all male cancers. The incidence rate of China's prostate cancer is lower than that of western countries. However, with the westernization of lifestyle, the westernization of life habits and the prolongation of life expectancy, the incidence rate of prostate cancer is increasing year by year. Androgen receptor (AR) plays an important role in the pathophysiological mechanism of prostate cancer. Inhibiting AR signal transduction pathway is the basis of prostate cancer treatment. For example, in the treatment of castration-resistant prostate cancer (CRPC), AR antagonists can competitively bind AR and block the binding of endogenous androgen. Thus, it interferes with the downstream response of androgen dependent cells and prevents the progression of prostate cancer. Androgen deprivation therapy (ADT) is the cornerstone in the treatment of prostate cancer. According to the consensus of domestic experts, the effective testosterone (T) level for ADT is less than 50 ng/dL. Accumulated studies have shown that patients with T < 20 ng/dL have better clinical prognosis. Lower T level (less than 20 ng/dL) results in more death of androgen-sensitive and some androgen-insensitive cells. During the treatment, androgen-sensitive cell populations can be obtained, thereby prolonging the duration to castration resistance. If T < 20 ng/dL cannot be achieved, some androgen-insensitive subpopulations may persist. These subpopulations will proliferate rapidly after retreatment and accelerate the progression of tumor resistance to castration. The safety and effectiveness of gonadotropin-releasing hormone agonist (GnRHa), which controls T levels, have been verified by laboratory and clinical evidence, providing the clinical feasibility of controlling T at the level less than 20 ng/dL. This article reviewed the advances in the relationship between T level and ADT, and exhibited the drug efficacy, safety and patient benefits from the treatment of prostate cancer.  
      关键词:Prostate cancer;Testosterone;Gonadotropin-releasing hormone agonist   
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    • Research progress of nerve and extracranial tumor growth

      王 钰
      Vol. 31, Issue 12, Pages: 1215-1219(2021) DOI: 10.19401/j.cnki.1007-3639.2021.12.010
        
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    • 郭 晔, 张陈平
      Vol. 31, Issue 12, Pages: 1220-1232(2021)
      摘要:Squamous cell carcinoma of the head and neck (SCCHN) is the most common head and neck tumor, with higher disease burden. More than 90% SCCHN patients with overexpression of epidermal growth factor receptor (EGFR). Therefore, one important method to inhibit EGFR signaling is through the specific high affinity binding of monoclonal antibody to EGFR. Among a variety of current drugs targeting EGFR and its pathway, cetuximab is the only targeted drug with definite efficacy and has been approved in China since February 2020 for the first-line treatment of recurrent/metastatic SCCHN (R/M SCCHN). With the gradual clinical application of cetuximab, the overall treatment model for patients with advanced SCCHN in China will continue to be improved and optimized. It is worth noting that although targeted and immune drugs have made great progress in the treatment of SCCHN, there are still many challenges. Consensus has not yet been reached for cetuximab on EGFR detection, drug application timing, combination regimen and suitable dosage, and adverse reaction management in the treatment of R/M SCCHN. This expert consensus has combined the literature and clinical practice in China to explain the efficacy and safety of cetuximab in first-line, second-line and combined immunotherapy of R/M SCCHN, and provides relevant recommendations regarding treatment strategies. It is hoped that this consensus will provide guidance for the standardized treatment of SCCHN patients with cetuximab and the optimization of clinical practice. After several rounds of discussion, experts of the consensus group have provided the following recommendations. In terms of molecular testing, patients with R/M SCCHN do not need routine testing of EGFR to inform clinical practice. Anti-EGFR monoclonal antibodies exert anti-tumor effect by inhibiting EGFR signaling. In first-line treatment, 6 cycles of cetuximab in combination with cisplatin 75 mg/m 2 and 5-FU 750 mg/m 2 are recommended for platinum-tolerant patients, followed with cetuximab maintenance monotherapy after disease response or stable disease until progressive disease; 4 cycles of cetuximab in combination with platinum (cisplatin 75 mg/m 2 , q3w) + docetaxel (75 mg/m 2 , q3w) are recommended for patients with contraindications to 5-FU, inconvenience with continuous intravenous infusion, dihydropyrimidine dehydrogenase (DPD) deficiency and poor treatment compliance, followed with cetuximab maintenance monotherapy after disease response or stable disease until progressive disease; cetuximab in combination with paclitaxel weekly is recommended for platinum-intolerant patients until progressive disease; and cetuximab maintenance monotherapy is recommended for elderly patients in good condition after 6 cycles of cetuximab + carboplatin + 5-FU. Multiple clinical studies and real-world data have shown consistent high objective response rate (ORR) and survival benefit with cetuximab in combination with chemotherapy in first-line treatment. In second-line treatment, for patients who have failed first-line platinum-based chemotherapy, weekly treatment with cetuximab monotherapy or in combination with paclitaxel is recommended; for patients who have failed first-line immune checkpoint inhibitor (ICI) treatment, cetuximab in combination with chemotherapy is recommended, and the combined drugs should be adjusted based on previous drug exposure. In terms of safety, the most common adverse events related to cetuximab treatment include skin reaction, infusion reaction and electrolyte disturbance. Most skin reactions are mild and manageable with precautions and generally will resolve without sequelae upon discontinuation or dose reduction of cetuximab. Infusion reactions can be effectively controlled by precautions before infusion, close monitoring during and after infusion and timely intervention. Adverse reactions associated with cetuximab treatment are generally well tolerated and acceptable compared with those associated with chemotherapy alone. In addition, the use of cetuximab in combination with immunotherapy or new targeted drugs is explored and will bring more possibilities for R/M SCCHN patients in the future.  
      关键词:Epidermal growth factor receptor;Anti-epidermal growth factor receptor antibody;Recurrent/metastatic squamous cell carcinoma of the head and neck;Consensus;Targeted therapy   
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      更新时间:2025-12-31
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