Clinical features of COVID-19 in cancer patients within Wuhan, China.

BACKGROUND: There have been few reports on cancer patients with COVID-19 since its outbreak. Our study aimed to understand the clinical features of cancer patients with COVID-19 and determine the impact of surgery and chemotherapy on the patients' conditions. METHODS: Seventy COVID-19 patients from Renmin Hospital of Wuhan University, including 18 cancer patients, were enrolled in this study. Patients were classified into moderate or severe cases of COVID-19 and as well as non-cancer or cancer patients. Cancer patients were further grouped into Group A (prevalent cases with cancer history) and Group B (incident cases who underwent cancer treatment recently). Laboratory results were analyzed to determine whether cancer-related surgery and chemotherapy worsened the condition of cancer patients. The patients presented with clinical symptoms of COVID-19, including fever, dry cough, and polypnea; blood tests also revealed decreased lymphocyte counts and cellular immune function, and examination of CT scans revealed patchy ground-glass opacity of lungs. RESULTS: The results showed a significant difference (P<0.05) in levels of CD3 CD4 T lymphocytes and D-dimer between non-cancer and cancer patients with moderate COVID-19; there was also a significant difference (P<0.05) in levels of D-dimer between non-cancer and cancer patients with severe COVID-19. Except for liver function, there was no significant difference (P>0.05) between cancer patients in Group A and B with moderate COVID-19. A significant difference (P<0.05) in neutrophil-to-lymphocyte ratio (NLR) and CD4 T lymphocytes was observed between cancer patients with moderate COVID-19 and those with severe COVID-19. CONCLUSIONS: The results indicated that chemotherapy and surgery might not worsen the conditions of COVID-19 patients. NLR and CD4 T lymphocyte might be used as effective indicators for the conditions of cancer patients with COVID-19.

Artificial Intelligence System Application in Miliary Lung Metastasis: Experience from a Rare Case.

INTRODUCTION: Miliary intrapulmonary carcinomatosis (MIPC) is very rare in the existing literature. We reported a lung adenocarcinoma patient presented with over 200 uniform size pulmonary nodules in all lung lobes at the initial examination. The application of artificial intelligence (AI) in lung cancer has been gradually reported, but not yet reported in MIPC. The application of AI in this rare disease is worth exploring. PATIENT INFORMATION: A 57-year-old woman received chest computed tomography (CT) scan because of dry cough, intermittent chest wall and back pain for 3 weeks. CT imaging found over 200 uniform size pulmonary nodules in an evenly dispersed pattern at bilateral lungs with a 38×45mm new creature at the dorsal segment of the lower lobe of the left lung. However, as a very reliable diagnostic assistant system in CT imaging of lung cancer, AI can only identify 18 nodules in such classic metastatic lung cancer case. CONCLUSION: This case provides classical imaging figures as textbook-like, even though there is no such classic imaging of lung metastases in the existing textbooks. This medical imaging material will impress medical students and help them learn about the disease deeply. This medical imaging material can warn patients to recognize the horror of lung cancer metastasis and has good popularization of science. This medical imaging material presents a new challenge for AI.

Long Noncoding RNA ADAMTS9-AS2 Inhibits the Proliferation, Migration, and Invasion in Bladder Tumor Cells.

BACKGROUND: Bladder tumor is the fifth most prevalent tumor in men, yet its pathogenesis remains to be fully identified. Albeit a host of long noncoding RNAs (lncRNA) are emerging as new players involved in bladder tumor, the functions of many lncRNAs are still enigmatic. Reports on the deluge of studies on lncRNA ADAMTS9-AS2 have been convincingly associated with various tumors, but without mention of its roles in bladder tumor. Therefore, the roles of ADAMTS9-AS2 in bladder tumor cells were explored in our study. MATERIALS AND METHODS: Quantitative real-time PCR assays and bioinformatic tools were applied in bladder tumor cells to identify the ADAMTS9-AS2 and ADAMTS9 expression. Western blot assays were performed to obtain the protein levels of bladder tumor related key molecules. CCK8, clonogenic assay, scratch wound healing, and transwell assays were separately applied to identify the functional roles of ADAMTS9-AS2 on proliferation, migration, and invasion in bladder tumor cells. RESULTS: First, ADAMTS9-AS2 downregulation in bladder tumor cells was identified. Overexpression and knockdown experiments showed that ADAMTS9-AS2 expression was positively related to ADAMTS9, which is in accordance with the results from GEO database. Second, ADAMTS9-AS2 contributed to the inhibition of proliferation, migration, and invasion in bladder tumor cells. Third, ADAMTS9-AS2 was linked with PI3K/AKT/mTOR pathway related-molecules, several key autophagy, and apoptotic proteins. CONCLUSION: Conjointly, our findings suggested that ADAMTS9-AS2 might function as a tumor suppressor to restrain the proliferation, migration, and invasion in bladder tumor cells. The potential mechanism of ADAMTS9-AS2 related to PI3K/AKT/mTOR signal pathway was further identified. Of note, we found that ADAMTS9-AS2 has a significant effect on several key autophagy and apoptotic proteins. Therefore, these observations will provide supportive evidence to ADAMTS9-AS2 as a potential biomarker in patients with bladder tumor.

Computational analysis reveals microRNA-mRNA regulatory network in esophageal squamous cell carcinoma.

MicroRNAs (miRNAs) are known to regulate post-transcriptional gene expression. They are involved in carcinogenesis and tumor progression. The aim of this study was to explore the microRNA-mRNA regulatory network in esophageal squamous cell carcinoma (ESCC) using comprehensive computational approaches. In this study we have selected a total of 11 miRNAs from one previously reported study in ESCC. The mRNA targets of these miRNAs were predicted using various algorithms. The expression profiles of these mRNA targets were identified on DNA microarray experiment dataset across ESCC tissue samples. Based on the miRNA-mRNA regulatory relationships, the network was inferred. A total of 23 miRNA-mRNA regulatory interactions, with 11 miRNAs and 13 mRNA targets, were inferred in ESCC. The miRNA-mRNA regulatory network with increased confidence provides insights into the progression of ESCC and may serve as a biomarker for prognosis or the aggressiveness of ESCC. However, the results should be examined with further experimental validation.

Chemosensitization and radiosensitization of a lung cancer cell line A549 induced by a composite polymer micelle.

Multidrug resistance (MDR) to Doxorubicin (DOX) remains a major obstacle to successful cancer treatment. The present study sought to overcome the MDR of lung cancer cells and achieve radiosensitization by developing a composite DOX-loaded micelle (M-DOX). M-DOX containing PEG-PCL/Pluronic P105 was prepared by the solvent evaporation method. Lung cancer cell line A549 was adopted in this study. In vitro cytotoxicity, cellular uptake behavior, subcellular distribution, and radiosensitivity were evaluated by the treatment with M-DOX, and free DOX was used as a control. A549 cells treated with M-DOX as opposed to free DOX showed greater cellular uptake as well as greater cytotoxicity. Furthermore, M-DOX reached the mitochondria and lysosome effectively after cellular uptake, and fluorescence used to track M-DOX was found to be surrounding the nucleus. Finally, colony-forming assays demonstrated that M-DOX treatment improved radiosensitization when compared to free DOX. Based on the increased cytotoxicity and radiosensitization, M-DOX could be considered as a promising drug delivery system to overcome MDR in lung cancer therapy.

HER2 overexpression reverses the relative resistance of EGFR-mutant H1975 cell line to gefitinib.

Gefitinib is an epidermal growth factor receptor tyrosine kinase inhibitor (EGFR TKI) that has been demonstrated to be clinically useful for the treatment of patients with non-small cell lung cancer (NSCLC). However, ~50% of patients do not respond to EGFR TKI treatment through the emergence of mutations, such as T790M. Therefore, it is important to determine which patients are eligible for treatment with gefitinib. As a preferred dimerization partner for EGFR, the role of EGFR 2 (HER2) in mediating sensitivity to gefitinib is poorly understood. In the present study, full-length human HER2 cDNA was introduced to the NSCLC cell lines H1975 and H1299, which have a low endogenous expression level of HER2. In addition, it was observed in the present study that the H1975 cell line harbored the L858R and T790M mutations in the EGFR kinase domain. Western blot analysis and MTT assay were used to evaluate the TKI sensitivity of HER2 expression status, and the activation of HER3 and HER2 downstream effectors. The results indicated that the sensitivity of H1975 cells to gefitinib was restored by the overexpression of HER2, which stimulated HER2-driven signaling cascades accompanied by the activation of protein kinase B. By contrast, ectopic HER2 overexpression in H1299 cells did not significantly alter the sensitivity to gefitinib treatment. In conclusion, the current study results suggested that the relatively resistance of the H1975 cell line to gefitinib could be reversed by the overexpression of HER2. Therefore, the expression of HER2 could also be considered when evaluate the patients' potential response to gefitinib, particularly in the subgroup of lung cancer patients who harbor an EGFR mutation.

Intravenous flurbiprofen axetil enhances analgesic effect of opioids in patients with refractory cancer pain by increasing plasma ß-endorphin.

BACKGROUND: The study aimed to investigate the analgesic effect of a combination of intravenous flurbiprofen axetil and opioids, and evaluate the relationship between refractory pain relief and plasma ß-endorphin levels in cancer patients. MATERIALS AND METHODS: A total of 120 cancer patients was randomly divided into two groups, 60 patients took orally morphine sulfate sustained-release tablets in group A, and another 60 patients receiving the combination treatment of intravenous flurbiprofen axetil and opioid drugs in group B. After 7 days, pain relief, quality of life improvement and side effects were evaluated. Furthermore, plasma ß-endorphin levels were measured by radioimmunoassay. RESULTS: With the combination treatment of intravenous intravenous flurbiprofen axetil and opioids, the total effective rate of pain relief rose to 91.4%, as compared to 82.1% when morphine sulfate sustained-release tablet was used alone. Compared with that of group A, the analgesic effect increased in group B (p=0.031). Moreover, satisfactory pain relief was associated with a significant increase in plasma ß-endorphin levels. After the treatment, plasma ß-endorphin level in group B was 62.4±13.5 pg/ml, which was higher than that in group A (45.8±11.2 pg/ml) (p<0.05). CONCLUSIONS: Our results suggest the combination of intravenous flurbiprofen axetil and opioids can enhance the analgesic effect of opioid drugs by increasing plasma ß-endorphin levels, which would offer a selected and reliable strategy for refractory cancer pain treatment.

Co-transduction of ribosomal protein L23 enhances the therapeutic efficacy of adenoviral-mediated p53 gene transfer in human gastric cancer.

Induction of murine double minute 2 (MDM2) expression is thought to be a determinant of resistance to p53 gene therapy for cancer. Previous studies have revealed that ribosomal protein L23 (RPL23) inhibits MDM2-mediated p53 degradation through direct binding to MDM2. In addition, ectopically expressed RPL23 was reported to interact with MDM2 in both the nucleus and cytoplasm, by which RPL23 indirectly inhibited MDM2-p53 binding. Based on the known molecular properties of the RPL23 protein, it was speculated that co-transduction of RPL23 may protect wild­type p53 protein from MDM2-mediated inactivation and, thus, improve the effect of delivering therapeutic exogenous p53. To test this hypothesis, we constructed a bicistronic adenoviral vector expressing both the RPL23 and p53 genes (Ad-RPL23/p53) and compared its tumor-suppressor activity in human gastric cancer with that of a single gene vector for p53 (Ad-p53). In the in vivo and in vitro experiments, we observed that treatment with Ad-RPL23/p53 resulted in a stronger antitumor response compared to that obtained using Ad-p53. Moreover, the antitumor response of the bicistronic adenovirus was obtained not only in MGC803 cells (endogenous mutant p53) but also in MKN45 cells (endogenous wild­type p53) which were initially resistant to p53 gene transfer, indicating that co-transduction of RPL23 also expanded the utility of p53 gene therapy. Furthermore, in an orthotopic nude mouse model of human gastric cancer, we found that the survival benefit was greater after Ad-RPL23/p53 treatment than after Ad-p53. Taken together, the data presented here demonstrate that co-transduction of RPL23 enhances the therapeutic efficacy of adenoviral-mediated p53 gene transfer in models of human gastric cancer and support the use of this strategy for cancer treatment.

MiR-26a regulates cell cycle and anoikis of human esophageal adenocarcinoma cells through Rb1-E2F1 signaling pathway.

Resistance to anoikis, the subtype of apoptosis induced by lack of matrix adhesion, contributes to malignant transformation and development of metastasis. MicroRNAs play key regulatory roles in tumorigenesis and metastasis. In this study, we described that miR-26a, which is usually downregulated in tumor cells, is involved in the acquisition of anoikis-resistance of human esophageal adenocarcinoma (EA) cells. Results of qRT-PCR in clinical samples showed that downregulated miR-26a expression is related to tumorigenesis and metastasis of EA. In vitro experiments determined that miR-26a directly participates in the regulation of cell cycle and anoikis of human EA OE33 cells. Further, we identified that Rb1 is the direct functional target of miR-26a, and revealed that the reduction of miR-26a expression leads to increased Rb1 protein level and thus inhibits the function of E2F1, by which it influences the phenotypes of cell cycle and anoikis. The findings we reported here presented the evidence that miR-26a may be involved in regulation of anoikis-resistance of EA cells. Targeting miR-26a may provide a novel strategy to inhibit metastasis.

Peritumoral lymphatic microvessel density is related to poor prognosis in lung adenocarcinoma: A retrospective study of 65 cases.

Although recent investigations have identified that lymphangiogenesis is associated with regional lymph node metastasis and tumor prognosis in non-small cell lung cancer (NSCLC), peritumoral lymphatic microvessel density (LMVD) and its prognostic significance in lung adenocarcinoma remain unknown. In the present study, we assessed peritumoral LMVD in lung adenocarcinoma and investigated its correlation with patient prognosis. Using immunohistochemistry (SP method), the D2-40-positive peritumoral LMVD count in lung adenocarcinoma was found to be 11.56±10.73, which was higher than intratumoral LMVD (P<0.001), and was found to be associated with lymphatic metastasis (P=0.003) and pTNM staging (P=0.046). Furthermore, a significant difference in the patient overall survival time was demonstrated between tumors with a high peritumoral LMVD and those with a low peritumoral LMVD (P=0.005). Finally, using multivariate analysis, it was determined that peritumoral LMVD, lymphatic metastasis and pTNM staging were independent prognostic factors. In conclusion, the results suggest that D2-40-positive peritumoral LMVD may predict the prognosis of lung adenocarcinoma.

Giant adenocarcinoma of unknown origin penetrating from the pelvic cavity to subcutaneous tissue: A case report and review of the literature.

In this study, we present a case of a 43-year-old female patient who was admitted to our hospital due to a giant mass on the left buttock. Imaging tests revealed that the mass was a solid-cystic tumor with a large size of 143×430×180 mm, penetrating from the pelvic cavity to the subcutaneous tissue. Pathology tests indicated a metastatic mucinous adenocarcinoma which was most likely of gastrointestinal origin. However, there was no evidence to confirm the existence of malignant changes in the gastrointestinal tract.

[Research on the DNA condensation properties by ultraviolet spectrum].

In order to explore the property and mechanism of DNA condensation, the authors studies the effect of different concentrations of spermine(SPM), spermidine (SPD) and hexamminecobalt(III) chloride on the ultraviolet (UV) absorption value of calf thymus DNA by UV spectrophotometer from the macro. The results showed that SPD and SPM interaction with the DNA had the similar characteristics in UV spectrum. The UV absorption value of calf thymus DNA at 260 nm appeared increased-decreased-increased with the increasing the concentration of SPD and SPM. The value of hexamminecobalt(III) chloride system showed decreased and then increased, suggesting that SPM, SPD and hexamminecobalt(III) chloride could make DNA condense, but in different ways. Relatively, hexamminecobalt(III) chloride was more sensitive than SPD and SPM. The result of UV spectral analysis coincided with recent single-molecule experimental results.

VISA is required for B cell expression of TLR7.

B cells play a critical role in the initialization and development of the systemic lupus erythematosus that is dependent on the expression of the endosomal ssRNA receptor TLR7. Previous studies have established that B cell expression of TLR7 is controlled by the type I IFN secreted by plasmacytoid dendritic cells. In this article, we report that VISA, also known as MAVS, IPS-1, and CardIf, essential for RIG-I/MDA5-mediated signaling following sensing of cytosolic RNA, regulate B cell expression of TLR7 and CD23. We found that B cells from a VISA(-/-) mouse express reduced TLR7 but normal basal levels of type I IFN. We also show that although IFN-ß and TLR7 agonists synergize to promote TLR7 expression in VISA(-/-) B cells, they do not fully complement the defect seen in VISA(-/-) cells. Cell transfer experiments revealed that the observed effects of VISA(-/-) are B cell intrinsic. The reduced TLR7 expression in B cells is correlated with impaired TLR7 agonist-induced upregulation of activation markers CD69 and CD86, cell proliferation, production of IFN-α, TNF, and IL-12, and NF-κB activation. Finally, studies indicate that genetic background may influence the observed phenotype of our VISA(-/-) mice, because VISA(-/-) B cells differ in CD23 and TLR7 expression when on C57BL/6 versus 129Sv-C57BL/6 background. Thus, our findings suggest an unexpected link between VISA-mediated cytosolic RLR signaling and autoimmunity.

Tumor-associated macrophages infiltration is associated with peritumoral lymphangiogenesis and poor prognosis in lung adenocarcinoma.

Tumor-associated macrophages (TAMs) have been implicated in promoting tumor progression. Nowadays, adenocarcinoma has surpassed squamous cell carcinoma as the most frequent type of lung cancer, but in lung adenocarcinoma, the correlation of TAMs with lymphangiogenesis patients remains unclear. The aim of this study was to examine the relationship between TAMs and lymphangiogenesis and the lung adenocarcinoma patients' prognosis. Tumor specimens from 65 patients with lung adenocarcinoma were determined for TAMs count and lymphatic microvessel density (LMVD) by immunohistochemistry. A positive correlation existed between TAMs count and D2-40-positive peritumoral LMVD (r=0.069, P<0.001). TAMs infiltration was significantly associated with P-TNM staging (P=0.042) and lymph node metastasis (P=0.037), and peritumoral LMVD was correlated with lymph node metastasis (P=0.003). A significant difference in overall survival was detected not only between tumors with a high TAMs count and a low TAMs count (P=0.009) but also between tumors with a high peritumoral LMVD and a low peritumoral LMVD (P=0.005). Both TAMs count and peritumoral LMVD were independent prognostic factors for overall survival. Our results indicate that TAMs infiltration correlates with tumor lymphangiogenesis and poor survival in lung adenocarcinoma.

Induction of apoptosis and inhibition of cell migration and tube-like formation by dihydroartemisinin in murine lymphatic endothelial cells.

Dihydroartemisinin (DHA) is a semisynthesized agent from the artemisinin first extracted from the Chinese plant Artemisia annua. Previous studies have shown that artemisinin derivates, apart from their antimalarial activity, possess antitumor, antiangiogenic, and anti-inflammatory effects. In the present investigation, DHA was found to have a potent ability in influencing lymphatic endothelial cells (LECs) behavior. Murine LECs were isolated from benign lymphangiomas induced by intraperitoneal injection of incomplete Freund's adjuvant and identified by indirect immunofluorescence assay and fluorescence-activated cell sorting analysis to examine the expression of the specific marker VEGFR-3/Flt-4. When LECs were treated with DHA at 10 microg/ml, the growth of LECs was inhibited, and LECs showed typical apoptotic morphological features, with a higher apoptotic rate as compared with the controls. DHA also exerted a significant inhibitory effect on migration and tube-like formation of LECs in a dose-dependent manner. Quantitative RT-PCR further showed that DHA remarkably downregulated the expression of antiapoptotic bcl-2 mRNA, but upregulated that of the proapoptotic gene bax mRNA. In addition, DHA could strongly attenuate the mRNA and protein levels of VEGFR-3/Flt-4. In summary, these findings indicate that DHA may be useful as a potential lymphangiogenesis inhibitor under induction of cell apoptosis, inhibition of the migration, and formation of tube-like structures in LECs.

[Efficacy of NO regimen and NP regimen on advanced non-small cell lung cancer: a prospective randomized trial].

BACKGROUND & OBJECTIVE: Oxaliplatin (LOHP) is an effective drug in treatment of non-small cell lung cancer (NSCLC) with mild toxicities to gastrointestinal tract, kidney, and bone marrow. Cisplatin (DDP) plus vinorelbine (NVB) constitute the first-line regimen (NP regimen) for NSCLC. This study was to compare the short-term response, long-term outcome, and adverse events between advanced NSCLC patients received NO regimen (LOHP plus NVB) and NP regimen. METHODS: A total of 90 patients with advanced NSCLC were randomized into NO group (58 patients, 25 mg/m(2) of NVB, day 1 and day 8; 130 mg/m(2) of LOHP, day 1) and NP group (32 patients, 25 mg/m(2) of NVB, day 1 and day 8; 50 mg/m(2) of DDP, day 2 and day 3). The short-term response, long-term outcome, adverse events, and survival status of the 2 groups were observed. RESULTS: The response rates were 33.33% in NO group, and 35.48% in NP group, but no significant difference was detected between the 2 groups (P > 0.05). The clinical benefit response rate was significantly higher in NO group than in NP group (80.70% vs. 64.52%, P < 0.05). The median time to progression (TTP) was 17 weeks in NO group, and 15 weeks in NP group; the median time of remission was 21 weeks in NO group, and 19 weeks in NP group; the median survival time was 39 weeks in NO group, and 37 weeks in NP group; the 1-year survival rate was 37.93% in NO group, and 31.25% in NP group. No significant differences were detected between the 2 groups. The incidence rates of phlebitis and grade I-II peripheral neuritis were significantly higher in NO group than in NP group (77.59% vs. 50.00%, P<0.01; 43.10% vs. 15.63%, P<0.01). The incidence rate of grade III-IV nausea/vomiting was significantly higher in NP group than in NO group (31.25% vs. 3.45%, P<0.05). CONCLUSIONS: The efficacy of NO regimen on advanced NSCLC is similar to that of NP regimen, but the clinical benefit response rate is higher in NO group than in NP group. In short, NO regimen may be recommended as the first-line chemotherapy regimen for advanced NSCLC.

Expression of NASG gene and its role in human nasopharyngeal homogenous tissue cells.

BACKGROUND: The NASG gene has been confirmed as a tumor-suppressor gene candidate related to nasopharyngeal carcinoma (NPC) by previous studies. We further investigated the expression and the role of NASG in the homogeneous tissue cells by microdissecting the samples of tissue from human NPC, and introduced a new way to study the expression of specific genes in tumor tissue. METHODS: The RNAlater reagent was used to preserve the samples of tissue from the nasopharynx of NPC patients. The samples were microdissected to harvest the homogeneous tissue cells and then total RNA was isolated from them. The antisense RNA (aRNA) was amplified from the total RNA by "in vitro transcription (IVT)". We investigated NASG expression in the homogeneous tumor cells of NPC (22 samples) and compared it with that in the pure epithelial pillar cells of normal nasopharyngeal (10 samples) by semi-quantitative reverse transcription-polymerase chain reaction (sqRT-PCR). RESULTS: The high quality total RNA could be harvested from the microdissected homogeneous tissue cells of the nasopharynx, then sufficient aRNA was derived from it. NASG gene expression was identified using aRNA by sqRT-PCR and showed that there was significant difference between the average value of case groups and that of control group (t = -5.275, df = 30, P < 0.001). The NASG gene in the subgroups WHOII tended to express lower levels than those in the subgroup WHOIII although this difference was not statistically significant (t = -1.584, df = 20, P = 0.129 > 0.05). CONCLUSIONS: Microdissection was an effective method to obtain the homogeneous tissue cells of nasopharyngeal tissue (including the samples of NPC and non-NPC) in our study. Sufficient aRNA from amplifying total RNA could be used in sqRT-PCR to analyse the expression of NASG in the pure tissue cells. NASG should be a tumor-suppression gene candidate regarding to NPC.

BRD7, a novel bromodomain gene, inhibits G1-S progression by transcriptionally regulating some important molecules involved in ras/MEK/ERK and Rb/E2F pathways.

Bromodomain is a 110 amino acid domain. It is evolutionally conserved and is found in proteins strongly implicated in signal-dependent transcriptional regulation. BRD7 is a novel bromodomain gene and it is downexpressed in nasopharyngeal carcinoma (NPC) biopsies and cell lines; its function is poorly understood. In the present study, tet-on inducible expression system was used to investigate the role of BRD7 in cell growth and cell cycle progression. We found that ectopic expression of BRD7 in NPC cells inhibited cell growth and cell cycle progression from G1 to S. We further performed cell cycle cDNA array to screen potential transcriptional targets of BRD7 in cell cycle. Thirteen important signaling molecules, mainly implicated in ras/MEK/ERK and Rb/E2F pathways, were differentially expressed by induction of BRD7. Moreover, we observed that BRD7 could regulate the promoter activity of E2F3, one of its targets. Taken together, the present study indicated that BRD7 inhibited G1-S progression by transcriptionally regulating some important molecules involved in ras/MEK/ERK and Rb/E2F pathways and suggested that BRD7 may present a promising candidate of NPC trade mark associated tumor suppressor gene.

[Prospective randomized study of HMVP, MVP, and HVP regimens in treatment of advanced non-small cell lung cancer].

BACKGROUND & OBJECTIVE: Non-small cell lung cancer (NSCLC) is hyposensitive to the normal first and second-line chemotherapy regimens. Camptothecin derivative is becoming a hot point in the treatment of advanced NSCLC. The objective of this article was to evaluate the response, toxicity, and survival time of HMVP, MVP, and HVP regimens (detail in below) in the treatment of advanced NSCLC. METHODS: A total of 134 cases with advanced NSCLC was randomized into three groups: HMVP group [46 patients, hydroxycamptothecin (HCPT) 12 mg/m(2) from d1 to d5, mitomycin C (MMC) 6 mg/m(2) d1, vindesine (VDS) 2.5-3 mg/m(2) d1 and d8, cisplatin (DDP) 50 mg/m(2) d2 and d3], MVP group (44 patients, MMC, VDS and DDP were the same as HMVP group) and HVP group (44 patients, HCPT, VDS, DDP were the same as HMVP group). RESULTS: The response rates were 39.54% (17/43), 35.57% (15/42), and 26.19% (11/42) in HMVP, MVP, and HVP groups, respectively; no significant difference was detected among the three groups (P >0.05). No significant difference was detected in the median time of remission, median survival time, and 1-, 2-year survival rates among the three groups. Moreover, no significant difference was detected in grade III-IV leukopenia, grade III-IV thrombocytopenia, grade III-IV nausea and vomiting and grade III-IV constipation among the three groups. CONCLUSION: The response rate of MVP regimen is slightly lower than that of HMVP regimen, but HMVP regimen do not show obvious superiority. It may increase toxicities such as leukopenia, nausea/vomiting, and constipation. The response rate of HVP regimen is slightly lower than that of MVP regimen.