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Private Set Intersection Cardinality that enable Multi-party to privately compute the cardinality of the set intersection without disclosing their own information. It is equivalent to a secure, distributed database query and has many practical applications in privacy preserving and data sharing. In this paper, we propose a novel quantum private set intersection cardinality based on Bloom filter, which can resist the quantum attack. It is a completely novel constructive protocol for computing the intersection cardinality by using Bloom filter. The protocol uses single photons, so it only need to do some simple single-photon operations and tests. Thus it is more likely to realize through the present technologies. The validity of the protocol is verified by comparing with other protocols. The protocol implements privacy protection without increasing the computational complexity and communication complexity, which are independent with data scale. Therefore, the protocol has a good prospects in dealing with big data, privacy-protection and information-sharing, such as the patient contact for COVID-19.

HOX gene-encoded homeobox proteins control body patterning during embryonic development; the specific expression pattern of HOX genes may correspond to tissue identity. In this study, using RNAseq data of 1019 human cancer cell lines that originated from 24 different anatomic sites, we established HOX codes for various types of tissues. We applied these HOX codes to the transcriptomic profiles of prostate cancer (PCa) samples and found that the majority of prostate adenocarcinoma (AdPCa) samples sustained a prostate-specific HOX code whereas the majority of neuroendocrine prostate cancer (NEPCa) samples did not, which reflects the anaplastic nature of NEPCa. Also, our analysis showed that the NEPCa samples did not correlate well with the HOX codes of any other tissue types, indicating that NEPCa tumors lose their prostate identities but do not gain new tissue identities. Additionally, using immunohistochemical staining, we evaluated the prostatic expression of HOXB13, the most prominently changed HOX gene in NEPCa. We found that HOXB13 was expressed in both benign prostatic tissues and AdPCa but its expression was reduced or lost in NEPCa. Furthermore, we treated PCa cells with all trans retinoic acid (ATRA) and found that the reduced HOXB13 expression can be reverted. This suggests that ATRA is a potential therapeutic agent for the treatment of NEPCa tumors by reversing them to a more treatable AdPCa.

Background  Colon cancer is a common cause of cancer and cancer-associated deaths in the United States. Many factors can influence the overall survival (OS) of patients with colon cancer, such as patient demographics, clinical presentation, and treatment characteristics. The goal of this study was to assess the influence of chemotherapy on OS in patients with colon cancer with similar baseline characteristics.  Materials and methods  A total of 70,876 patients with stage II and III colon cancer, confirmed by pathology, over the age of 18, and who were diagnosed with colon cancer between 2004 and 2019, were selected from the de-identified National Cancer Database (NCDB). All of the patients included in the study underwent surgical treatment. Patients who received hormonal therapy, radiation therapy, immunotherapy, palliative care, or any treatment modality besides chemotherapy were excluded from the analysis. Calculation of the propensity score was performed by computing the probability of patients being in the chemotherapy group using logistic regression. The propensity score matching (PSM) was done via the PSMATCH procedure with the SAS software (SAS Institute, Cary, NC, USA) on patients who received chemotherapy compared to patients who received a treatment other than chemotherapy. The greedy nearest neighbor matching method was then utilized to match one chemotherapy patient to one non-chemotherapy patient with a caliper of 0.2. An exact match was done for sex, race, tumor stage, and year diagnosed at the time of patient diagnosis. Multivariate Cox regression analysis was then used to estimate the effect of chemotherapy on OS before and after PSM.  Results  A total of 70,876 patients were included in the study before PSM, with 44,992 receiving chemotherapy and 25,884 not receiving chemotherapy. Before PSM, the OS was 17.55 years for patients who received chemotherapy, compared to 14.12 years for those who did not. After matching 23,356 patients, the OS was 17.77 years for patients who received chemotherapy and 12.18 years for those who did not. Following PSM, patients who received chemotherapy were 46% less likely to die compared to those who did not receive chemotherapy. Conclusion  Our findings, per the PSM method, demonstrate that receiving chemotherapy can be a significant predictor of OS among patients with stage II and III colon cancer. Other variables such as tumor stage, age, and insurance type were also found to be significant predictors of OS in colon cancer patients. Prospective clinical studies are necessary and should be performed to determine the true effects of chemotherapy on OS.

Shikonin, a small-molecule natural product which inhibits the activity of pyruvate kinase M2 (PKM2), has been studied as an anti-cancer drug candidate in human cancer models. Here, our results demonstrate that shikonin is able to sensitize human breast cancer cells to chemotherapy by paclitaxel (taxol). Human breast adenocarcinoma MBA-MD-231 cells, which have higher levels of PKM2 expression and activity compared with MCF-7 cells, were selected to study further. The concentrations of shikonin and taxol were first selected at which they did not significantly induce cytotoxicity when treated alone, whereas the combination induced apoptosis. Surprisingly, PKM2 activity was decreased by shikonin, but not by the combination treatment. To identify the potential targets of this combination, human phospho-kinase antibody array analysis was performed and results indicated that the combination treatment inhibited the activation of ERK, Akt, and p70S6 kinases, which are known to contribute to breast cancer progression. Finally, how the combination affects breast cancer cell growth in vivo was tested using a xenograft tumor model. The results indicated that shikonin plus taxol prolonged animal survival and reduced tumor size than the vehicle treatment group. In summary, our results suggest that shikonin has a potential as an adjuvant for breast cancer therapy.

BackgroundAfter long-term androgen deprivation therapy, 25–30% prostate cancer (PCa) acquires an aggressive neuroendocrine (NE) phenotype. Dysregulation of YAP1, a key transcription coactivator of the Hippo pathway, has been related to cancer progression. However, its role in neuroendocrine prostate cancer (NEPC) has not been assessed.MethodsImmunohistochemistry and bioinformatics analysis were conducted to evaluate YAP1 expression levels during PCa initiation and progression.ResultsYAP1 expression was present in the basal epithelial cells in benign prostatic tissues, lost in low-grade PCa, but elevated in high-grade prostate adenocarcinomas. Interestingly, the expression of YAP1 was reduced/lost in both human and mouse NEPC.ConclusionsThe expression of YAP1 is elevated in high-grade prostate adenocarcinomas but lost in NEPC.

Emergent cancer drug resistance and further metastasis can mainly be attributed to altered expression levels and functional activities of multiple genes of cancer cells under chemotherapy. In response to challenge with anticancer drugs, enhanced ceramide glycosylation catalyzed by glucosylceramide synthase (GCS) confers drug resistance and enrichment with cancer stem cells. p53 mutations, which gain function in tumor progression, are prevalently extant in ovarian cancers. Via integrated gene expression assessments, we characterized GCS-responsive genes in ovarian cancer cells treated with dactinomycin. NCI/ADR-RES cells dominantly expressed a p53 mutant (7 aa deleted in exon-5) and displayed anti-apoptosis; however, silencing GCS expression rendered these cells sensitive to dactinomycin-induced apoptosis. Microarray analyses of NCI/ADR-RES and its GCS transfected sublines found that elevated GCS expression or ceramide glycosylation was associated with altered expression of 41 genes, notably coding for ABCB1, FGF2, ALDH1A3, apolipoprotein E, laminin 2, chemokine ligands, and IL6, with cellular resistance to induced apoptosis and enrichment with cancer stem cells, promoting cancer progression. These findings were further corroborated through integrated genomic analyses of ovarian cancer from The Cancer Genome Atlas (TCGA) and cancer resistance to platinum-based chemotherapy. Altogether, our present study indicates that altered ceramide glycosylation can modulate expression of these GCS-responsive genes and alter cancer cell attributes under chemotherapy.

Background Thymoquinone (TQ) is a compound extracted from Black Caraway seeds of Nigella Sativa and is active against various cancers. Cisplatin (CDDP) is the most active chemotherapeutic agent in Lung Cancer. Here we report activity of TQ against non-small cell lung cancer (NSCLC) and small cell lung cancer (SCLC) cell lines alone and in combination with Cisplatin (CDDP). Methods For proliferation MTT assay, cell viability trypan blue assay and for apoptosis Annexin-V FITC assay were used in NCI-H460 and NCI-H146 cell lines. Inhibition of invasion by TQ was assessed using Matrigel assay and its affect on release of various cytokines was determined using RayBio Human Cytokine detection kit. Mouse xenograft model using NCI-H460 was used to determine in vivo activity of TQ and CDDP. Inhibition of LPS induced NF-κB expression by TQ was determined using transgenic mice expressing a luciferase reporter. Results TQ was able to inhibit cell proliferation, reduce cell viability and induce apoptosis. TQ at 100 μM and CDDP at 5 μM inhibited cell proliferation by nearly 90% and the combination showed synergism. TQ was able to induced apoptosis in both NCI-H460 and NCI-H146 cell lines. TQ also appears to affect the extracellular environment inhibiting invasion and reducing the production of two cytokines ENA-78 and Gro-alpha which are involved in neo-angiogenesis. Using a mouse xenograft model we were able to demonstrate that combination of TQ and CDDP was well tolerated and significantly reduced tumor volume and tumor weight without additional toxicity to the mice. In the combination arms (TQ5 mg/kg/Cis 2.5 mg/kg) tumor volume was reduced by 59% and (TQ20 mg/kg/Cis 2.5 mg/kg) by 79% as compared to control which is consistent with in vitro data. TQ down regulated NF-κB expression which may explain its various cellular activities and this activity may prove useful in overcoming CDDP resistance from over expression of NF-κB. Conclusions Thus TQ and CDDP appear to be an active therapeutic combination in lung cancer.

Introduction Cancer cachexia affects many advanced non-small-cell lung cancer (NSCLC) patients. Cachexia index (CXI) was developed to assess the degree of cachexia in these patients. Methods Patients with metastatic NSCLC diagnosed between January 1, 2000, and June 30, 2011, at our institution were retrospectively studied. Abdominal computed tomography scans done within 1 month of diagnosis were reviewed to estimate skeletal muscle area (SMA) and skeletal muscle index (SMI) at the L3 level. CXI was developed as follows: CXI=SMI×A1bNLR where SMI is the skeletal muscle index, Alb is the serum albumin, and NLR is the NLR neutrophil-to-lymphocyte ratio. Progression-free survival (PFS) and overall survival (OS) were estimated using the Kaplan–Meier method. Survival among various factors was calculated using the log-rank test. Multivariate Cox regression was used to perform survival analysis in order to estimate the effects of various factors. Results Patients were divided into two groups around the median into stage I cachexia (CXI ≥35, n = 56) and stage II cachexia (CXI <35, n = 56). Groups did not differ in age, gender, ethnicity, or histology of cancer. Patients with stage II cachexia had significantly worse PFS (2.45 vs 5.43 months, P < 0.0001) and OS (3.45 vs 8.8 months, P = 0.0001) than those with stage I cachexia. On multivariate analysis adjusting for gender, race, and histology, patients with stage II cachexia were found to have worse PFS (hazard ratio [HR] 1.94, 95% confidence interval [CI] 1.27–2.95) and OS (HR 1.53, 95% CI 1.0009–2.34). Conclusion The CXI is a novel index for estimating cachexia that also correlates with prognosis in both men and women with advanced NSCLC.

Abstract BACKGROUND: Ventriculoperitoneal shunting is the most widely used neurosurgical procedure for the management of hydrocephalus. OBJECTIVE: To evaluate our long-term single-institution experience in the management of adult hydrocephalus patients with ventriculoperitoneal shunts. METHODS: Adult patients who underwent ventriculoperitoneal shunt placement for hydrocephalus from October 1990 to October 2009 were included. Medical charts, operative reports, imaging studies, and clinical follow-up evaluations were reviewed and analyzed retrospectively for clinical outcome in adult hydrocephalus patients. RESULTS: A total of 683 adult patients were included in the study. The most common etiologies of hydrocephalus include idiopathic (29%), tumors and cysts (20%), postcraniotomy (13%), and subarachnoid hemorrhage (13%). The overall shunt failure rate was 32%, and the majority (74%) of shunt revisions occurred within the first 6 months. The median time to first shunt revision was 9.31 months. Etiology of hydrocephalus showed a significant impact on the incidence of shunt revision/failure and on the median time to shunt revision. Similarly, the type of hydrocephalus had a significant effect on the incidence of shunt failure and the median time to shunt revision. CONCLUSION: A large proportion of patients (32%) experience shunt failure after shunt placement for hydrocephalus. Although the overall incidence of shunt revision was comparable to previously reported studies, the fact that a large proportion of adult populations with shunt placement experience shunt failure is a concern.

The rapid development of the Internet of Things (IoT), big data and artificial intelligence (AI) technology has brought extensive IoT services to entities. However, most IoT services carry the risk of leaking privacy. Privacy-preserving set intersection in IoT is used for a wide range of basic services, and its privacy protection issues have received widespread attention. The traditional candidate protocols to solve the privacy-preserving set intersection are classical encryption protocols based on computational difficulty. With the emergence of quantum computing, some advanced quantum algorithms may undermine the security and reliability of traditional protocols. Therefore, it is important to design more secure privacy-preserving set intersection protocols. In addition, identity information is also very important compared to data security. To this end, we propose a quantum privacy-preserving set intersection protocol for IoT scenarios, which has higher security and linear communication efficiency. This protocol can protect identity anonymity while protecting private data.