Kinds Of Cancers Research Articles

AQP5 promotes epithelial-mesenchymal transition and tumor growth through activating the Wnt/β-catenin pathway in triple-negative breast cancer

BackgroundEmerging data identifies aquaporin 5 (AQP5) as a vital player in many kinds of cancers. Over expression of AQP5 was associated with increased metastasis and poor prognosis, suggesting that AQP5 may facilitate cancer cell proliferation and migration. Our previous studies also showed that AQP3 and AQP5 were highly expressed in triple-negative breast cancer (TNBC) and the expression of AQP3 and AQP5 in TNBC tissue was positive correlated with advanced clinical stage. ObjectiveWe aim to investigate the role of AQP5 in TNBC oncogenesis and development. MethodsMDA-MB-231 cells were transfected with siRNA-AQP5 and AQP5 overexpression vector to establish a differential expression system for AQP5. Cell proliferation and apoptosis of MDA-MB-231 cells were detected by CCK-8 (Cell Counting Kit-8) and FCM (flow cytometry), respectively. Cell migration and invasion abilities were evaluated by wound healing assay and transwell assay. The qRT-PCR and western blot assays were used to study the effect of AQP5 expression level on the expression of epithelial-to-mesenchymal transition (EMT) related molecules. The effects of ICG-001, a Wnt/β-catenin signaling pathway inhibitor, on the invasive and migratory capabilities of overexpressed AQP5 cells and downstream molecules were measured. Results1. The expression of AQP5 in the MDA-MB-231 cells was significantly higher than that in the MCF-10A cells. 2. Up-regulation of AQP5 significantly promoted the proliferation, migration and invasion of TNBC cells, while inhibited the cell apoptosis; in addition, up-regulation of AQP5 increased the expression of Bcl-2 and decreased the expression of Caspase-3. However, knockdown of AQP5 presented the adverse effects of AQP5 overexpression. 3. Overexpressed AQP5 induced the overexpression of EMT-related factors, which further promoted the migration and invasion of cells. 4. Overexpression of AQP5 could up-regulate the expression of β-catenin in the nucleus followed by increasing the expression levels of downstream genes in Wnt/β-catenin signaling pathway. Moreover, ICG-001, the inhibitor of Wnt/β-catenin signaling pathway, could significantly attenuate the effect of overexpression of AQP5 on cells, further confirming that AQP5 may promote the proliferation, migration and invasion of TNBC cells by activating Wnt/β-catenin signaling pathway. ConclusionsIn the TNBC cells, AQP5 modulates the expression levels of EMT-related proteins through activation of Wnt/β-catenin signaling pathway, thus enhancing the cell proliferation, migration and invasion while inhibiting the cell apoptosis.

Treating Cancer From the Inside Out

In this article, we will talk about a special treatment that doctors can use to help people who have cancer. This kind of treatment is called brachytherapy. Brachytherapy uses little pieces of materials that give off radiation to treat cancer from the inside out. We will explore what radiation is, what it means when something is radioactive, and why radiation can be used for cancer treatment. We will discuss different types of brachytherapy, because sometimes doctors use small, implanted capsules and sometimes they use a special robot. Toward the end of the article, we will see how this treatment can be used for different kinds of cancers.

CRTAC1 identified as a promising diagnosis and prognostic biomarker in lung adenocarcinoma

CRTAC1, one of the pyroptosis-related genes, has been identified as a protective factor in certain kinds of cancer, such as gastric adenocarcinoma and bladder cancer. The study aimed to investigate the role of CRTAC1 in lung adenocarcinoma (LUAD). LUAD datasets were obtained from Gene Expression Omnibus (GEO) database and The Cancer Genome Atlas (TCGA), pyroptosis-related genes from GeneCard. Limma package used to find differentially expressed genes (DEGs), least absolute shrinkage and selection operator (LASSO) regression and weighted genes co-expression network analysis (WGCNA) to identify CRTAC1 as hub gene. CRTAC1 expression was confirmed in a real-world cohort using quantitative polymerase chain reaction (qPCR) and Western Blot (WB) analyses. Cellular experiments were conducted to investigate CRTAC1’s potential oncogenic mechanisms. CRTAC1 mRNA expression was significantly lower in LUAD tissues (p < 0.05) and showed high accuracy in diagnosing LUAD. Reduced CRTAC1 expression was associated with a poor prognosis. Higher CRTAC1 expression correlated with increased immune cell infiltration. Individuals with high CRTAC1 expression showed increased drug sensitivity. Additionally, qPCR and WB analyses showed that CRTAC1 expression was lower in tumor tissue compared to adjacent normal tissue at both the RNA and protein levels. Upregulation of CRTAC1 significantly inhibited LUAD cell proliferation, invasion, and migration in cellular experiments. CRTAC1 has the potential to serve as a diagnostic and prognostic biomarker in LUAD.

CRISPR-Cas9: An Evolutionary Technique for the Treatment of Breast and Cervical Carcinoma

CRISPR/Cas9 has transformed genome editing methods in several scientific domains, including the study of human cancer. Globally, breast cancer (BC) affects women more than any other kind of cancer and triple-negative breast cancer (TNBC) has the greatest fatality rate. The diagnosis and treatment of breast cancer have come a long way, yet many patients still experience metastases or relapses. One of the potential techniques for correcting faulty genes and curing different cancers is gene therapy. Certain mutations associated with cancer onset and development might be repaired in model organisms as a first step toward translational applications using the CRISPR/Cas9 technology. The CRISPR/Cas9 system, which consists of a single readily modified guide RNA (sgRNA) sequence coupled to a Cas9 nuclease, has transformed genome editing owing to its simplicity and effectiveness when compared to previous methods. CRISPR/Cas9 allows for the knockdown of over-expressed genes, the reversal of mutations in defected genes, and the remodeling of the regulatory environment to inhibit BC proliferation. CRISPR/Cas9-based treatment mixed with traditional chemotherapy has proven to be beneficial in combating drug resistance and tumor inhibition difficulties. The CRISPR cas9 system may edit many genes at the same time by generating numerous sgRNAs that target different genomic regions, considerably increasing its therapeutic potential and making it a unique technique for treating cervical lesions. This review focuses on the therapeutic applications of CRISPR/Cas9 in the treatment of cervical cancer and breast cancer.

The Functional Roles of the Src Homology 2 Domain-Containing Inositol 5-Phosphatases SHIP1 and SHIP2 in the Pathogenesis of Human Diseases.

The src homology 2 domain-containing inositol 5-phosphatases SHIP1 and SHIP2 are two proteins involved in intracellular signaling pathways and have been linked to the pathogenesis of several diseases. Both protein paralogs are well known for their involvement in the formation of various kinds of cancer. SHIP1, which is expressed predominantly in hematopoietic cells, has been implicated as a tumor suppressor in leukemogenesis especially in myeloid leukemia, whereas SHIP2, which is expressed ubiquitously, has been implicated as an oncogene in a wider variety of cancer types and is suggested to be involved in the process of metastasis of carcinoma cells. However, there are numerous other diseases, such as inflammatory diseases as well as allergic responses, Alzheimer's disease, and stroke, in which SHIP1 can play a role. Moreover, SHIP2 overexpression was shown to correlate with opsismodysplasia and Alzheimer's disease, as well as metabolic diseases. The SHIP1-inhibitor 3-α-aminocholestane (3AC), and SHIP1-activators, such as AQX-435 and AQX-1125, and SHIP2-inhibitors, such as K161 and AS1949490, have been developed and partly tested in clinical trials, which indicates the importance of the SHIP-paralogs as possible targets in the therapy of those diseases. The aim of this article is to provide an overview of the current knowledge about the involvement of SHIP proteins in the pathogenesis of cancer and other human diseases and to create awareness that SHIP1 and SHIP2 are more than just tumor suppressors and oncogenes.

Multi-Gene Single Nucleotide Polymorphism Detection in Gastric Cancer Based on Ion Semiconductor Sequencing Platform.

Gastric cancer is a common heterogeneous tumor. Most patients have advanced gastric cancer at the time of diagnosis and often need chemotherapy. Although 5-fluorouracil (5-FU) is widely used for treatment, its therapeutic sensitivity and drug tolerance still need to be determined, which emphasizes the importance of individualized administration. Pharmacogenetics can guide the clinical implementation of individualized treatment. Single nucleotide polymorphisms (SNPs), as a genetic marker, contribute to the selection of appropriate chemotherapy regimens and dosages. Some SNPs are associated with folate metabolism, the therapeutic target of 5-FU. Methylenetetrahydrofolate reductase (MTHFR) rs1801131 and rs1801133, dihydrofolate reductase (DHFR) rs1650697 and rs442767, methionine synthase (MTR) rs1805087, gamma-glutamyl hydrolase (GGH) rs11545078 and solute carrier family 19 member 1 (SLC19A1) rs1051298 have been investigated in different kinds of cancers and antifolate antitumor drugs, which have potential forecasting and guiding significance for application of 5-FU. The ion torrent next-generation semiconductor sequencing technology can rapidly detect gastric cancer-related SNPs. Each time a base is extended in a DNA chain, an H+ will be released, causing local pH changes. The ionic sensor detects pH changes and converts chemical signals into digital signals, achieving sequencing by synthesis. This technique has low sample requirement, simple operation, low cost, and fast sequencing speed, which is beneficial for guiding individualized chemotherapy by SNPs.

Multifaceted role of TRIM21 in inflammation.

Tripartite motif (TRIM) family members participate in a variety of cellular activities, such as intracellular signaling, development, cellular death, protein quality control, immunological defense, waste degradation, and the emergence of cancer. These proteins usually act as E3 ubiquitin ligase. The final line of resistance against infectious viruses is a cytosolic ubiquitin ligase and antibody receptor called TRIM containing 21. TRIM21, a protein with a tripartite structure, has been linked to autoimmune erythematosus, Sjogren's disorder, and innate immunity. TRIM21 may either promote the formation of specific cancer-activating proteins, resulting in their proteasomal degradation, or it may do neither, depending on the kind of cancer and cancer-causing trigger. The current research has shown that the antiviral action of TRIM mostly depends on their role as E3-ubiquitin ligases and a significant portion of the TRIM family mediates the transmission of innate immune cell signals and the subsequent production of cytokines. We highlighted the function of TRIM family members in various inflammatory diseases.

Association of glucagon-like peptide-1 receptor agonists with risk of cancers-evidence from a drug target Mendelian randomization and clinical trials.

Glucagon-like peptide-1 receptor (GLP1R) agonists have been approved by Food and Drug Administration for management of obesity. However, the causal relationship of GLP1R agonists (GLP1RA) with cancers still unclear. The available cis-eQTLs for drugs target genes (GLP1R) were used as proxies for exposure to GLP1RA. Mendelian randomizations (MR) were performed to reveal the association of genetically-proxied GLP1RA with 14 common types cancer from large-scale consortia. Type 2 diabetes was used as positive control, and the GWASs data including 80154 cases and 853816 controls. Replicating the findings in the FinnGen study and then pooled with meta-analysis. Finally, all the related randomized controlled trails (RCTs) on GLP1RA were systematically searched from PubMed, Embase, and the Cochrane Library to comprehensively synthesize the evidence to validate any possible association with cancers. A total of 22 significant cis-eQTL single-nucleotide polymorphisms were included as genetic instrument. The association of genetically-proxied GLP1RA with significantly decreased type 2 diabetes risk [OR (95%)=0.82 (0.79-0.86), P <0.001], which ensuring the effectiveness of identified genetic instruments. The authors found favorable evidence to support the association of GLP1RA with reduced breast cancer and basal cell carcinoma risk [0.92 (0.88-0.96), P <0.001, 0.92 (0.85-0.99), P =0.029, respectively], and with increased colorectal cancer risk [1.12 (1.07-1.18), P <0.001]. In addition, there was no suggestive evidence to support the association of GLP1RA with ovarian cancer [0.99 (0.90-1.09), P =0.827], lung cancer [1.01 (0.93-1.10), P =0760], and thyroid cancer [0.83 (0.63-1.10), P =0.187]. Our findings were consistent with the meta-analysis. Finally, 80 RCTs were included in the systematic review, with a low incidence of different kinds of cancer. Our study suggests that GLP1RA may decrease the risk of breast cancer and basal cell carcinoma, but increase the risk of colorectal cancer. However, according to the systematic review of RCTs, the incidence of cancer in patients treated with GLP1RA is low. Larger sample sizes of RCTs with long-term follow-up are necessary to establish the incidence of cancers and evaluate the risk-benefit ratios.

Narrative Testimony and Characteristics of Rottlerin for the Treatment of Various Kinds of Cancer

Abstract: From ancient times until now, scientists have focused on herbal medicaments for treating various diseases. Rottlerin, a potent PKCδ inhibitor, is one of the greatest herbal medications. Over the years, it was identified that rottlerin has several cellular and molecular targets that could be involved in the fight against cancer. The past and present research has clearly shown that rottlerin inhibits the transcription factors, enzymes, and signaling molecules that regulate the death and life of cancer cells. Although the anticancer property of rottlerin has primarily been attributed to the induction of autophagy and apoptosis, current research has revealed the existence of different damage pathways. The major part described in this mini-review is the antitumor/anticancer effects of rottlerin in various organs of the human body affected by breast cancer, pancreatic cell cancer, bladder cancer, NSCLC, prostate cancer, ovarian cancer, nasopharyngeal cancer, etc.

Assessment of structural and activity-related contributions of various PIM-1 kinase inhibitors in the treatment of leukemia and prostate cancer.

One of the most perilous illnesses in the world is cancer. The cancer may be associated with the mutation of different genes inside the body. The PIM kinase, also known as the serine/threonine kinase, plays a critical role in the biology of different kinds of cancer. They are widely distributed and associated with several biological processes, including cell division, proliferation, and death. Aberration of PIM-1 kinase is found in varieties of cancer. Prostate cancer and leukemia can both be effectively treated with PIM-1 kinase inhibitors. There are several potent compounds that have been explored in this review based on heterocyclic compounds for the treatment of prostate cancer and leukemia that have strong effects on the suppression of PIM-1 kinase. The present review summarizes the PIM-1 kinase pathway, their inhibitors under clinical trial, related patents, and SAR studies of several monocyclic, bicyclic, and polycyclic compounds. The study related to their molecular interactions with receptors is also included in the present manuscript. The study may be beneficial to scientists for the development of novel compounds as PIM-1 inhibitors in the treatment of prostate cancer and leukemia.

RETRACTED: ODRNN: Optimized Deep Recurrent Neural Networks for Automatic Detection of Leukaemia

Leukaemia, a kind of cancer that may occur in individuals of all ages, including kids and adults, is a significant contributor to worldwide death rates. This illness is currently diagnosed by manual evaluation of blood samples obtained using microscopic imaging, which is frequently slower, lengthy, imprecise. Additionally, inspection under a microscope, leukemic cells look and develop similarly to normal cells, making identification more difficult. Convolutional Neural Networks (CNN) for Deep Learning has provided cutting-edge techniques for picture classification challenges throughout the previous several decades, there is still potential for development with regard to performance, effectiveness, and learning technique. As a consequence, the study provided a unique deep learning approach known as Optimized Deep Recurrent Neural Network (ODRNN) for identifying Leukaemia sickness by analysing microscopic images of blood samples. Deep recurrent neural networks (DRNN) are used in the recommended strategy for diagnosing Leukaemia, then the Red Deer Optimization algorithm (RDOA) applies to optimize the weight gained by DRNN. The mass of DRNN from RDOA will be tuned on the deer roaring rate behavior. The model that has been proposed is evaluated on two openly accessible Leukaemia blood sample datasets, AML, ALL_IDB1 and ALL_IDB2. It is possible to create an accurate computer-aided diagnosis for Leukaemia malignancy by using the proposed deep learning model, which shows encouraging results. The research work uses statistical metrics related to disease including specificity, recall, accuracy, precision and F1 score to assess the effectiveness of the proposed model for identification and classification. The proposed method achieves highly impressive results, with scores of 98.96%, 99.85%, 99.98%, 99.23%, and 99.98%, respectively.

A Nomogram Model Based on the Inflammation-Immunity-Nutrition Score (IINS) and Classic Clinical Indicators for Predicting Prognosis in Extranodal Natural Killer/T-Cell Lymphoma.

Systemic inflammation, immunity, and nutritional status are closely related to patients' outcomes in several kinds of cancers. This study aimed to establish a new nomogram based on inflammation-immunity-nutrition score (IINS) to predict the prognosis of extranodal natural killer/T-cell lymphoma (ENKTL) patients. The clinical data of 435 patients with ENTKL were retrospectively reviewed and randomly assigned to training cohort (n=305) and validation cohort (n=131) at a ratio of 7:3. Cox regression analysis was employed to identify independent prognostic factors and develop a nomogram in the training cohort. Harrell's concordance index (C-index), calibration curve, receiver operating characteristic (ROC) curve, and decision curve analysis (DCA) curve were employed to assess the performance of the nomogram and compare it with traditional prognostic systems (PINK, IPI, KPI). Internal validation was performed using 1000 bootstrap resamples in the validation cohort. Kaplan-Meier survival analyses were conducted to compare the overall survival (OS) of patients in different risk groups. In the training cohort, in addition to several classic parameters, IINS was identified as an independent prognostic factor significantly associated with the OS of patients. The nomogram established based on the independent prognostic indicators showed superior survival prediction efficacy, with C-index of 0.733 in the training cohort and 0.759 in the validation cohort compared to the PINK (0.636 and 0.737), IPI (0.81 and 0.707), and KPI (0.693 and 0.639) systems. Furthermore, compared with PINK, IPI, and IPI systems, the nomogram showed relatively superior calibration curves and more powerful prognostic discrimination ability in predicting the OS of patients. DCA curves revealed some advantages in terms of clinical applicability of the nomogram compared to the PINK, IPI, and IPI systems. Compared with traditional prognostic systems, the nomogram showed promising prospects for risk stratification in ENKTL patient prognosis, providing new insights into the personalized treatment.

Tiny But Mighty: Unveiling the Nutritional Powerhouse of Watermelon Seeds

Abstract: The Curcubitaceae family includes the significant horticultural crop known as watermelon (Citrulus lantus). Many researchers have demonstrated watermelon's nutraceutical potential, making it a superior option for a functional diet. Numerous illnesses, including those connected to age, obesity, diabetes, ulcers, and several kinds of cancer, have been treated with watermelon. Citruline, lycopene, and other polyphenolic substances are among the significant phytochemicals of pharmacological significance that provide watermelon its therapeutic qualities. Watermelon serves as a crucial supplier of l-citrulline, a neutralalpha amino acid that serves as a precursor to l-arginine, an essential amino acid required for the synthesis of proteins. Numerous health benefits were demonstrated in both in vitro and in vivo trials when l-citrulline and lycopene supplements were given.

Abstract 7588: Discovery of NSP-5033: A novel and potent PARP7/12 dual inhibitor

Abstract PARP7 is a mono-ADP-ribosyl transferase that catalyzes the transfer of single units of ADP-ribose onto substrate proteins to regulate their functions. One of its substrates is TANK binding kinases 1 (TBK1), whose MARylation by PARP7 inhibits its activation and thereby represses the type I IFN response to cytosolic nucleic acid. PARP7 is upregulated in many kinds of cancers and acts as a brake in cytosolic nucleic acid sensing, which leads to the suppression of type I IFN signaling and immune response. Therefore, PARP7 is a novel and promising target in cancer immunotherapy. Herein, we describe the discovery of a novel small molecule NSP-5033 as a dual PARP7/PARP12 inhibitor, which potently inhibits PARP7 and PARP12 enzymes with sub-nanomolar and low nanomolar activities, respectively. It displayed potent anti-proliferative activities against a number of cancer cell lines in vitro. NSP-5033 also increased the mRNA level of IFNβ and CXCL10 and stimulated STAT1 phosphorylation, suggesting that it restored the type I IFN response in tumor cells. With excellent ADME and pharmacokinetic properties, NSP-5033 demonstrated potent in vivo efficacy in human lung cancer xenografts with tumor regression and induced antitumor immunity in tumor-bearing immunocompetent mice. NSP-5033 has been nominated as a preclinival candidate for treatment of solid tumors and is undergoing IND-enabling studies. Citation Format: Qin Chen, Qionglin Huang, Ke Zhang, Yuli Hao, Zixuan Wang, Bing Li. Discovery of NSP-5033: A novel and potent PARP7/12 dual inhibitor [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2024; Part 1 (Regular Abstracts); 2024 Apr 5-10; San Diego, CA. Philadelphia (PA): AACR; Cancer Res 2024;84(6_Suppl):Abstract nr 7588.

Association between Autism Spectrum Disorder and Cancer - a Review from the Literature

Introduction: Autism spectrum disorder (ASD) is neurodevelopmental polygenic disorder with strong genetic component. In adult period, it is associated with many chronic diseases including diabetes, hypertension, cardiovascular disease, and cancer.&#x0D; The aim of this article is to show possible connection between autism spectrum disorder and some kinds of cancers, and to show possible pathways for prevention and treatment.&#x0D; Methodology: The PubMed and Google Scholar databases were searched using the keywords: autism spectrum disorder, genetics, cancer, prevention and treatment.&#x0D; Results: Autism spectrum disorder is associated with high rates of genomic aberrations, including chromosomal rearrangements and de novo copy-number variations. Autism and cancer share 43 risk genes, suggesting that common mechanisms underlying the functions of some of these genes could conceivably be leveraged to develop therapies not just for cancer but for autism as well. Pleiotropy, whereby gene variants exert effects on multiple phenotypes, has been the source of increasing research attention with ASD and cancer.&#x0D; Germline loss-of-function PTEN mutations increase the rate of benign and malignant tumors and also manifest as ASD and macrocephaly. Mutations in TSC1 and TSC2 genes cause tuberous sclerosis complex which is characterized by cortical tubers, and neurocognitive phenotypes including epilepsy, ASD, and intellectual disability (ID).&#x0D; Conclusion: There is may be an association between autism and specific forms of cancer. Further epidemiologic research in large populations is needed to elucidate the association between autism and cancer and identify explanatory factors. Approved drugs targeting oncogenic pathways might also have therapeutic value for treating autism spectrum disorder.

78 Targeting tumor-promoting myeloid cell functions in head & neck cancer

Myeloid cells are a major component of immune cells infiltrating tumors, interacting with each other, with tumor cells and other stromal cells, and demonstrating a prominent plasticity. Tumor-associated myeloid cells, such as neutrophils (or so-called MDSCs: suppressory neutrophils) contribute to cancer progression via multiple mechanisms. Neutrophils are the most abundant myeloid blood cells, which have been shown to exert heterogeneous phenotypic and functional states: reaching from anti- to protumoral. On the one hand these cells can suppress anti-tumor immune responses, support tumor angiogenesis or metastatic dissemination. On the other hand, neutrophils actively kill tumor cells, or activate T-cell dependent immune responses.There is still little information on tumor-infiltrating neutrophils and their clinical relevance. Nevertheless, neutrophils were demonstrated to be associated with poor clinical outcome in patients with different kinds of cancer, including renal cancer, non-small-cell lung carcinoma, melanoma and head and neck cancer. Enrichment of neutrophils was also associated with metastases in various tumor entities. The recruitment of neutrophils within the tumor microenvironment is strictly regulated by chemokines, such as CXCL2 or CXCL8/IL-8.Neutrophil activity strongly depends on the stimulus present in the microenvironment. Since these cells are highly plastic and can easily alter their functionality, they are an ideal target for designing anti-tumor therapies. However, most of therapeutic strategies to target neutrophils in tumor-bearing hosts are dealing with the blocking of their migration into the tumor site. The efficiency of such approaches is, however, limited, as it does not address heterogeneity of these cells, and thus depletes as well antitumoral cells, leading to cancer progression and infectious complications.Given a critical role of neutrophils in tumor progression, we tested several alternative strategies to neutralize pro-tumoral activity of these cells, including reprogramming and inhibition of their immunosuppressive functions. Our recent data using own designed CCL2 peptide MyeloMIB show promising therapeutic results in head and neck cancer preclinical models. Application of this peptide leads not only to the specific inhibition of neutrophil migration into tumor tissue, but also reprograms these cells into anti-tumoral state. These results suggest a dual-edged role of neutrophils as essential regulators of anti-cancer immune responses and argue for approaches fostering anti-cancer activity of these cells, not only their migration, during cancer immunotherapy.

An in-silico Approach for Recognition of Long non-coding RNA-Associated Competing Endogenous RNA Axes in Prostate Cancer.

Prostate cancer is among the most central sources of cancer-related mortalities. In order to find novel candidates for therapeutic strategies in this kind of cancer, we developed an in-silico method for identification of competing endogenous RNA network. According to the microarray data analyses between prostate tumor and normal specimens, we attained 1312 differentially expressed (DE)mRNAs, including 778 down-regulated DEmRNAs (such as CXCL13 and BMP5) and 584 up-regulated DEmRNAs (such as OR51E2 and LUZP2), 39 DElncRNAs, including 10 down-regulated DElncRNAs (such as UBXN10-AS1 and FENDRR) and 29 up-regulated DElncRNAs (such as PCA3 and LINC00992) and 10 DEmiRNAs, including 2 down-regulated DEmiRNAs (such as MIR675 and MIR1908) and 8 up-regulated DEmiRNAs (such as MIR6773 and MIR4683). We constructed the ceRNA network between these transcripts. We also evaluated the related signaling pathways and the significance of these RNAs in prediction of survival of patients with prostate cancer. This study provides novel candidates for construction of specific treatment routes for prostate cancer.

Gut Microbiome and Cancer: From Cancer Development to Therapeutics with a Special Focus on Hepatocellular Carcinoma.

The body of a human has a vast array of microorganisms termed the microbiome that impacts almost every function of the body. Gene-environment interactions play a major role in making us susceptible to cancer and the microbiome is such an environmental factor that we are exposed to from the very beginning of our lives to the very end. Increasing pieces of evidence are pointing towards an association of cancer and the microbiome. The bacteria inside our body might help us prevent some cancers as well as may increase the risk of carcinogenesis and treatment responses. Many studies are suggesting that tinkering with the microbiome might be a new way to treat and prevent many kinds of cancer. Although information on the roles of the microbiome in carcinogenesis is scant and almost no direct links have been found between these two yet. This review offers some of the recent evidences of the association between cancer and the microbiome, discuss the impact of gut bacteria on cancer and provide a detailed discussion on gut microbiota mediated therapeutic approaches with a special focus on Hepatocellular Carcinoma. The implementation of the new knowledge discovered in this subject calls for a great deal of research.

Using temperament and character dimensions (TCI) to analyze the personality profiles of adults and older adults with cancer managed in outpatient settings.

This study aimed to investigate profiles of personality evaluated by temperament and character dimensions (TCI) in 638 adult and older adult patients (CP) who had recently been diagnosed with breast, colon, lung, and other kinds of cancer (female and male subjects were assessed). Tests: Temperament and Character Inventory (TCI). Statistical analysis: cluster K-means analysis for personality traits. Two different personality profiles emerged: "Low self-determination and pessimism" (Profile 1) and "Self-determination and self-caring (medium)" (Profile 2). The following significant differences were observed in the TCI dimensions between the two profiles: Temperament-Novelty-Seeking (NS) (p < 0.001); Harm-Avoidance (HA) (p < 0.001); Reward-Dependence (RD) (p < 0.001); Persistence (PS) (p < 0.001); Character-Self-Directness (SD) (p < 0.001); Cooperativeness (C) (p > 0.001); Self-Transcendence (ST) (p < 0.001). No differences in the two profiles were found between adult and elderly patients. Profile 1 - "Low self-determination and pessimism": Patients with this profile present low resistance to frustration, poor search for novelty and solutions (NS), anxiety and pessimism (medium HA), high social attachment and dependence on the approval of others (medium-high RD), and low self-determination (PS) as temperament dimensions; and medium-low self-direction, low autonomy and ability to adapt (SD-medium-low), medium cooperativeness (C), and low self-transcendence (ST) as character dimensions. Profile 2 - "Self-determination and self-caring (medium)": Patients with this profile have resistance to frustration, ability to search for novelty and solutions (medium-NS), low anxiety and pessimism (HA), low social attachment and dependence on approval (medium-low-RD), and determination (medium-high PS) as dimensions of temperament; and autonomy and capacity for adaptation and self-direction (SD), capacity for cooperation (high-CO), and self-transcendence (medium-high-ST) as character dimensions. Personality screening allows a better understanding of the difficulties of the individual patient and the planning of targeted psychotherapeutic interventions that promote quality of life and good adaptation to the disease course.

White Blood Cells Classification using CNN

One kind of cancer that arises from an overabundance of white blood cells produced by the patient's bone marrow and lymph nodes is leukaemia. Since white blood cells are the primary source of immunity, or the body's defence, it is imperative to determine the type of leukocyte cell the patient has leukaemia from as soon as possible. Failure to do so could result in a more serious condition. Haematologists typically use a light microscope to examine the necessary cell traces in order to classify and identify the features of the cell cytoplasm or nucleus in order to diagnose leukaemia in a patient. One form of cancer is leukaemia, which develops when a patient's bone marrow and lymph nodes produce an excessive amount of white blood cells. It is vital to determine the type of leukocyte cell the patient has leukaemia from as soon as possible because postponing diagnosis can worsen the situation. Our white corpuscles are the primary source of immunity, which is the body's defence. In order to define and identify the features found in the cell cytoplasm or nucleus, hematopathologists typically use a light microscope to examine the necessary cell traces in order to diagnose leukaemia in patients.