Survival Rate Of Cancer Patients Research Articles

TGF-β promotes proliferation and inhibits apoptosis of liver cancer Huh-7 cells by regulating MiR-182/CADM1

Purpose: To investigate the mechanism of liver cancer cell tolerance to the antiproliferative effect of transforming growth factor beta (TGF-β) based on miRNA levels.Methods: MiRNA microarray and quantitative reverse transcription-polymerase chain reaction (qRTPCR) were used to identify differentially expressed miRNAs in liver cancer Huh-7 cells treated with TGF-β. The effect of these miRNAs on patient survival was analyzed using Kaplan-Meier Plotter. Involvement of Smad2/Smad3 in TGF-β-induced miR-182 expression was determined using shRNA knockdown and qRT-PCR. Dose-dependent effect of TGF-β on miR-182 expression was investigated in Huh-7 cells and mouse primary liver cells using qRT-PCR. The effect of miR-182 on Huh-7 cell proliferation and apoptosis was studied using CFSE and Annexin V/PI assay. Direct targets of miR-182 in Huh-7 cells were identified using a luciferase reporter gene assay, while the influence of Recombinant Cell Adhesion Molecule 1 (CADM1) overexpression on Huh-7 cell proliferation and apoptosis treated with miR-182 was examined using lentivirus experiments, and CFSE and Annexin V/PI assays.Results: The expression levels of hsa-miR-181a, hsa-miR-182, hsa-miR-483, and hsa-miR-143 were significantly higher in serum samples from liver cancer patients (p < 0.05). Survival analysis showed that low expression of hsa-miR-182 and high expression of hsa-miR-483 increased the survival rate of liver cancer patients. Furthermore, TGF-β increased miR-182 expression in Huh-7 cells, but not in mouse primary liver cancer cells. The MiR-182 promoted Huh-7 cell proliferation and inhibited apoptosis. It targeted CADM1 mRNA 3'-UTR, decreasing CADM1 expression. Overexpression of MiR-182 significantly reduced cell proliferation and increased apoptosis in Huh-7 cells with CADM1 overexpression (p < 0.05).Conclusion: Transforming growth factor beta (TGF-β) facilitates the proliferation and repression of apoptosis of Huh-7 cells by increasing miR-182 expression and inhibiting CADMI expression.

Tumor characteristics and survival rate of HER2-low breast cancer patients: a retrospective cohort study

HER2 is an important prognostic marker in breast cancer (BC) patients, which also plays a crucial role in their therapeutic plan. Consequently, a great desire is to thoroughly assess the patients based on their HER2 status. In the current study, we aimed to evaluate HER2-low breast cancer as a new subtype in the standard classification of BC patients and review its characteristics and survival rate in a tertiary center in Iran. We retrospectively evaluated disease-free survival (DFS), overall survival (OS), and clinicopathological characteristics of BC patients referred to the Cancer Research Center in Tehran, Iran from 1991 to 2022. Patients’ clinical characteristics, including HER2 status, which is classified as HER2-low, HER2-positive, or HER2-negative, were obtained from prospectively maintained registries. Among the total 3582 recruited patients, 60.2%, 13.6%, and 26.2% were HER2-negative, HER2-low, and HER2-positive, respectively. HER2-positive patients showed a significantly higher Hazard Ratio (HR) for DFS (HR 1.44, 95% CI 1.01–2.05) and OS (HR 2.05, 95% CI 1.31–3.20), compared to HER2-low. Moreover, HER2-low and HER2-negative were found to show the same proportion of high-grade tumors (28 and 28.4%), while 40% of the HER2-positive tumors were high-grade. Accordingly, HER2-low patients had a lower metastasis risk than the others (P-value = 0.01). The Ki67 percentage was significantly lower in the HER2-low group compared to the HER2-positive (P-value < 0.001). HER2-low, a new subtype of HER2-status classification with distinct biological and clinicopathological traits, represented the highest survival rate and less invasive characteristics. This difference was statistically significant when compared to HER2-positive, but not when compared to HER2-negative.Research registration unique identifying number: NCT05754047.

A macrophage related signature for predicting prognosis and drug sensitivity in ovarian cancer based on integrative machine learning

BackgroundOvarian cancer ranks the leading cause of gynecologic cancer-related death in the United States and the fifth most common cause of cancer-related mortality among American women. Increasing evidences have highlighted the vital role of macrophages M2/M1 proportion in tumor progression, prognosis and immunotherapy.MethodsWeighted gene co-expression network analysis (WGCNA) was performed to identify macrophages related markers. Integrative procedure including 10 machine learning algorithms were performed to develop a prognostic macrophage related signature (MRS) with TCGA, GSE14764, GSE140082 datasets. The role of MRS in tumor microenvironment (TME) and therapy response was evaluated with the data of CIBERSORT, MCPcounter, QUANTISEQ, XCELL, CIBERSORT-ABS, TIMER and EPIC, GSE91061 and IMvigor210 dataset.ResultsThe optimal MRS developed by the combination of CoxBoost and StepCox[forward] algorithm served as an independent risk factor in ovarian cancer. Compared with stage, grade and other established prognostic signatures, the current MRS had a better performance in predicting the overall survival rate of ovarian cancer patients. Low risk score indicated a higher TME score, higher level of immune cells, higher immunophenoscore, higher tumor mutational burden, lower TIDE score and lower IC50 value in ovarian cancer. The survival prediction nomogram had a good potential for clinical application in predicting the 1-, 3-, and 5-year overall survival rate of ovarian cancer patients.ConclusionAll in all, the current study constructed a powerful prognostic MRS for ovarian cancer patients using 10 machine learning algorithms. This MRS could predict the prognosis and drug sensitivity in ovarian cancer.

Classification techniques using gray level co-occurrence matrix features for the detection of lung cancer using computed tomography imaging

&lt;span lang="EN-US"&gt;Lung cancer, which causes the majority of fatalities worldwide each year, is one of the deadliest diseases. The survival rate of cancer patients could be improved with better cancer detection methods. Image processing and machine learning have both been used to aid in lung cancer detection, but a method that both increase accuracy and increases a patient’s survival rate has yet to be identified. In an effort to find the most effective method for the accurate lung cancer recognition, this paper analyses and compares several classification algorithms. Lung computed tomography (CT) images are enhanced by removing noise using a median filter. For filtered image, threshold segmentation is used to segment it into distinct parts. From the segmented image different features are extracted using the grey level co-occurrence matrix (GLCM). several classification strategies, including support vector machine (SVM), random forest (RF), k-nearest neighbor (KNN), and decision tree (DT) methods, are used to classify lung images as malignant or normal based on the extracted features. Methods are evaluated based on a number of various performance measures, like accuracy, a precision, the recall, and the F1-Score. Based on the experimental outcomes, SVM outperforms other classification methods in accurately detecting lung cancer with an accuracy of 99.32%.&lt;/span&gt;

Long-term survival rates of cancer patients achieved by deuterium depletion as an adjuvant treatment in spinal astrocytic glioma, carcinoma mammae and melanoma malignum

The anticancer effect of deuterium depletion has been proved in various types of cancer, either in combination with conventional therapies or as a single treatment. Here we present 3 case studies illustrating 3 different cancer types. The first patient was diagnosed with spinal astrocytic glioma, a very rare cancer type. In her case, conventional therapy was and could not be used, but she consumed Deuterium-Depleted Water (DDW). Her follow-up time was 21 years. The second one was diagnosed with carcinoma mammae, worldwide the second most common cause of cancer-related death in women. She was operated, left side mastectomy was done, and metastases were found in 8 out of the 9 removed lymph nodes. She received chemo- and radiotherapy and started DDW consumption one month after the surgery. Her follow-up time was 24 years. The third patient was diagnosed with malignant melanoma, a highly aggressive skin cancer, currently the fifth most common cancer in men and seventh in women. He was operated, then 3 years later liver metastasis was detected, and chemoembolization was done. Afterwards, the patient started a oneyear DDW cure, then repeated several cures of various durations, in the subsequent 26 years. These cases confirm that deuterium depletion is effective both as a single treatment and in parallel or subsequent use with conventional therapies. DDW causes regression of the tumors and is an efficient therapeutic modality to achieve better patient outcomes.

Multidimensional quantitative phenotypic and molecular analysis reveals neomorphic behaviors of p53 missense mutants

Mutations in the TP53 tumor suppressor gene occur in >80% of the triple-negative or basal-like breast cancer. To test whether neomorphic functions of specific TP53 missense mutations contribute to phenotypic heterogeneity, we characterized phenotypes of non-transformed MCF10A-derived cell lines expressing the ten most common missense mutant p53 proteins and observed a wide spectrum of phenotypic changes in cell survival, resistance to apoptosis and anoikis, cell migration, invasion and 3D mammosphere architecture. The p53 mutants R248W, R273C, R248Q, and Y220C are the most aggressive while G245S and Y234C are the least, which correlates with survival rates of basal-like breast cancer patients. Interestingly, a crucial amino acid difference at one position—R273C vs. R273H—has drastic changes on cellular phenotype. RNA-Seq and ChIP-Seq analyses show distinct DNA binding properties of different p53 mutants, yielding heterogeneous transcriptomics profiles, and MD simulation provided structural basis of differential DNA binding of different p53 mutants. Integrative statistical and machine-learning-based pathway analysis on gene expression profiles with phenotype vectors across the mutant cell lines identifies quantitative association of multiple pathways including the Hippo/YAP/TAZ pathway with phenotypic aggressiveness. Further, comparative analyses of large transcriptomics datasets on breast cancer cell lines and tumors suggest that dysregulation of the Hippo/YAP/TAZ pathway plays a key role in driving the cellular phenotypes towards basal-like in the presence of more aggressive p53 mutants. Overall, our study describes distinct gain-of-function impacts on protein functions, transcriptional profiles, and cellular behaviors of different p53 missense mutants, which contribute to clinical phenotypic heterogeneity of triple-negative breast tumors.

Study on Dosimetric Benefits of Adaptive Brachytherapy in the Treatment of Postoperative Cervical Cancer Patients

Image-guided adaptive brachytherapy (IGABT) has been proven to improve the local control and survival rate of cervical cancer patients, while reducing the side effects. However, IGABT is time-consuming and difficult to achieve in countries or hospitals with intense medical resources. Compared with radical cervical cancer patients, the anatomical change of postoperative patients during brachytherapy is small. We hypothesis that the dosimetric benefits of adaptive brachytherapy in the treatment of postoperative cervical cancer patients is limited. This study investigates whether there is a balance between the treatment quality and treatment efficiency in postoperative cervical cancer patients without using IGABT. We retrospectively studied 30 postoperative cervical cancer patients who underwent brachytherapy. Each patient had a primary CT (PCT) and an adaptive CT (ACT). The plan developed on the PCT (PCT plan) was introduced into ACT for dose calculation (P-ACT plan) to evaluate the dosimetric effect of anatomy change. The dose difference between P-ACT plan and ACT plan and was compared. The mean value of HRCTV D100% and V150% in P-ACT plan are 4.95% and 0.75% lower than those of ACT plan, the difference is not statistically significant (P>0.05). The D0.1cm³ of bladder, rectum and sigmoid in P-ACT plan are higher 2.13%, 3.17%, and 0.71% than ACT plan, respectively, but the increment is insignificant (P>0.05). The D2cm³ of bladder and rectum is slightly lower in ACT plan, while the D2cm³ of sigmoid is slightly lower in P-ACT plan. The dosimetric benefits of IGABT is not remarkable for postoperative cervical cancer patients. The preliminary results of this study show that IGBAT is optional for postoperative patients with cervical cancer in countries or hospitals with tight medical resources. It is necessary to conduct a larger sample and more detailed research further.

High expression of MRPL13 promotes cell cycle progression and proliferation of gastric cancer cells by inhibiting p53 signaling to affect long-term prognosis

To determine the expression of mitochondrial ribosomal protein L13 (MRPL13) in gastric cancer and its impact on long-term prognosis and explore the possible mechanism. We analyzed MRPL13 expression level in gastric cancer and its association with the patients' prognosis based on the public cancer database the data of 100 gastric cancer patients undergoing radical gastrectomy in our hospital from January, 2014 to October, 2017. We further assessed the effects of MRPL13 overexpression and knockdown on proliferation and cell cycle of gastric cancer MGC-803 and SGC-7901 cells in vitro and on subcutaneous xenograft growth in nude mice. Both bioinformatic analysis and the patients' data demonstrated that the expression level of MRPL13 was significantly higher in gastric cancer than in adjacent tissues (P<0.05) and positively correlated with peripheral blood Ki67, CEA and CA19-9 levels (P<0.05). High expression of MRPL13 was an independent risk factor affecting the 5-year survival rate of gastric cancer patients (HR: 3.284; 95% CI: 1.537-7.016). Gene set enrichment analysis suggested that MRPL13 was involved in cell cycle and p53 signaling. In cultured gastric cancer cells, MRPL13 overexpression significantly promoted cell proliferation, G1/S phase transition and the expressions of cyclin D1 and CDK6 (P<0.05), and MRPL13 knockdown produced the opposite effects (P<0.05). MRPL13 overexpression significantly promoted gastric cancer cell xenograft growth (P<0.05), and MRPL13 knockdown obviously inhibited tumor growth in nude mice (P<0.05). In both cultured gastric cancer cells and the xenografts in nude mice, MRPL13 overexpression significantly decreased while MRPL13 knockdown enhanced the expressions of p53 and p21 (P<0.05). MRPL13 is highly expressed in gastric cancer and affects the long- term prognosis of the patients possibly by inhibiting p53 signaling to promote cancer cell proliferation and cell cycle progression.

High expression of CAMSAP2 promotes invasion and metastasis of gastric cancer cells by upregulating TGF-β signaling

To investigate the expression of calmodulin-regulated spectrin-associated protein 2 (CAMSAP2) in gastric cancer and its effect on gastric cancer cell invasion and metastasis. The association of CAMSAP2 expression levels with progression and prognosis of gastric cancer was analyzed using public cancer data and in 106 patients receiving radical gastrectomy in our hospital from October, 2013 to October, 2017. The biological functions of CAMSAP2 were predicted using bioinformatics analysis. Gastric cancer MGC803 cells with CAMSAP2 overexpression and knockdown were observed for epithelial-mesenchymal transition (EMT), migration and invasion. A nude mouse model bearing orthotopic gastric cancer cell xenografts was established for verifying the results and exploring the underlying molecular mechanism. Gastric cancer tissues expressed high levels of CAMSAP2, which were positively correlated with CEA and CA19-9 (P<0.001). Cox regression analysis showed that CAMSAP2 expression level was an independent risk factor affecting the 5-year survival rate of gastric cancer patients (HR=2.969, 95% CI: 1.031-8.548). Enrichment analysis suggested that CAMSAP2 was involved in epithelialmesenchymal transition (EMT) and TGF-β signaling. In gastric cancer cells, CAMSAP2 overexpression significantly increased the expressions of vimentin and N-cadherin, inhibited the expression of E-cadherin, and enhanced cell migration and invasion (P<0.05); CAMSAP2 knockdown produced the opposite effects in the cells (P<0.05). In the tumor- bearing mice, xenografts overexpressing CAMSAP2 showed enhanced metastasis (P<0.05), increased vimentin and N-cadherin expressions and lowered E-cadherin expression (P<0.05), and the xenografts with CAMSAP2 knockdown showed the opposite changes (P<0.05). Both the in vivo and in vitro experiments showed that CAMSAP2 overexpression increased and CAMSAP2 knockdown lowered the levels of TGF-β and p-Smad2/3 in the gastric cancer cells (P<0.05). The high expression of CAMSAP2 contributes to disease progression and poor prognosis of gastric cancer possibly by upregulating TGF-β signaling to promote EMT.

Predictive factors and prognosis of upper gastrointestinal bleeding in gastric cancer: A large population-based study (UGIB-GC trial).

Gastric cancer remains the fourth leading cause of cancer-related death worldwide. Significant number of gastric cancer patients presented with bleeding. This study aimed to identify risk factors and overall survival rates of bleeding gastric cancer patients. This retrospective cohort study was conducted between 2007-2022 at tertiary care center in Thailand. Clinical information, endoscopic findings and histological type were extensively reviewed and were compared between bleeders and non-bleeders. Patients were monitored for at least 5 years. There were 20,981 patients who underwent upper gastrointestinal endoscopy during study period. Total of 201 gastric cancer patients were included in this study, 21 were excluded due to incomplete medical records. 180 gastric cancer patients were included with mean age of 60.5±14.3 years. There were 65 (36.1%) patients with gastrointestinal bleeding. Hypertension and chronic kidney disease were significantly more common in bleeders than non-bleeders (43.1% vs 23.5%, OR2.51, 95%CI 1.14.-5.52, p = 0.022; and 16.9% vs 5.2%, OR2.00, 95%CI 1.56-6.63, p = 0.025, respectively). current H. pylori infection was also significantly more common in bleeders than non-bleeders (84.6% vs. 55.7%, OR 4.39, 95%CI 1.90-10.12, p<0.001). Median overall survival of bleeders was significantly lower than non-bleeders (7±0.93 vs 10±2.10 months, p = 0.001). Bleeding gastric cancer was not an uncommon condition. Majority of patients presented at advanced stage with grave prognosis. Male gender, hypertension, chronic kidney disease, and current H. pylori infection were reliable predictors for bleeding. Early diagnosis and prompt treatment are the key to improve clinical outcome.

An Update on Potential Molecular Biomarkers of Dietary Phytochemicals Targeting Lung Cancer Interception and Prevention.

Since ancient times, dietary phytochemicals are known for their medicinal properties. They are broadly classified into polyphenols, terpenoids, alkaloids, phytosterols, and organosulfur compounds. Currently, there is considerable interest in their potential health effects against various diseases, including lung cancer. Lung cancer is the leading cause of cancer deaths with an average of five-year survival rate of lung cancer patients limited to just 14%. Identifying potential early molecular biomarkers of pre-malignant lung cancer cells may provide a strong basis to develop early cancer detection and interception methods. In this review, we will discuss molecular changes, including genetic alterations, inflammation, signal transduction pathways, redox imbalance, epigenetic and proteomic signatures associated with initiation and progression of lung carcinoma. We will also highlight molecular targets of phytochemicals during lung cancer development. These targets mainly consist of cellular signaling pathways, epigenetic regulators and metabolic reprogramming. With growing interest in natural products research, translation of these compounds into new cancer prevention approaches to medical care will be urgently needed. In this context, we will also discuss the overall pharmacokinetic challenges of phytochemicals in translating to humans. Lastly, we will discuss clinical trials of phytochemicals in lung cancer patients.

Подовження інтервалу QT як значуще кардіоваскулярне ускладнення під час системного лікування хворих на рак

Стрімке впровадження нових протипухлинних засобів та технологій лікування сприяло підвищенню виживання хворих на рак. Однак, розвиток серцево-судинних ускладнень на тлі протипухлинного лікування нерідко призводить до зниження якості та тривалості життя онкологічних хворих.Одним з проявів серцево-судинних ускладнень при застосуванні протипухлинних лікарських засобів є подовження інтервалу QT з різними порушеннями серцевого ритму.Стаття базується на аналізі рандомізованих клінічних досліджень і метааналізів та рекомендаціях Європейського товариства кардіологів з кардіо-онкології. Наведено опис факторів ризику і класифікація подовження інтервалу QT, спричиненого протипухлинною терапією. Проаналізовані основні групи протипухлинних лікарських засобів, які індукують зміни інтервалу QT. Розглянуті етапи і кратність огляду онкологічних хворих при різних патологічних станах та порушеннях гемостазу, що можуть призводити до подовження інтервалу QT під час лікування та в різні періоди після його проведення.Огляд присвячений аналізу змін інтервалу QT та клінічному застосуванню алгоритмів прийняття рішень щодо мінімізації кардіотоксичності з метою підвищення ефективності протипухлинного лікування онкологічних хворих.

CNIH4 governs cervical cancer progression through reducing ferroptosis

Cervical cancer is one of the most leading causes of cancer death worldwide, and ferroptosis is implicated in the progression of cervical cancer. Cornichon family AMPA receptor auxiliary protein 4 (CNIH4) is involved in the progression of various human cancers; however, its function in cervical cancer remains unclear. The present study aims to investigate the role and mechanism of CNIH4 in cervical cancer using gain- and loss-of-function studies in vitro. SiHa and CaSki cells were infected with lentiviral vectors to manipulate the expression of CNIH4 in vitro, and cell viability, migration, invasion as well as ferroptosis were evaluated. Transcriptome sequencing analysis was performed to further validate the mechanism through which CNIH4 regulated the progression of cervical cancer. The expression of CNIH4 was upregulated in human cervical cancer tissues and cells, and strongly correlated with the decreases in overall survival and disease free survival rates of cervical cancer patients. CNIH4 silence inhibited, while CNIH4 overexpression facilitated the survival of human cervical cancer cells. Mechanistically, CNIH4 elevated solute carrier family 7 member 11 (SLC7A11)-mediated cystine import, and subsequently increased intracellular glutathione synthesis and glutathione peroxidase 4 activity, thereby inhibiting ferroptosis of human cervical cancer cells. SLC7A11 silence significantly abolished CNIH4-mediated inhibition of ferroptosis in cervical cancer cells in vitro. Our study for the first time reveals that CNIH4 inhibits ferroptosis of human cervical cancer cells through upregulating SLC7A11, defining CNIH4 as an attractive therapeutic and prognostic target for cervical cancer.

Role of Lactobacillus and calcium in colorectal cancer

Colorectal cancer (CRC) is the third most cancer which is prevalent globally. It is the second most leading cause of mortality worldwide. In Asia Colorectal cancer is most abundant type of cancer. Causative factors involved are genetic pattern, western lifestyle, alcohol, smoking, etc. The commonest therapy for colorectal cancer is the combination therapy of 5-fluorouracil with Leucovorin which is either co-administered with alkylating agent Oxaliplatin or with a topoisomerase inhibitor Irinotecan. There is still a need of therapeutic agent that increases the survival rate in colorectal cancer patients. Probiotics are well known to increase the proliferation of beneficial bacteria and recently they are widely researched for regression of carcinogenesis. a commonly used probiotic, is observed to increase the expression of apoptotic ligand by modulating TNF action. has also shown to represses cyclin D1 and inhibit the Wnt/β-catenin signaling thereby, not only prevent the proliferation of cancerous cells but also ensure the apoptosis of CRC cells. Calcium is a vital element in many biological pathways including cancer signaling pathway. A wide variety of research reflects the role of calcium in suppression of cancerous cells. Recently calcium has shown its role in inhibiting Wnt/-catenin signaling canonical pathway in colorectal cancer cells. The review focuses on the role of calcium and probiotic as a natural therapeutic option in the treatment of CRC.

Liquid ImmunoBiopsy-based detection of early stage lung cancer in a volunteer subject recruited as a ‘healthy donor’ of a lung cancer diagnosis clinical trial study: A case report

Background: Developing early detection diagnostic methods, especially non-invasive methods, is a critical component in raising the overall survival rate and prognosis for lung cancer (LC) patients. Recently, we described a novel Liquid ImmunoBiopsy™ test to detect early stage LC with high accuracy. As a part of our ongoing clinical trials for early detection of LC, a blood specimen was received from a ‘healthy’ volunteer, nonsmoker male, who was recruited as a part of the trial’s control group. The Liquid ImmunoBiopsy™ test result of this subject clearly indicated a lung-related malignant lesion. The objective of this article is to provide a detailed description of the subsequent investigation of this case, up to the surgical intervention.

Clinical significance of MATN1-AS1 as ceRNA of Mir-200b in tissues and serum of patients with cervical cancer

To analyze the clinical significance of MATN1-AS1 as ceRNA of Mir-200b in the tissues and serum of cervical cancer patients. A total of 50 patients with cervical cancer admitted to our hospital from March 2018 to March 2019 were selected as the research objects. All patients underwent surgical resection of cancer tissues in our hospital, and cervical cancer tissues and adjacent tissues more than 2 cm away from the edge of cancer tissues were retained. Patients with cervical cancer were selected as the research group, and 50 patients with benign uterine lesions were selected as the control group. The expressions of MATN1-AS1 and Mir-200b in cervical cancer tissues and serum were detected by real-time PCR, and the correlation between MATN1-AS1 and Mir-200b was analyzed. The relationship between MATN1-AS1, Mir-200b and clinical features was analyzed, and the 3-year survival rate of cervical cancer patients was analyzed. Compared with adjacent tissues, the relative expression levels of MATN1-AS1 and Mir-200b in cancer tissues were significantly increased (P < 0.05). Compared with the control group, the relative expression levels of MATN1-AS1 and mir-200b in the study group were increased (P < 0.05). The expression levels of matn1-as1 and mir-200b were higher in poorly differentiated, tumor ≥ 4 cm, FIGO stage iii–iv, and lymph node metastasis patients (P < 0.05). Correlation analysis showed that MATN1-AS1 was positively correlated with Mir-200b (r = 0.625, P = 0.001). Compared with blank control group, the relative expression levels of MATN1-AS1 and Mir-200b in MATN1-AS1 silencing group were decreased (P < 0.05). The 3-year survival rate of 48 patients with cervical cancer was 66.67% (32/48). The survival rate of patients with high expression of MATN1-AS1 was lower than that of patients with low expression of MATN1-AS1, and the survival rate of patients with high expression of Mir-200b was lower than that of patients with low expression of Mir-200b (x2 = 4.251, 5.244, P = 0.011, 0.008). There is a potential binding point between MATN1-AS1 and Mir-200b. The expressions of MATN1-AS1 and Mir-200b are increased in the tissues and serum of cervical cancer patients, and they are positively correlated. Silencing of MATN1-AS1 in cervical cancer cell lines can reduce the expression of Mir-200b. Matn1-as1 can regulate the expression of Mir-200b and participate in the occurrence and development of cervical cancer.

Emphasizing the Role of Multi-omics Approach to Increase Survival Rate of Breast and Prostate Cancer Patients

The understanding of cancer biology has greatly advanced since the advent of genomics. A remarkable heterogeneity at the whole-genome (or omics) level exists amongst even histologically comparable cancers, demonstrating the enormous complexity of the cancer genome. A powerful resource that has the potential to translate high-throughput omics to better and quick overall survival is the massive accrual and public accessibility of multi-omics databases with accompanying clinical annotation, including tumor histology, patient response, and outcome. In this new era of high-throughput omics, this paper emphasizes the distinct benefits of a multidimensional approach to genomic analysis. It discusses the implications of translational omics research for the cancer population. Single-level data analysis of high-throughput technologies has constraints because it only displays a small window of cellular processes. Understanding the links across several cellular organization levels made possible by data integration across various platforms, including genomes, epigenomics, transcriptomics, proteomics, and metabolomics, is important. This review examines a few popular frameworks for integrating multi-omics data. It provides a general overview of multi-omics applications in tumor classification, prognosis, diagnostics, and the function of data integration in searching for novel biomarkers and treatment options.

Improvement in neoantigen prediction via integration of RNA sequencing data for variant calling.

Neoantigen-based immunotherapy has emerged as a promising strategy for improving the life expectancy of cancer patients. This therapeutic approach heavily relies on accurate identification of cancer mutations using DNA sequencing (DNAseq) data. However, current workflows tend to provide a large number of neoantigen candidates, of which only a limited number elicit efficient and immunogenic T-cell responses suitable for downstream clinical evaluation. To overcome this limitation and increase the number of high-quality immunogenic neoantigens, we propose integrating RNA sequencing (RNAseq) data into the mutation identification step in the neoantigen prediction workflow. In this study, we characterize the mutation profiles identified from DNAseq and/or RNAseq data in tumor tissues of 25 patients with colorectal cancer (CRC). Immunogenicity was then validated by ELISpot assay using long synthesis peptides (sLP). We detected only 22.4% of variants shared between the two methods. In contrast, RNAseq-derived variants displayed unique features of affinity and immunogenicity. We further established that neoantigen candidates identified by RNAseq data significantly increased the number of highly immunogenic neoantigens (confirmed by ELISpot) that would otherwise be overlooked if relying solely on DNAseq data. This integrative approach holds great potential for improving the selection of neoantigens for personalized cancer immunotherapy, ultimately leading to enhanced treatment outcomes and improved survival rates for cancer patients.

Enhancing the invasive traits of breast cancers by CYP1B1 via regulation of p53 to promote uPAR expression

Human cytochrome P450 1B1 (CYP1B1) catalyzes estrogen metabolism to produce metabolites that promote the progression of breast cancer. Since the invasive properties of cancer cells cause cancer relapse, which dramatically reduces patient survival, we investigated the new pro-invasive mechanism involving CYP1B1 in breast cancer. Exploring clinical data from invasive breast cancer patients revealed that CYP1B1 exhibits a potential correlation with urokinase-type plasminogen activator receptor (uPAR). Interestingly, uPAR mRNA expression was elevated in invasive breast cancer patients carrying TP53 genes with driver mutations, and our results showed that CYP1B1 activates the uPAR pathway following regulation of p53 according to its mutant status. CYP1B1 suppressed wild-type (WT) p53 whereas it induced the oncogenic gain-of-function mutant p53R280K, not only via transcriptional regulation but also the protein stabilization and activation following phosphorylation on Ser15 residue of p53R280K. Intriguingly, results from CYP1B1 polymorphic gene study and 4-hydroxyestradiol (4-OHE2) treatment showed that CYP1B1 regulates p53s and uPAR through its enzymatic activity. Furthermore, effects of DMBA and TMS on uPAR expression disappeared in HCT116p53−/− cells, indicating that p53 is critical for uPAR induction by CYP1B1. Collectively, our results demonstrate that CYP1B1 may reduce the relapse-free survival rate of breast cancer patients by inducing invasive traits in cancer cells via p53 regulation based on the mutation status of TP53 genes and further activation of the uPAR pathway. The elucidation of the previously unknown molecular mechanism of CYP1B1 may provide evidence for the development of effective anti-cancer therapeutic strategies that target the progression of cancer invasion.

Power Exponentiated Weibull Distibution: Application in Survival Rate of Cancer Patients

Power Exponentiated Weibull Distibution: Application in Survival Rate of Cancer Patients