• YPEL3's role as a novel tumor suppressor and its involvement in cellular proliferation were discovered during experiments to investigate p53 dependent cell cycle arrest. (wikipedia.org)
  • As a part of the p53 pathway response and its anti-proliferation role, cellular senescence has gained attention for its working relationship with tumor suppressor genes. (wikipedia.org)
  • Hypoxia and genetic defects that chronically drive proliferation leave such tumors dependent on a steady supply of nutrients, especially glucose. (springer.com)
  • Moreover, in adults, Merkel cells undergo slow turnover and are replaced by cells originating from epidermal stem cells, not through the proliferation of differentiated Merkel cells. (medscape.com)
  • Inactivation of tumor suppressor genes, whose products normally provide negative control of cell proliferation, contributes to malignant transformation in various cell types. (medscape.com)
  • Thus, unlike other tumor suppressors, RPL5/RPL11 play an essential role in normal cell proliferation, a function cells have evolved to rely on in lieu of a cell cycle checkpoint. (nih.gov)
  • Cell proliferation and invasion were assayed using the kidney cell lines HEK293 with wild-type p53 and a ccRCC cell line MZ1257RC mutated for p53. (frontiersin.org)
  • HEK293 cells demonstrated a restriction of ERV-K113 env expression and invasion with no changes in proliferation in the absence of Aza. (frontiersin.org)
  • Cell proliferation involves the replication of all cellular contents with the required energy for this to happen. (hindawi.com)
  • To prevent aberrant cell proliferation, these pathways are tightly regulated. (hindawi.com)
  • This activation is necessary for both cell proliferation as well as glucose uptake and use. (hindawi.com)
  • Retroviral vectors expressing short hairpin RNAs (shRNAs) against CDC2 caused efficient deletion of CDC2, cellular G2/M arrest concluding in apoptosis and inhibition of proliferation in human glioma cells U251 and SHG-44 cell lines ex vivo. (biomedcentral.com)
  • CDC2 gene plays an important role in the proliferation of human gliomas. (biomedcentral.com)
  • In addition, compared to the mono-treatment, combination of Polo-like kinase 1 inhibition with anti-mitotic or DNA damaging agents boosts more severe mitotic defects, effectually triggers apoptosis and strongly inhibits proliferation of cancer cells with functional p53. (oncotarget.com)
  • 1] 'Multiforme,' which refers to a heterogenous histologic appearance and proliferation of multiple cell types, was abandoned from the revised nomenclature in the 2007 World Health Organization Classification of Tumors of the Central Nervous System, and is now simply called 'glioblastoma. (cancernetwork.com)
  • 2] Glioblastoma is histologically defined by neoplastic cells with astrocytic characteristics and the presence of either endothelial proliferation-often in a glomeruloid morphology-and/or necrosis, which may resemble a pseudopalisading pattern (a false fence of neoplastic cells surrounding an area of necrotic tissue). (cancernetwork.com)
  • Low to moderate levels of CIN seems to be well tolerated and can promote cancer proliferation, genetic diversity, and tumor evolution. (encyclopedia.pub)
  • CIN can promote selective advantage to cancer cells by increasing the probability of novel chromosomal abnormalities, which can change the expression profile of the genes regulating cell division and differentiation, resulting in high proliferation rates [ 3 ] [ 4 ] . (encyclopedia.pub)
  • These CIN mechanisms and their signatures can be largely found in acute myeloid leukemia (AML), a heterogeneous disease characterized by abnormal proliferation and accumulation of myeloid precursor cells in the bone marrow [ 13 ] . (encyclopedia.pub)
  • MTT colorimetric assays, colony formation assays and 5‑ethynyl‑20‑deoxyuridine incorporation assays were also conducted to evaluate ACC cell proliferation. (cancerindex.org)
  • Many factors are involved in causing and permitting the unregulated proliferation of cells that occurs in cancer. (msdmanuals.com)
  • Overview of Cancer Cancer is an unregulated proliferation of cells. (msdmanuals.com)
  • The importance of functioning p53 in the regulation of the cell cycle is evident in that 55% of human cancers exhibit p53 mutations. (wikipedia.org)
  • DUSP4 alterations lead to hyperactivation of MAPK signaling in many cancers, including breast cancer, which often harbor mutations in cell cycle checkpoint genes, particularly in TP53. (biomedcentral.com)
  • This study identifies a novel mechanism for breast tumorigenesis implicating Dusp4 loss and p53 mutations in cellular acquisition of Dbf4 upregulation as a driver of cellular replication and cell cycle checkpoint escape. (biomedcentral.com)
  • BLBCs are nearly always accompanied by inactivating mutations in TP53 , encoding p53 [ 15 ]. (biomedcentral.com)
  • We find that together with loss-of-function mutations in p53 and, to some degree, potentiated by cMyc overexpression, Dusp4 deletion aids in cell cycle checkpoint escape while simultaneously potentiating hallmarks of replicative stress, including multinucleation and Chk1 phosphorylation. (biomedcentral.com)
  • The mutations of BRCA2 gene predispose the cells towards neoplastic development. (biomedcentral.com)
  • Mutations in this gene have been associated with Peutz-Jeghers syndrome, an autosomal dominant disorder characterized by the growth of polyps in the gastrointestinal tract, pigmented macules on the skin and mouth, and other neoplasms. (cancerindex.org)
  • PJS is autosomal-dominant condition caused by mutations of STK11, characterized by gastrointestinal polyposis, mucocutaneous pigmentation, and predisposition to a range of epithelial cancers: including colorectal, gastric, pancreatic, breast, ovarian cancers and sex cord tumors with annular tubules). (cancerindex.org)
  • However, cancer cells overcome these controls, in particular by acquiring genetic mutations leading to the activation of oncogenes (pten, myc) or loss of tumor suppressors (p53) [ 1 ]. (hindawi.com)
  • Several genetic alterations have been described in SCCHN, including mutations in the p53 tumor suppressor gene and mutations in genes that encode cell cycle proteins such as p16 and cyclin D1. (oncotarget.com)
  • 11- 13 The finding of breast cancer associated mutations within the RING finger domain of BRCA1 , disrupting BRCA1/BARD1 interaction, 11, 14 and the occurrence of BARD1 missense mutations in breast cancer patients, 15- 17 implies participation of BARD1 in BRCA1 mediated tumour suppression. (bmj.com)
  • These studies reveal that recurrent somatic mutations occur in only a handful of genes, with an overall mutational burden of roughly 1-2 per Mb. (springer.com)
  • In addition to performing nucleotide sequencing for 5 cases of ovarian cancer, TP53 mutations were analyzed via immunohistochemical staining for P53. (biomedcentral.com)
  • Both intensive P53 immunohistochemical staining and complete absence of signal were associated with the occurrence of TP53 mutations. (biomedcentral.com)
  • Thus, somatic mutations, and the consequent genomic instability may be an important driving force for the development of chemoresistance in malignant tumors. (biomedcentral.com)
  • 3] Patients are classified into one of two distinct categories based on the presence or absence of mutations in the IDH1 or IDH2 genes. (cancernetwork.com)
  • COHORT I: Patients that have cancer-associated DNA-repair gene mutations receive olaparib orally (PO) twice daily (BID) on days 1-28 of each cycle. (bcan.org)
  • COHORT II: Patients that do not have cancer-associated DNA-repair gene mutations undergo blood sample collection at baseline. (bcan.org)
  • ALL cancers have lots of additional changes, the so-called 'passenger' mutations, that may contribute to the cancer, but are not the main genes. (cancerquest.org)
  • TP53 mutations are seen in 5-10% of de novo MDS and AML, but 25-40% of therapy-related MDS and AML. (mdpi.com)
  • Both STARD12 and STARD14 were corelated with epigenetic regulation, especially TP53 mutation and m6A modification. (medsci.org)
  • Germline mutation of one TP53 allele is found in patients with Li-Fraumeni syndrome who generally inherit a mutated TP53 gene from an affected parent. (medscape.com)
  • Recent research has classified lung adenocarcinoma patients with KRAS mutation into three subtypes by co-occurring genetic events in TP53 (KP subgroup), STK11/LKB1 (KL subgroup) and CDKN2A/B inactivation plus TTF-1 low expression (KC subgroup). (cancerindex.org)
  • A mutation, or (increased or abnormal) methylation, in a tumour suppressor gene may adversely affect the expression or transcription of the gene so that the amino acid sequence and hence the primary structure of its polypeptide product is altered. (biotopics.co.uk)
  • If a mutation occurs in the proto-oncogene, producing an oncogene , more of these proteins are produced and this leads to unregulated cell division, a slower rate of cell differentiation and increased inhibition of the normal cell death, so cells build up, causing cancer and forming a tumour. (biotopics.co.uk)
  • Genomic instability caused by mutation of the checkpoint molecule TP53 may endow cancer cells with the ability to undergo genomic evolution to survive stress and treatment. (biomedcentral.com)
  • We attempted to gain insight into the potential contribution of ovarian cancer genomic instability resulted from TP53 mutation to the aberrant expression of multidrug resistance gene MDR1 . (biomedcentral.com)
  • TP53 mutation status was assessed by performing nucleotide sequencing and immunohistochemistry. (biomedcentral.com)
  • Moreover, in 161 epithelial ovarian cancer patients, multivariate logistic analysis identified late FIGO (International Federation of Gynecology and Obstetrics) stage, serous histotype, G3 grade and TP53 mutation as independent risk factors for ovarian cancer recurrence. (biomedcentral.com)
  • TP53 mutation-associated genomic instability may promote chromosome 7 accumulation and MDR1 amplification during ovarian cancer chemoresistance and recurrence. (biomedcentral.com)
  • In this regard, restoration of p53 in tumor cells with loss or mutation of p53 will reinforce the cytotoxicity of combined Polo-like kinase 1 therapy and provide a proficient strategy for combating relapse and metastasis of cancer. (oncotarget.com)
  • Up to 10% of patients with glioblastoma harbor a mutation in the IDH1 or IDH2 genes, an early event in gliomagenesis. (cancernetwork.com)
  • To explore tumor-mutational profiles in metastatic tumor biopsies, saliva "normal" DNA, changes in tumor or peripheral immune characteristics, or tumor associated somatic mutation load in blood DNA in response to treatment. (bcan.org)
  • An important checkpoint in a complex pathway, activated p53 has been shown to bind DNA and transcriptionally regulate genes that can mediate a variety of cellular growth processes including DNA repair, growth arrest, cellular senescence and apoptosis. (wikipedia.org)
  • Although studies in murine myeloid precursor cell lines indicated YPEL3 to have a role in apoptosis, human YPEL3 failed to demonstrate an apoptotic response using sub-G1 or poly ADP ribose polymerase cleavage as accepted indicators of programmed cell death. (wikipedia.org)
  • RT can directly induce cancer cell death through various mechanisms, such as apoptosis, necrosis, and autophagy. (nature.com)
  • The TP53 gene is also capable of stimulating apoptosis of cells containing damaged DNA. (medscape.com)
  • TP53 activates the expression of genes involved in apoptosis, cell cycle regulation (p21), and MDM2. (medscape.com)
  • A successful therapy must therefore eliminate these cells known to be highly resistant to apoptosis. (hindawi.com)
  • In this paper, we describe the metabolic changes as well as the mechanisms of resistance to apoptosis occurring in cancer cells and cancer stem cells, underlying the connection between these two processes. (hindawi.com)
  • EPCs from human umbilical cord and adult peripheral blood activate different mechanisms upon high-dose x-ray radiation treatment: CB-EPCs undergo p53 stabilization, Bax-dependent apoptosis and p21-dependent G 1 and G 2 /M cell cycle checkpoints, while PB-EPCs undergo only radiation-induced senescence [ 13 ], indicating unique gene expression patterns in EPCs of different sources. (biomedcentral.com)
  • Treating SCCHN cell lines with a pan-Aurora kinase inhibitor resulted in defective cytokinesis, polyploidy and apoptosis, which was effective irrespective of the EGFR status. (oncotarget.com)
  • Our results demonstrate that combined targeting of EGFR and Aurora kinases represents a therapeutic means to activate cell cycle checkpoints and apoptosis in SCCHN. (oncotarget.com)
  • Tumour suppression is achieved via the inhibition of cell division, induction of apoptosis (cell death) to remove altered cells, DNA damage repair, and inhibition of mechanisms that cause spread of cancer cells to other parts of the body (metastasis). (biotopics.co.uk)
  • In fact they they often code for proteins that stimulate cell division, prevent cell differentiation or regulate programmed cell death (apoptosis) within normal tissues and in this way they cause a controlled turnover of functional cells within an organ. (biotopics.co.uk)
  • TP53 is a checkpoint molecule that maintains genomic stability, prevents cell mitosis and induces apoptosis following abnormal chromosome segregation or chemical damage to DNA sequences [ 9 , 10 ]. (biomedcentral.com)
  • Western Blotting was used to determine the level of expression of CDC2 protein as measure to quantify down regulation of CDC2 expression along with use of flow cytometry to investigate effect of shRNAs on cell cycles and detection of apoptosis. (biomedcentral.com)
  • Upon treatment with Plk1 inhibitors, p53 in tumor cells is activated and induces strong apoptosis, whereas tumor cells with inactive p53 arrest in mitosis with DNA damage. (oncotarget.com)
  • We determined in six neuroblastoma cell lines the cytotoxicity of TPZ using DIMSCAN, a digital imaging fluorescence assay, apoptosis and mitochondrial membrane potential (ΔΨ m ) by flow cytometry, and protein expression by immunoblotting. (aacrjournals.org)
  • 46% of cells in p53-functional cell lines but failed to cause apoptosis in p53 nonfunctional cell lines. (aacrjournals.org)
  • Thus, TPZ cytotoxicity for neuroblastoma cell lines in hypoxia occurred via a p53-dependent mitochondrial pathway that caused induction of p53 and p21, ΔΨ m decrease, GSH depletion, and apoptosis. (aacrjournals.org)
  • On the other hand, extreme levels of CIN could lead to decreased cell fitness or apoptosis [ 9 ] . (encyclopedia.pub)
  • Tumour cells acquire the ability to proliferate uncontrollably, resist apoptosis, sustain angiogenesis and evade immune surveillance. (researchgate.net)
  • Although the conventional activities of p53 such as cell cycle arrest, senescence, and apoptosis are well accepted as the major checkpoints in stress responses, accumulating evidence implicates the importance of other tumor suppression mechanisms. (nature.com)
  • Is p53-dependent ferroptosis sufficient for tumor suppression in the absence of cell cycle arrest, senescence, and apoptosis? (nature.com)
  • To date, various mechanisms have been suggested to explain the powerful tumor-suppressive effect of p53, including the induction of cell cycle arrest, senescence, and apoptosis. (nature.com)
  • Epigenetics is the study of changes in gene activity that do not involve alterations to genetic code, or DNA. (wikipedia.org)
  • Analyzing preinvasive tumors of different sizes can therefore shed light on the sequence of these alterations. (biomedcentral.com)
  • In addition, these alterations affect 3 principal categories of genes, as follows: proto-oncogenes, tumor suppressor genes, and DNA repair genes. (medscape.com)
  • However, alterations to tumour suppressor genes can lead to the development of tumours. (biotopics.co.uk)
  • Chromosome instability (CIN) is an increased rate where chromosome acquire alterations due to errors in cell division. (encyclopedia.pub)
  • Chromosomal instability (CIN) is the increasing rate in which cells acquire new chromosomal alterations. (encyclopedia.pub)
  • Recent innovations have helped to develop prescription drugs against certain prostate cancer types, showing gene alterations that prevent the repair of damaged DNA or activate the body's anti-cancer natural immune defense. (mdpi.com)
  • A panel of genes has been identified whose cancer genome alterations may predict whether non-metastatic prostate cancer would go on to metastasize. (mdpi.com)
  • Aggressive tumors typically demonstrate a high glycolytic rate, which results in resistance to radiation therapy and cancer progression via several molecular and physiologic mechanisms. (springer.com)
  • Metabolic reprogramming plays an important role in tumor progression and antitumor immunity. (medsci.org)
  • The CDK4-cyclinD complex normally phosphorylates the retinoblastoma protein (Rb protein), leading to release of the E2F transcription factor and cell cycle progression. (medscape.com)
  • Deregulated signaling pathways are a hallmark feature of oncogenesis and driver of tumor progression. (biomedcentral.com)
  • Unexpectedly, we found that their depletion in primary human lung fibroblasts failed to induce cell cycle arrest but strongly suppressed cell cycle progression. (nih.gov)
  • We show that the effects on cell cycle progression stemmed from reduced ribosome content and translational capacity, which suppressed the accumulation of cyclins at the translational level. (nih.gov)
  • One potential mechanism of BRCA2 involvement in breast cancer progression may be through deregulation of the BRCA2 gene expression. (biomedcentral.com)
  • Although for years most studies have focused on tumor cells, allowing the discovery of numerous key (epi)-genetic aberrations and oncogenic pathways, it is now widely accepted that ecosystem integration is also critical for the understanding of cancer progression. (haematologica.org)
  • Accumulating evidence shows that cancer stem cells are key drivers of tumor formation, progression, and recurrence. (hindawi.com)
  • The most relevant articles summarising existing knowledge on RCC genomics, including tumour cell evolution and progression, were selected for this review. (springer.com)
  • In response to DNA damage and replication blocks, cell cycle progression is halted through the control of critical cell cycle regulators. (affbiotech.com)
  • Abnormalities in cell cycle regulation are reported to be strongly associated with tumorigenesis and progression of tumors. (biomedcentral.com)
  • In the present study, we investigated the relationship of gene expression profiles with malignant progression of human glioma. (biomedcentral.com)
  • Tumor specimens were obtained with informed consent from a 37-year-old female patient who underwent initial surgical removal in January 1999 and subsequent recurrent resections of a right temporal tumor July 1999 and February 2001 at the 2nd Affiliated Hospital of Soochow University (Suzhou, China) and did not receive chemotherapy and radiation between these stages of progression. (biomedcentral.com)
  • Mitotic chromosomal instability - the inability to faithfully segregate equal chromosome complements to two daughter cells during mitosis - is a widespread phenomenon in solid tumours that is thought to serve as the fuel for tumorigenic progression. (researchgate.net)
  • Cycles repeat every 28 days in the absence of disease progression or unacceptable toxicity. (bcan.org)
  • Of the 30,000 or so genes that are currently thought to exist in the human genome , there is a small subset that seems to be particularly important in the prevention, development, and progression of cancer. (cancerquest.org)
  • Yippee-like 3 (Drosophila) is a protein that in humans is encoded by the YPEL3 gene. (wikipedia.org)
  • SUAP later attained its current designation as YPEL3 (Yippee like three), after it was discovered to be one of five human genes possessing homology with the Drosophila Yippee protein. (wikipedia.org)
  • While investigating the p53 tumor suppressor protein, microarray studies which targeted Hdmx and Hdm2, both p53 negative regulators, revealed YPEL3 as a potential p53 regulated gene in MCF7 breast cancer cells. (wikipedia.org)
  • p53 is a tumor suppressor protein encoded by the human gene TP53 whose function is to prevent unregulated cell growth. (wikipedia.org)
  • [ 1 ] His prediction was subsequently supported by the cloning of the retinoblastoma tumor suppressor gene ( RB1 ) and by functional studies of the retinoblastoma protein, Rb. (medscape.com)
  • Like Rb protein, many of the proteins encoded by tumor suppressor genes act at specific points in the cell cycle. (medscape.com)
  • For example, the TP53 gene, located on chromosome 17, encodes a 53-kd nuclear protein that functions as a cell cycle checkpoint. (medscape.com)
  • The p19ARF protein, which is encoded by the same locus as p16, also leads to cell cycle arrest by inhibiting the ability of MDM2 to inactivate TP53. (medscape.com)
  • The p16INK4A protein is a cell-cycle inhibitor that acts by inhibiting activated cyclin D:CDK4/6 complexes, which play a crucial role in the control of the cell cycle by phosphorylating Rb protein. (medscape.com)
  • A1742P results in decreased kinase activity in patient cells ( PMID: 16014569 ), and therefore, is predicted to lead to a loss of Atm protein function. (jax.org)
  • A2062V results in failure to induce expression of TP53 target genes upon DNA damage in patient-derived cells in culture ( PMID: 23585524 ), and therefore, is predicted to lead to a loss of Atm protein function. (jax.org)
  • A2067D confers a loss of function to Atm, resulting in reduced Atm protein expression and decreased Atm kinase activity in cell culture ( PMID: 25077176 ). (jax.org)
  • A220V restores cell viability of ATM-deficient cells upon irradiation in culture ( PMID: 29059438 ) and therefore, is predicted to have no effect on Atm protein function. (jax.org)
  • A2274T results in phosphorylation levels of Atm and downstream targets similar to wild-type Atm in response to irradiation in cultured cells ( PMID: 19431188 ), and leads to kinase activity, radiosensitivity, and radiation-induced chromosome aberrations similar to wild-type protein in cultured cells ( PMID: 11805335 ), and therefore, is predicted to have no effect on Atm protein function. (jax.org)
  • Dual specificity protein phosphatase 4 (DUSP4) is a critical negative regulator of the mitogen-activated protein kinase (MAPK) pathway and is often deleted or epigenetically silenced in tumors. (biomedcentral.com)
  • As loss of RPL5/RPL11 abrogates ribosome biogenesis and protein synthesis to the same extent as loss of other essential 60S RPs, we reasoned the loss of RPL5 and RPL11 would induce a p53-independent cell cycle checkpoint. (nih.gov)
  • While studying the activity of BRCA2 gene promoter in breast cancer cells, we discovered that this promoter has bi-directional activity and the product of the reverse activity (a ZAR1-like protein, we named ZAR2) silences the forward promoter at the G0/G1 phase of the cell. (biomedcentral.com)
  • Standard techniques like cell synchronization by serum starvation, flow cytometry, N-terminal or C-terminal FLAG epitope-tagged protein expression, immunofluorescence confocal microscopy, dual luciferase assay for promoter evaluation, and chromatin immunoprecipitation assay were employed during this study. (biomedcentral.com)
  • What does this gene/protein do? (cancerindex.org)
  • What pathways are this gene/protein implicaed in? (cancerindex.org)
  • Research has intensified to understand ERV protein function and their role as tumor antigens and targets for cancer (immune) therapy. (frontiersin.org)
  • High ERV-K env total protein expression of all tumor subtypes significantly correlated with low tumor grading and a longer disease specific survival using multivariable analyses. (frontiersin.org)
  • Patients characterized by elevated EGFR and elevated Aurora-A protein expression in tumor tissue represent a risk group with poor disease-free and overall survival (EGFR low Aurora-A low versus EGFR high Aurora-A high , p=0.024). (oncotarget.com)
  • Oestrogen enters target cells, and binds with a receptor protein. (biotopics.co.uk)
  • The protein encoded by this gene is a cell cycle checkpoint regulator and putative tumor suppressor. (affbiotech.com)
  • Following this, the differentially expressed genes (DEGs) were included in Gene Ontology enrichment, and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway, protein‑protein interaction network and survival analyses. (cancerindex.org)
  • Genes whose protein products stimulate or enhance the division and viability of cells. (cancerquest.org)
  • Genes whose protein products can directly or indirectly prevent cell division or lead to cell death. (cancerquest.org)
  • As an example TP 53 refers to the gene and p53 refers to the protein. (cancerquest.org)
  • Inflammasomes refer to the cytoplasmic multimeric protein complexes that sense pathogen- or danger-associated molecular patterns (PAMPs or DAMPs, respectively) to mediate the inflammatory response and induce programmed cell death known as pyroptosis [ 1 ]. (thno.org)
  • DNA methylation of a CpG island near the YPEL3 promoter as well as histone acetylation may represent possible epigenetic mechanisms leading to decreased gene expression in human tumors. (wikipedia.org)
  • Although carcinogenic roles for the INK4B, INK4C, INK4D, CIP1, KIP1, and KIP2 genes appear to be limited, INK4A is among the most commonly mutated genes in human tumors. (medscape.com)
  • Scholars@Duke publication: Genomic evaluation of tumor mutational burden-high (TMB-H) versus TMB-low (TMB-L) metastatic breast cancer to reveal unique mutational features. (duke.edu)
  • Background: Tumor mutational burden (TMB) has emerged as an imperfect biomarker of immune checkpoint inhibition (ICI) outcomes in solid tumors. (duke.edu)
  • Genetic testing revealed a high loss of heterozygosity score and high tumor mutational burden (TMB). (spandidos-publications.com)
  • We used a molecular pathway-based approach to analyze transcriptomic profiles of 59 colorectal tumors representing early and late preinvasive stages and the invasive stage of tumorigenesis. (biomedcentral.com)
  • DNA damage increases TP53 levels through an ATM-dependent pathway. (medscape.com)
  • Interestingly, Wnt Pathway we found a significant increase in tyrosine phosphorylation at the corresponding molecular weight of hTERT in K562 cells compared to HL60 cells. (rafinhibitors.com)
  • This was supported by our finding that the levels of tricarboxylic Estrogen Receptor Pathway acid cycle intermediates change divergently upon hyper activation of Bcr Abl: the intracellular concentrations of fumarate and malate were increased whereas the citrate and isocitrate levels were decreased. (rafinhibitors.com)
  • These data uncovered the IL32β/BAFF axis as a previously undescribed pathway involved in lymphoma-associated macrophage polarization and tumor survival, which could be counteracted through selective NIK inhibition. (haematologica.org)
  • The corresponding genes for the DFS-SEs were significantly enriched in mitochondria and their associated pathways according to Gene Ontology annotation and in the pathways of fatty acid metabolism, oxidative phosphorylation and Huntington's disease according to a Kyoto Encyclopedia of Genes and Genomes pathway analysis. (spandidos-publications.com)
  • Ferroptosis acts as an independent pathway for suppressing tumor growth and is tightly connected with metabolism and oxidative stress responses. (nature.com)
  • I. To determine the proportion of patients with DNA-repair pathway-mutated genes in metastatic non-prostate GU cancer (patient cohort referred for screening). (bcan.org)
  • To determine the effectiveness of using next-generation sequencing (NGS) to identify DNA-repair pathway gene defects in tumor samples and circulating DNA and identify patients with non-prostate GU cancer suitable for PARP inhibition. (bcan.org)
  • Although RT is an important modality for cancer treatment, the consequential changes caused by RT in the tumor microenvironment (TME) have not yet been fully elucidated. (nature.com)
  • Furthermore, inflammatory mediators released by irradiated dying cells can attract and regulate immune cells in the tumor microenvironment (TME), further killing cancer cells. (nature.com)
  • Aggressive B-cell malignancies, such as mantle cell lymphoma (MCL), are microenvironment-dependent tumors and a better understanding of the dialogs occurring in lymphoma-protective ecosystems will provide new perspectives to increase treatment efficiency. (haematologica.org)
  • This integrated analysis led to the discovery of microenvironment-dependent and tumor-specific secretion of interleukin-32 beta (IL32β), whose expression was confirmed in situ within MCL lymph nodes by multiplex immunohistochemistry. (haematologica.org)
  • Finally, we demonstrated the efficacy of selective NIK/alternative-NFkB inhibition to counteract microenvironment-dependent induction of IL32β and BAFF-dependent survival of MCL cells. (haematologica.org)
  • Evidence demonstrating that the tumor ecosystem plays a central role in tumoral expansion and treatment resistance has continued to accumulate since the emergence of the tumor microenvironment concept more than a century ago. (haematologica.org)
  • In contrast, cancer cells shift their metabolism toward lactate production even in the presence of oxygen [ 4 ], partly through genetic modifications that stabilize the transcription factor Hypoxia Inducible Factor (HIF) involved in the adaptation of the cells to hypoxia, under nonhypoxic conditions as well as generating an adaptive response to the hypoxic microenvironment (Figure 1 ). (hindawi.com)
  • DNA signature analyses including APOBEC and homologous recombination repair deficiency, as well as gene expression profiling to assess immune-related signatures and tumor microenvironment are underway. (duke.edu)
  • TP53 inhibition allows LINE-1 + cells to grow, and genome-wide-knockout screens show that these cells require replication-coupled DNA-repair pathways, replication-stress signaling and replication-fork restart factors. (nih.gov)
  • As shown in Figure 4c, Gleevec treatment resulted in almost complete inhibition of hTERT phosphorylation at tyrosine residues compared to control cells. (rafinhibitors.com)
  • On the contrary, enhanced glycolysis could be linked to the cell death observed 48 hours after imatinib withdrawal as inhibition of glycolysis by 2 deoxyglucose completely rescued cells from imatinib withdrawal induced death. (rafinhibitors.com)
  • A significant, although incomplete, inhibition of cell death was also observed upon partial deprivation of glutamine from the medium and inhibition Celastrol of glutaminase activity using the glutaminase inhibitor 6 diazo 5 oxo l norleucine. (rafinhibitors.com)
  • Concurrent predictive biomarkers of response to immune checkpoint inhibition such as MSI-H and PDL-1 positivity are also more prevalent in TMB-H MBC. (duke.edu)
  • Thus, inactive p53 is not associated with a susceptible cytotoxicity of Polo-like kinase 1 inhibition and could rather foster the induction of polyploidy/aneuploidy in surviving cells. (oncotarget.com)
  • Inflammasome inhibition reverted the therapeutic failure of ICB in inflammasome-activated tumors. (thno.org)
  • Even as the nature of the exact cell in which Merkel cell carcinoma oncogenesis occurs is controversial, there is strong support for the notion that Merkel cell carcinoma results from of one of two distinct pathways. (medscape.com)
  • GSEA analysis found STARD12 and STARD14 were associated with glycolysis, oxidative phosphorylation and tumor related signaling pathways. (medsci.org)
  • Random set analysis was used to identify biological pathways enriched for genes differentially regulated in tumors (compared with 59 samples of normal mucosa). (biomedcentral.com)
  • Of the 880 canonical pathways we investigated, 112 displayed significant tumor-related upregulation or downregulation at one or more stages of tumorigenesis. (biomedcentral.com)
  • S transition in the cell cycle, upregulated expression of tumor-promoting microenvironmental factors, and profound dysregulation of metabolic pathways (e.g., increased aerobic glycolysis, downregulation of pathways that metabolize drugs and xenobiotics). (biomedcentral.com)
  • Lipids, amino acids, and nucleotides necessary for the biosynthesis of the daughter cells are mostly provided by intermediate metabolites of these pathways. (hindawi.com)
  • The term "oncotarget" encompasses all molecules, pathways, cellular functions, cell types, and even tissues that can be viewed as targets relevant to cancer as well as other diseases. (oncotarget.com)
  • We shall consider each subtype in turn describing genes and pathways of oncogenesis and how these relate to prognosis and treatment response. (springer.com)
  • Here, we review the role of ferroptosis in p53-mediated tumor suppression, with a focus on what cellular factors are critical for p53-dependent ferroptosis during tumor suppression and how p53 modulates both the canonical (GPX4-dependent) and the non-canonical (GPX4-independent) ferroptosis pathways. (nature.com)
  • Once activated, p53 coordinates multiple downstream pathways, thereby maintaining the homeostasis of the host cell or organism (if the stress is mild, transient, and repairable) or eliminating damaged cells (if the stress is acute, prolonged, and difficult to resist). (nature.com)
  • However, since the heterogeneity of the tumors and the small sample size analyzed, we recommend complementary and centralized germline studies to discard the early onset as an additional criterion to take into account to improve the identification of cancer genetic predisposition syndromes in neonates. (bvsalud.org)
  • Intra-tumour heterogeneity appears to hamper the clinical applicability of sparsely sampled tumours. (springer.com)
  • To determine the expression of Schlafen 11 (SLFN11) in tumor versus (vs.) stroma cells, and the potential tumor heterogeneity based on SLFN11 expression. (bcan.org)
  • During later sequence analysis of human chromosome 22, researchers identified a gene family YPEL1-YPEL5, which had high homology with the Drosophila Yippee gene. (wikipedia.org)
  • We found that Dusp4 loss alone is insufficient in mediating tumorigenesis, but alternatively converges with loss in Trp53 and MYC amplification to induce tumorigenesis primarily through chromosome 5 amplification, which specifically upregulates Dbf4 , a cell cycle gene that promotes cellular replication by mediating cell cycle checkpoint escape. (biomedcentral.com)
  • The higher incidence of ccRCC in male patients may partially be accounted by mono-allelic inactivation of the chromatin remodelling gene, KDM5C on the X chromosome [ 6 ]. (springer.com)
  • This gene is localized to chromosome 20 and has pseudogenes which reside on chromosomes 1 and 22. (cancerindex.org)
  • The identified DEGs included 20 downregulated genes and 51 upregulated genes, which were highly associated with the cell cycle, organelle fission, chromosome segregation, cell division and spindle stability. (cancerindex.org)
  • [ 2 ] Targeted disruption of TP53 in the mouse leads to the development of various tumors (see image below). (medscape.com)
  • Increasingly numerous results have demonstrated overexpression of CDC2/Cyclin B1 in various tumors however there is still no report of CDC2/Cyclin B1 expression in clinical samples from patients with gliomas. (biomedcentral.com)
  • An important development in cancer research over the past 2 decades has been the recognition that genetic changes drive the pathogenesis of tumors of both adulthood and childhood. (medscape.com)
  • however, germline genetic analysis is not usually performed in neonatal cancer patients PATIENTS AND METHODS: To improve the identification of cancer genetic predisposition syndromes, we retrospectively review clinical characteristics in 45 patients with confirmed tumor diagnosis before 28 days of age, and we carried out germline genetic analysis in 20 patients using next-generation sequencing and directed sequencing. (bvsalud.org)
  • CONCLUSIONS: Our results suggest that genetic factors have almost no higher impact in most neonatal tumors. (bvsalud.org)
  • In this review, we consider what is currently known of the genetic landscape of the commonest subtypes of renal cell cancer (RCC). (springer.com)
  • p53, the guardian of the genome, is the most important tumor suppressor. (oncotarget.com)
  • Another important class of tumor suppressor genes involved in cell cycle control and in the generation of human cancers is the cyclin-dependent kinase (CDK) inhibitors. (medscape.com)
  • Renal cell carcinoma (RCC) is one of the ten most common cancers for men and women with an approximate 75% overall 5-year survival. (frontiersin.org)
  • Approximately 5-10% of all breast and ovarian cancers are thought to arise from a hereditary predisposition to the disease, 1 BRCA1 and BRCA2 being the most important susceptibility genes. (bmj.com)
  • The most common non-clear cell renal cancers have also undergone genomic profiling and are characterised by distinct genomic landscapes. (springer.com)
  • Correlation with outcome needs to be more comprehensively furnished, particularly for small renal masses, rarer non-clear cell renal cancers, and for all tumours undergoing targeted therapy. (springer.com)
  • A diagram showing the major cancer genes for some cancers. (cancerquest.org)
  • After subsequent cloning and sequencing experiments Yippee was found to be a conserved gene family of proteins present in a diverse range of eukaryotic organisms, ranging from fungi to humans. (wikipedia.org)
  • 6, 7 BRCA1 interacts with a variety of proteins and is involved in multiple cellular processes including DNA repair, transcription, and checkpoint control. (bmj.com)
  • 8- 10 In attempts to identify new breast and ovarian cancer susceptibility genes, much research has focused on BRCA1 associated proteins. (bmj.com)
  • Note that by convention gene names are italicized and the proteins they make are not. (cancerquest.org)
  • The majority of glioblastomas are IDH wild-type and correspond to the longstanding clinical description of primary glioblastomas, which arise rapidly from non-neoplastic brain cells and progress quickly. (cancernetwork.com)
  • A small proportion of these tumors show large ducts lined by neoplastic cells, the so-called large-duct variant of adenocarcinoma. (coek.info)
  • The phenomenon of field cancerization (the existence of histologically abnormal tissue beyond a neoplastic area that predisposes to tumour formation) was described in the 1950s on the basis of analyses of squamous cell carcinomas (SCCs). (researchgate.net)
  • YPEL3 was discovered to be a possible p53 target after a screen for such genes was performed in MCF7 breast cancer cells following RNAi knockdown of p53 negative inhibitors. (wikipedia.org)
  • Immunotherapy mainly includes immune checkpoint inhibitors (ICIs), such as inhibitors of PD-1 (programmed cell death 1)/programmed cell death ligand 1 (PD-L1). (nature.com)
  • To further determine whether BCR ABL phosphorylates Raf Inhibitors hTERT, we treated K562 cells with 1 M Gleevec, and evaluated the phosphorylation status of hTERT. (rafinhibitors.com)
  • Plk1 inhibitors target all rapidly dividing cells irrespective of tumor cells or non-transformed normal but proliferating cells. (oncotarget.com)
  • PARP inhibitors, such as olaparib, can keep PARP from working, so tumor cells can't repair themselves, and they may stop growing. (bcan.org)
  • Typically, rapidly proliferating tumor cells have glycolytic rates up to 200 times higher than those of their normal tissue of origin, even in the presence of oxygen [ 3 ]. (hindawi.com)
  • In this review, we discuss the changes in irradiated cancer cells and immune cells in the TME under different RT regimens and describe existing and potential molecules that could be targeted to improve the therapeutic effects of RT. (nature.com)
  • We review the possible roles for calorie restriction (CR) and very low carbohydrate ketogenic diets (KDs) in modulating the five R's of radiotherapy to improve the therapeutic window between tumor control and normal tissue complication probability. (springer.com)
  • Stimulating the expression of angiogenic microRNAs or genes in EPCs of low activity (such as those from patients with cardiovascular diseases) might allow the development of novel therapeutic strategies. (biomedcentral.com)
  • Thus, umbilical cord blood EPCs hold great therapeutic potential for cell therapy and vascular engineering. (biomedcentral.com)
  • While the standard workup did not identify the primary tumor, genomic profiling analysis was useful in therapeutic management. (spandidos-publications.com)
  • Polo-like kinase 1, a pivotal regulator of mitosis and cytokinesis, is highly expressed in a broad spectrum of tumors and its expression correlates often with poor prognosis, suggesting its potential as a therapeutic target. (oncotarget.com)
  • Moreover, based on the proposed classification and therapeutic implications, an open website was established to provide tumor patients with comprehensive information on inflammasome signaling. (thno.org)
  • These findings highlight the importance of inflammasome evaluation in tumor classification and provide a foundation for improving relevant therapeutic regimens. (thno.org)
  • Gliomas are the most common and aggressive primary brain tumors for which unfortunately no effective treatment modalities exist despite advances in molecular biology as the knowledge base to unravel the extremely complex molecular mechanisms of tumorigenesis is limited. (biomedcentral.com)
  • Although individualized targeted therapies are routinely used for patients with lung and breast tumors, personalized medicine has not achieved the same degree of success in the pancreas. (coek.info)
  • In addition, STARD12/14 could regulate the ferroptosis related genes. (medsci.org)
  • The notion could be that unique cellular mechanisms are triggered in the breast cancer cells to stimulate BRCA2 gene expression as a temporary measure to regulate the growth of the breast cancer cells. (biomedcentral.com)
  • Some proto-oncogenes work to regulate cell death. (cancerquest.org)
  • Most cases of breast cancer do not 'run in families', but the well-known genes BRCA1 and BRCA2 can increase the risk of developing breast cancer (and also ovarian cancer). (biotopics.co.uk)
  • Ovarian cancer cell DNA ploidy was determined using Feulgen-stained smears or flow cytometry. (biomedcentral.com)
  • Several alkylating agents are commonly used in chemotherapy but may induce DNA damage to cancer cells as well as normal cells. (frontiersin.org)
  • Characterized by the limited ability of cultured normal cells to divide, senescence has been shown to be triggered through oncogenic activation( premature senescence) as well as telomere shortening as the result of successive rounds of DNA replication (replicative senescence). (wikipedia.org)
  • STARD12 co-expressed genes participated in cell cycle and DNA replication, and STARD14 were enriched in ECM-receptor interaction. (medsci.org)
  • The early preinvasive stage was characterized by cell-cycle checkpoint activation triggered by DNA replication stress and dramatic downregulation of basic transmembrane signaling processes that maintain epithelial/stromal homeostasis in the normal mucosa. (biomedcentral.com)
  • Interestingly, replication stress in Brca2-null cells activates p53 and the expression of its target genes, including senescence-inducing Ink4/Arf. (biomedcentral.com)
  • Given the previously reported role of DUSP4 as a p53 target, a potential cell cycle checkpoint, and in mediating senescence downstream of replication stress, we hypothesized that DUSP4 may be a critical oncogenic driver in breast cancer. (biomedcentral.com)
  • This article briefly discusses tumor suppressor genes and then focuses on the role of proto-oncogenes in childhood cancer. (medscape.com)
  • The normal versions of genes in the first group are called proto-oncogenes. (cancerquest.org)
  • Numerous genes have been identified as proto-oncogenes. (cancerquest.org)
  • The proto-oncogenes that have been identified so far have many different functions in the cell. (cancerquest.org)
  • The genes in the second group are called tumor suppressors. (cancerquest.org)
  • A useful analogy to consider when thinking about tumor suppressors and oncogenes is an automobile. (cancerquest.org)
  • In this investigation a human RCC tissue microarray (TMA) (n=374) predominantly consisting of the most common histological tumor subtypes was hybridized with an ERV-K env antibody and correlated with patient clinical data. (frontiersin.org)
  • They are fairly spherical structures composed of fibrous and muscle tissue, and they develop in response to oestrogen, which has the effect of thickening the lining of the uterine wall as part of the menstrual cycle. (biotopics.co.uk)
  • The activated version of this acts as a transcription factor regulating various gene expression events involved in the development of breast tissue in puberty and pregnancy. (biotopics.co.uk)
  • Tissue microarrays were utilized to investigate the expression of genes in a large number of tumor samples and to identify overexpressed genes which could be potentially causing tumorigenesis. (biomedcentral.com)
  • Its prominent properties are A lack of cell differentiation Local invasion of adjoining tissue Metastasis, which is spread to distant sites through. (msdmanuals.com)
  • Furthermore, these three genes predicted overall survival and recurrence‑free survival in patients with ACC from the TCGA cohort. (cancerindex.org)
  • In addition, tumor-associated antigens (TAAs) produced by irradiated tumor cells can be captured by antigen-presenting cells (APCs) in the TME and presented to T cells. (nature.com)
  • The methylation specific polymerase chain reaction in conjunction with sequencing verification was used to establish the methylation patterns of the 14 genes in the liver tissues of four healthy liver donors, as well as tumor and the paired non-cancerous tissues of 30 HCC patients. (wjgnet.com)
  • Both glutathione S-transferase pi ( GSTpi ) (80%, 24/30 in tumor and 56.7%, 17/30 in the paired non-cancerous tissues) and cystic fibrosis transmembrane conductance regulator, ATP-binding cassette (sub-family C, member 7) ( CFTR ) (77%, 23/30 in tumor and 50%, 15/30 in the paired non-cancerous tissues) genes were prevalently hypermethylated in HCC as well as their neighboring non-cancerous tissues. (wjgnet.com)
  • Can ferroptosis be specifically induced in tumors but not in normal tissues? (nature.com)
  • Although most circulating cancer cells die, an occasional cell may penetrate into tissues, generating a metastasis at a distant site. (msdmanuals.com)
  • The cell cycle is a complex process with myriad genes involved and elaborate and complex signaling mechanisms to allow for this critical cellular process. (biomedcentral.com)
  • The extremely low 5-year overall survival of patients is, in part, due to pancreatic cancer cells having several mechanisms of resistance to different chemotherapeutic treatments, one of which is their capacity to efficiently repair alkylating agent-induced DNA damage. (frontiersin.org)
  • With the advent of improved immunohistochemical profiling, the tumor was reclassified as Merkel cell carcinoma because shared epithelial and neuroendocrine markers, along with ultrastructural features suggestive of neural crest origin, were observed in both the constituent tumor cell and the physiologic Merkel cell of the skin. (medscape.com)
  • Within skin, Merkel cells have also been shown to cluster in the basal layers of the interfollicular epidermis in specialized epithelial structures called touch domes, where they are juxtaposed with epidermal keratinocytes. (medscape.com)
  • [ 5 , 6 ] Furthermore, experiments have demonstrated that epidermal progenitors in the touch domes are capable of producing Merkel cell lines and that epithelial progenitor populations in adults have the capacity to give rise to both neuroendocrine and squamous lineages. (medscape.com)
  • Other suggested cells of origin include the neural crest‒derived cell of amine precursor uptake and decarboxylation (APUD) system, dermal fibroblasts, pre or pro B cells, residual epidermal stem cells, and epithelial, non-Merkel cell progenitors. (medscape.com)
  • Using a genetically engineered mouse model, we generated mammary-specific Dusp4 -deleted primary epithelial cells to investigate the necessary conditions in which DUSP4 loss may drive breast cancer oncogenesis. (biomedcentral.com)
  • In addition, the effects of reduced Bard1 expression have been studied in murine mammary epithelial cell cultures, where it was associated with complex cellular changes suggestive of a premalignant phenotype. (bmj.com)
  • Basal cell carcinoma (BCC) is a nonmelanocytic skin cancer (ie, an epithelial tumor) that arises from basal cells (ie, small, round cells found in the lower layer of the epidermis). (medscape.com)
  • We find that nontransformed cells undergo a TP53-dependent growth arrest and activate interferon signaling in response to LINE-1. (nih.gov)
  • Most women have a 12% chance of developing breast cancer in their lifetime, and women with mutated BRCA1 or BRCA2 genes may have as much as an 80% chance, and they are more likely to develop it at an early age. (biotopics.co.uk)
  • 22, 23 The significance of BARD1/BRCA1 collaboration has also been emphasised by studies of its ubiquitin ligase activity that might contribute to tumour suppression and other biological functions of BRCA1. (bmj.com)
  • 26 The suggested role in TP53 dependent apoptotic signalling 27 and interaction with the ankyrin repeats of proto-oncoprotein BCL3, thereby possibly modulating the activity of transcription factor NFKB, 28 represent BRCA1 independent functions of BARD1. (bmj.com)
  • We identified a colorectal cancer wherein a fast-growing tumor subclone downregulated LINE-1, prompting us to examine how LINE-1 expression affects cell growth. (nih.gov)
  • Compared to HL60 cells, the tyrosine phosphorylation level in K562 cells was markedly increased, suggesting that the increase in tyrosine phosphorylation is due to BCR ABL tyrosine kinase activity, which was confirmed by the expression of BCR ABL shown only in K562 cells. (rafinhibitors.com)
  • To evaluate this possibility, hTERT was immunoprecipitated by anti hTERT antibody from both K562 and HL60 cell lysates and resolved by SDS PAGE followed by immunoblotting with anti phosphorylation antibody. (rafinhibitors.com)
  • We found that hTERT tyrosine phosphorylation was significantly elevated in K562 cells compared to HL60 cells. (rafinhibitors.com)
  • To demonstrate that the decrease in tyrosine phosphorylation of hTERT was not due to reduced hTERT expression level, western blot was performed and we did not observe a difference in hTERT expression level in Gleevec treated K562 cells compared to control cells. (rafinhibitors.com)
  • Gleevec inhibits hTERT nucleoli translocation in K562 BCR ABL positive cells It is known that phosphorylation of hTERT is important for its nuclear translocation. (rafinhibitors.com)
  • In normal cells, glucose participates in cellular energy production through glycolysis as well as through its complete catabolism via the tricarboxylic acid (TCA) cycle and oxidative phosphorylation (OXPHOS). (hindawi.com)
  • BRCA2 gene expression is tightly regulated during the cell cycle in human breast cells. (biomedcentral.com)
  • The expression of BRCA2 gene is silenced at the G0/G1 phase of cell growth and is de-silenced at the S/G2 phase. (biomedcentral.com)
  • Human BRCA2 gene promoter is active in both the forward and the reverse orientations. (biomedcentral.com)
  • In the G0/G1 growth phase ZAR2 is predominantly located inside the nucleus of the breast cells, binds to the BRCA2 promoter and inhibits the expression of BRCA2. (biomedcentral.com)
  • BRCA2 gene promoter has bi-directional activity, expressing BRCA2 and a novel C4-type zinc finger containing transcription factor ZAR2. (biomedcentral.com)
  • Subcellular location of ZAR2 and its expression from the reverse promoter of the BRCA2 gene are stringently regulated in a cell cycle dependent manner. (biomedcentral.com)
  • ZAR2 binds to BRCA2/ZAR2 bi-directional promoter in vivo and is responsible, at least in part, for the silencing of BRCA2 gene expression in the G0/G1 phase in human breast cells. (biomedcentral.com)
  • BRCA2 gene expression is stringently regulated during the cell cycle. (biomedcentral.com)
  • Initially discovered in a gene expression profiling assay of p53 activated MCF7 cells, induction of YPEL3 has been shown to trigger permanent growth arrest or cellular senescence in certain human normal and tumor cell types. (wikipedia.org)
  • Recognized hallmarks of cellular senescence include senescence associated(SA)beta galactosidase staining and the appearance of senescence-associated heterochromatic foci(SAHF) within the nuclei of senescent cells. (wikipedia.org)
  • Studies in U2OS osteosarcoma cells and MCF7 breast cancer cells have also demonstrated increased cellular senescence upon YPEL3 induction. (wikipedia.org)
  • Confocal microscopy was carried out to study Gleevec,s effect on hTERT cellular distribution in K562, HL60, and Jurkat cells. (rafinhibitors.com)
  • Importantly, this enhanced cellular metabolic activity upon acute hyper activation of Bcr Abl was not beneficial for the cells as proposed by Warburg. (rafinhibitors.com)
  • These solo-LTRs contain functional sequences like promoters, enhancers, polyadenylation signals and are frequently located near cellular genes. (frontiersin.org)
  • Plk3 is expressed throughout the cell cycle and involved in cellular response to DNA damage [ 9 ]. (oncotarget.com)
  • This receptor is found in moderate levels on some normal cells and as the gene's name implies, it is involved in cellular responses to growth factors. (cancerquest.org)
  • Methods: Tumor samples (N = 5621) obtained from patients with MBC were analyzed by next-generation sequencing (NGS) of DNA (592-gene panel or whole exome sequencing) and RNA (whole transcriptome sequencing) at Caris Life Sciences (Phoenix, AZ). (duke.edu)
  • Here, we tested whether ALKBH6 plays a significant role in preventing alkylating DNA damage and decreasing genomic instability in pancreatic cancer cells. (frontiersin.org)
  • The initiation and development of tumor cell is accompanied by elevated stresses, such as oncogene activation, DNA damage, genome instability, and reprogrammed tumor metabolism. (nature.com)
  • Although epigenetically silenced, endogenous retroviral (ERV) genes become activated in tumors and function to ignite immune responses. (frontiersin.org)
  • RT-induced damage to cancer cells leads to different outcomes, such as survival, senescence, or death. (nature.com)
  • Transfecting these cell lines with a codon optimized ERV-K113 env overexpressing CMV vector was performed with or without 5'-Aza-2'-deoxycytidine (Aza) treatment to sustain promoter de-methylation. (frontiersin.org)
  • Methylation profile of the promoter CpG islands of 14 "drug-resistance" genes in hepatocellular carcinoma. (wjgnet.com)
  • To establish the DNA methylation patterns of the promoter CpG islands of 14 "drug-resistance" genes in hepatocellular carcinoma (HCC). (wjgnet.com)
  • The mutated or otherwise damaged versions of these genes are called oncogenes. (cancerquest.org)
  • In normal cells, both internal and external signals control the activity of the oncogenes. (cancerquest.org)
  • We have two copies of each gene and for oncogenes, a single defective copy is enough to cause a cell to divide. (cancerquest.org)
  • As stated in the introduction to this section, the defective versions of these genes, known as oncogenes, can cause a cell to divide in an unregulated manner. (cancerquest.org)
  • A phase II study showed that patients with resected local-regionally advanced head and neck squamous cell carcinoma (HNSCC) had improved survival when pembrolizumab was added to adjuvant RT (NCT02641093). (nature.com)
  • Merkel cell carcinoma is a rare primary cutaneous neuroendocrine carcinoma with growing incidence and high metastatic potential. (medscape.com)
  • This skin cancer has been called by several other names, including primary small-cell carcinoma of the skin, APUDoma, primary undifferentiated carcinoma of the skin, and the Toker tumor. (medscape.com)
  • [ 2 ] As neuroendocrine carcinomas were thought to be of neural crest origin, in 1978 Tang and Toker proposed that this carcinoma might be derived from Merkel cells. (medscape.com)
  • Ultimately, it is unclear whether the eponymous Merkel cell is truly a histiogenic precursor of Merkel cell carcinoma. (medscape.com)
  • [ 7 , 8 ] Sunshine et al offer that perhaps there are multiple cell-line precursors of Merkel cell carcinoma. (medscape.com)
  • [ 9 ] Since our understanding of the histogenesis is still evolving, some authors choose to refer to Merkel cell carcinoma as neuroendocrine carcinoma of the skin or cutaneous neuroendocrine carcinoma. (medscape.com)
  • Also see Merkel Cell Tumors of the Head and Neck and Merkel Cell Carcinoma and Rare Appendageal Tumors . (medscape.com)
  • Sixteen histological tumor subtypes exist and the most common are papillary, chromophobe and clear cell renal cell carcinoma (ccRCC) representing 85% of all RCC. (frontiersin.org)
  • Pathological diagnosis based on a biopsy sample of the para‑aortic lymph nodes indicated that the tumor was a high‑grade serous carcinoma of possible gynecological organ origin. (spandidos-publications.com)
  • The former includes adenocarcinoma of the axillary lymph nodes, papillary serous carcinoma of the peritoneum (redefined as peritoneal cancer), squamous cell carcinoma of the cervical lymph nodes and extragonadal germ cell tumors in young men, which are derived from the middle of the body ( 4 ). (spandidos-publications.com)
  • On the other hand, the unfavorable subset (majority of patients) includes patients with adenocarcinoma metastasis to the liver or other organs, poorly differentiated carcinoma and squamous cell carcinoma of the abdominal cavity ( 1 ). (spandidos-publications.com)
  • Basal cell carcinoma of the right lower lid. (medscape.com)
  • Expression profiles analysis identifies the values of carcinogenesis and the prognostic prediction of three genes in adrenocortical carcinoma. (cancerindex.org)
  • risk of esophageal squamous cell carcinoma. (who.int)
  • A prospective of five cervical cancer screening tests assessed the risk of esophageal squamous cell carcinoma. (who.int)
  • Mesquita HB, Gross M, Helzlsouer K, Jacobs EJ, mous cell carcinoma in a high-risk region in Iran. (who.int)
  • Lung cancer is the first leading diagnosed malignant tumor globally [ 1 ]. (medsci.org)
  • Glioblastoma is an aggressive primary tumor of the central nervous system. (cancernetwork.com)
  • Although DON turned out to be toxic in presence of imatinib, it significantly reduced imatinib withdrawal induced cell death. (rafinhibitors.com)
  • For subcutaneous tumors, injection of CDC2-shRNA retroviruses significantly decreased tumor weight and volume compared with control. (biomedcentral.com)
  • 0.05) frequencies were significantly increased in TMB-H tumors. (duke.edu)
  • In particular, the loss of ALKBH6 in human pancreatic cancer cells increases alkylating agent-induced DNA damage and significantly decreases cell survival. (frontiersin.org)
  • However, some immune cells are immunosuppressive or transform into immunosuppressive phenotypes under specific conditions, leading to the development of radioresistance. (nature.com)
  • 4 According to the number of tumor-infiltrating lymphocytes, tumors can be divided into three phenotypes: immune-inflamed, immune-excluded, and immune-desert types. (nature.com)
  • Immune-inflamed tumors are called hot tumors, while the latter two are collectively referred to as cold tumors, and they respond poorly to immunotherapy. (nature.com)
  • One study reported an increased survival benefit with simultaneous RT compared with sequential administration, 8 while another study found no significant difference between the two strategies, 9 possibly because simultaneous RT plus immunotherapy and the administration of an ICI before RT may kill cancer cells as well a substantial number of immune cells, leading to poor systemic response and toxic side effects. (nature.com)
  • STARD14 was negatively associated with the infiltration of CD8+T cells, while positively with CCL28 and immune checkpoints, including CTLA4 as well as PD-L2. (medsci.org)
  • IHC was performed for PD-L1 (Ventana SP142 ≥1% immune cells). (duke.edu)
  • Inflammasome signaling is a reaction cascade that influences immune response and cell death. (thno.org)
  • Cancer cells often present neoantigens on their cell surface that can be detected as "non-self" by the immune system, resulting in an attack by the immune system. (msdmanuals.com)
  • MDM2 binds to and inhibits TP53 activity. (medscape.com)
  • p53 represses the promoter of Polo-like kinase 1, whereas Polo-like kinase 1 inhibits p53 and its family members p63 and p73 in cancer cells lacking functional p53. (oncotarget.com)
  • p53-mediated ferroptosis is required for its tumor suppression in mouse models. (nature.com)
  • What is the physiological ferroptosis inducer(s) for p53 during tumor suppression? (nature.com)
  • With regards to treatment, the role of surgical resection, radiotherapy, chemotherapy, and tumor-treating fields will be presented. (cancernetwork.com)
  • 4. Department of Radiotherapy, The Affiliated Tumor Hospital of Guangxi Medical University, Nanning, China. (thno.org)
  • On the other hand, LTR-retrotransposons, so called mammalian apparent LTR retrotransposons (MaLRs) represent 3.6% of the genome and lack primer binding sites and gag-pol genes ( 1 ). (frontiersin.org)
  • Clear cell, papillary cell, and chromophobe renal cell carcinomas (RCCs) have now been well characterised thanks to large collaborative projects such as The Cancer Genome Atlas (TCGA). (springer.com)
  • Overall, our data suggest that ALKBH6 is required to maintain the integrity of the genome and promote cell survival of pancreatic cancer cells. (frontiersin.org)
  • The analyzed gene datasets were downloaded from the Gene Expression Omnibus and The Cancer Genome Atlas (TCGA) database. (cancerindex.org)
  • A total of 9881 patients across 33 tumor types from The Cancer Genome Atlas database were included in this study. (thno.org)
  • In contrast to normal cells, most cancer cells predominantly produce energy by a high rate of glycolysis followed by lactate fermentation, even in the presence of oxygen, a less efficient metabolism compared to a low rate of glycolysis followed by mitochondrial oxidation of pyruvate [ 2 ]. (hindawi.com)
  • The current models for CIN involve telomere dysfunction, defective spindle assembly, sister chromatid cohesion, DNA double-strand breaks (DSB) repair, genes involved in the cell cycle, and epigenetic regulators. (encyclopedia.pub)
  • The top 14 hub genes were subsequently confirmed by reverse transcription‑quantitative polymerase chain reaction in ACC and adrenocortical adenoma samples. (cancerindex.org)
  • It was identified that the nuclear division cycle 80, cyclin B2 and topoisomerase 2‑α may serve important roles in adrenocortical tumor development. (cancerindex.org)
  • Glioblastoma, previously known as glioblastoma multiforme, is the most aggressive among infiltrative gliomas, a group of primary tumors arising from the central nervous system (CNS). (cancernetwork.com)
  • Postoperative radiation can also be a useful adjunct when patients have aggressive tumors that were treated surgically or when surgery has failed to clear the margins of the tumor. (medscape.com)
  • The activity of these genes may help to guide treatment decision for non-metastatic cancer with the choice for non-aggressive versus debilitating aggressive options. (mdpi.com)
  • microRNAs have emerged as master regulators of stem cell lineage differentiation and angiogenesis [ 14 ]. (biomedcentral.com)
  • Using ex vivo models of primary MCL cells (n=23), we demonstrated that, through the secretion of IL32β, the tumor was able to polarize monocytes into specific MCL-associated macrophages, which in turn favor tumor survival. (haematologica.org)
  • We highlighted that while IL32β-stimulated macrophages secreted several protumoral factors, they supported tumor survival through a soluble dialog, mostly driven by BAFF. (haematologica.org)
  • This study supports ERV-K env as a single prognostic indicator for better survival of RCC, which we propose represents a new tumor antigen. (frontiersin.org)
  • Following ex vivo study, viral particles containing small interfering RNA for CDC2 were subsequently injected into xenogeneic graft tumor of nude mice and the weight of human glioma xenografts, survival and resulting phenotypic changes of target gene were investigated. (biomedcentral.com)
  • To correlate levels of baseline circulating tumor cells (CTCs) with survival in untreated patients. (bcan.org)
  • The unique course of the disappearance of the effusion and the absence of tumor in the adnexa might be associated with the high immunogenicity of the tumor characterized by the high TMB. (spandidos-publications.com)
  • What this means for cells is that they divide continuously even in the absence of any signals telling them to divide. (cancerquest.org)
  • This gene, which encodes a member of the serine/threonine kinase family, regulates cell polarity and functions as a tumor suppressor. (cancerindex.org)
  • This gene encodes a DNA topoisomerase, an enzyme that controls and alters the topologic states of DNA during transcription. (cancerindex.org)
  • HER2/neu (also called ERB B2 ) is the gene that encodes the human epidermal growth factor receptor type 2. (cancerquest.org)
  • Alpha-ketoglutarate-dependent dioxygenase (ALKBH) is a DNA repair gene involved in the repair of alkylating DNA damage. (frontiersin.org)
  • Among these unconventional activities, an iron-dependent form of non-apoptotic cell death, termed ferroptosis, attracts great interest. (nature.com)
  • The cell division process is dependent on a tightly controlled sequence of events. (cancerquest.org)
  • These events are dependent on the proper levels of transcription and translation of certain genes. (cancerquest.org)
  • TP53 -mutated acute myeloid leukemia (AML) and myelodysplastic syndromes (MDS) are among the myeloid malignancies with the poorest prognosis. (mdpi.com)