Chromosome tumor suppressor protein p53. Medical search. Frequent questions

Point mutations in K-ras and p53 were studied by PCR restriction fragment length polymorphism analysis and DNA sequencing. (cdc.gov)
There were no point mutations observed in codons 12, 13, and 61 of K-ras or in exons 4-10 of p53 and no observed differences in the levels of any of the proteins studied. (cdc.gov)
Scope includes mutations and abnormal protein expression. (cancerindex.org)
Our recent report indicated that tumor suppressor gene ( p53 ) mutations and protein aberrant expression were detected in pterygium. (molvis.org)
TP53 mutations define a maladaptive pathway with enhanced leukemic potential by inactivating tumor suppressor checkpoints without correcting the ribosome defect. (nature.com)
The majority of classical LFS families harbour germline mutations of the p53 tumour suppressor gene. (bmj.com)
These had all been previously screened for the presence of p53 mutations in exons 2 and 4-11 by single strand conformational polymorphism (SSCP) analysis and DNA sequencing as previously described. (bmj.com)
These molecules are able to oxidize cellular macromolecules and DNA, potentially resulting in damage and mutations to proteins and genes that usually manage cell growth, proliferation or apoptosis. (5dok.net)
Mistakes in the duplication or distribution of the chromosomes lead to mutations that may be passed forward to every new cell produced from an abnormal cell. (openstax.org)
In addition, it has to be emphasized, that stromal cells, lymphocytes and endothelial cells in the clinical samples are essential as internal positive tissue controls especially for carcinomas with TP53 mutations causing absence and loss of p53 expression in the tumour cells. (nordiqc.org)
Clinical implications of p53 mutations in lung cancer. (nordiqc.org)
Mutations in cis-acting splicing elements or changes in the activity of constitutive or alternative splicing could have a profound regulatory proteins that compromise the accuracy of either impact on human pathogenesis, in particular in tumor development and progression. (biologists.com)
These data suggest that TP53 mutations may play a role in astrocytoma development and are predominantly associated with higher grade tumors. (nih.gov)
Most of these mutations lead to production of little or no functional p16(INK4A) protein. (medlineplus.gov)
The CDKN2A gene mutations found in melanoma result in a nonfunctional p16(INK4A) protein. (medlineplus.gov)
Together, the germline and somatic mutations impair the function of proteins that regulate division and senescence, leading to uncontrolled cell growth and the formation of a melanoma. (medlineplus.gov)
CDKN2A gene mutations involved in cancer impair production of functional p16(INK4A) or, less commonly, p14(ARF), which can result in uncontrolled cell growth and tumor formation. (medlineplus.gov)

Scholars@Duke publication: Chromosome end-to-end associations and telomerase activity during cancer progression in human cells after treatment with alpha-particles simulating radon progeny. (duke.edu)
Chromosome end-to-end associations seen at metaphase involve telomeres and are commonly observed in cells derived from individuals with ataxia telangiectasia and most types of human tumors. (duke.edu)
however, it is not clear why some immortal cells display chromosome end-to-end associations. (duke.edu)
In the present study we evaluated chromosome end-to-end associations, telomere length and telomerase activity with the tumorigenic status of human bronchial epithelial cells immortalized with human papillomavirus. (duke.edu)
The fewest chromosome end associations and lowest telomerase activity were observed in the parental immortalized cells. (duke.edu)
The tumorigenic cells that were telomerase positive and had the highest frequency of cells with chromosome end-to-end associations were also metastatic. (duke.edu)
Remarkably, increases in chromosome copy number, multinucleation, and cytokinesis failure are also promoted while MCT-1 is induced in p53-deficient cells. (tmu.edu.tw)
Given a p53-silencing background, MCT-1 malignantly transforms normal breast epithelial cells that are satisfactory for stimulating cell migration/ adhesion and tumorigenesis. (tmu.edu.tw)
Detailed analyses of MCT-1 oncogenicity in H1299 p53-null lung cancer cells have shown that ectopically expressed MCT-1 advances xenograft tumorigenicity and angiogenesis, which cannot be completely suppressed by induction of p53. (tmu.edu.tw)
Sarcomatoid renal cell carcinoma (SRCC) is currently defined in the 2004 World Health Organization (WHO) classification of renal tumors as any histologic type of renal cell carcinoma (RCC) containing foci of high-grade malignant spindle cells. (medscape.com)
Focal spindling due to noncohesion of tumor cells is not considered to represent sarcomatoid differentiation. (medscape.com)
however, occasional tumors composed entirely of rhabdoid cells have been described in which no RCC component is detected despite extensive sampling. (medscape.com)
RR CC was named for its morphologic resemblance to pediatric malignant rhabdoid tumor (MRT) of the kidney, which is a highly aggressive tumor characterized by cells that resemble rhabdomyoblasts and by genetic alterations involving chromosome 22, particularly the hSNF5/INI1 gene on 22q11.2. (medscape.com)
It is recommended to add 0.1 mL of RIPA Lysis Buffer to each well of a 6-well plates (the protein content in different cells may vary, and the volume of the lysate added can be appropriately adjusted). (elabscience.com)
Fgf overexpression or ectodermal wounding, both of which potently activate Erk, reduce Cic protein levels in embryonic cells. (bvsalud.org)
This may be due to the fact that elephants contain 20 copies of p53, making apoptosis much more likely, whereas humans only possess one copy of p53 in their genetic code, which means that human cells are less likely to trigger apoptosis upon DNA damage, increasing the likelihood of cancer. (longevitywiki.org)
It turned out that old cells, on the one hand, act as tumor suppressors (since they irreversibly stop dividing themselves and reduce the risk of transformation of surrounding cells), and on the other hand, the specific metabolism of old cells can cause inflammation and degeneration of neighboring precancerous cells into malignant ones. (vechnayamolodost.ru)
Tax-expressing cells also exhibit nuclear morphological aberrancy, frequent multinucleation, aneuploidy, and loss of function of the tumor suppressor protein p53. (nih.gov)
The chromosomal constitution of cells which deviate from the normal by the addition or subtraction of CHROMOSOMES, chromosome pairs, or chromosome fragments. (lookformedical.com)
A type of CELL NUCLEUS division by means of which the two daughter nuclei normally receive identical complements of the number of CHROMOSOMES of the somatic cells of the species. (lookformedical.com)
These changes can be inherited and are, therefore, found in every cell, but more often, they are somatically acquired and restricted to tumor cells. (medscape.com)
Lymph accumulates in the tiny spaces between tissue cells and contains proteins, fats, and certain white blood cells known as lymphocytes. (rarediseases.org)
Chromosomal double-strand breaks (DSBs) occurring in mammalian cells can initiate genomic instability, and their misrepairs result in chromosomal deletion, amplification, and translocation, common findings in human tumors. (soken.ac.jp)
In contrast, no chromosomal alterations were observed in TK-deficient mutants from TK6-20C cells expressing wild-type p53. (soken.ac.jp)
In wild-type p53 cells, spontaneous DSBs appear to be promptly repaired through recombination between homologous chromosomes. (soken.ac.jp)
In addition, NK cells stimulated with lunasin plus cytokines displayed higher tumoricidal activity than those stimulated with cytokines alone using in vitro and in vivo tumor models. (weeksmd.com)
Eukaryotic expression vectors containing genes encoding plant proteins for killing of cancer cells. (weeksmd.com)
consequently, genes encoding some of these proteins are being used to design constructs for the inhibition of multiplying cancer cells. (weeksmd.com)
The p53 (phospho-)protein (p53), 53 kDa, is expressed in the nuclei of all normal cells, but usually not immunohistochemically detectable due to a very short half-life (10-20 min. (nordiqc.org)
Normal (wild type - WT) p53 is accumulated in damages cells, e.g., in virus infections, where the protein is bound (e.g., to protein E6 of human papilloma virus) and prevented from break down. (nordiqc.org)
Marked p53 accumulation (at least 20-50% of the cells stained) largely reflects an underlying mutation. (nordiqc.org)
As a guideline for an accurate p53 IHC test more than 20% of germinal centre B-cells must show a weak to moderate nuclear staining reaction, while less than 10% of the mantle zone B-cells should be demonstrated in tonsil. (nordiqc.org)
In this study, we examined whether normal human cells could tolerate telomere uncapping and showed that p53 wild-type diploid cells reacted but rapidly adapted to telomere uncapping," the authors noted. (genengnews.com)
Myeloma cells produce harmful proteins that can cause kidney damage and even failure. (healthline.com)
Doctors diagnose multiple myeloma when there is evidence of a plasma cell tumor or a minimum of 10 percent of plasma cells in the bone marrow. (healthline.com)
i.e ., radiation or chemotherapy) provide temporary palliation, but eventually prostate cancer cells become resistant to chemotherapy and radiation, with ensuing failure to control tumor growth. (aacrjournals.org)
ARA55, ARA54, ARA70, BRCA1, and heat-shock proteins) may allow cells to become independent of androgens (intrinsic activation). (aacrjournals.org)
Here, we show that chronic (6-month) exposure of human lung epithelial cells to single-walled (SW) CNTs at the workplace-relevant concentration induced an emergence of lung CSCs, as indicated by the induction of CSC tumor spheres and side population (SP). (oncotarget.com)
Using gene manipulation strategies, we reveal for the first time that Cav-1 plays an essential role in CSC regulation and aggressiveness of SWCNT-transformed cells partly through p53 dysregulation, consistent with their suggested role by microarray and gene ontology analysis. (oncotarget.com)
Evolving research in stem cells and cancer biology have provided strong evidence for the existence of cancer stem cells (CSCs) in various human solid tumors, including brain, breast, bone marrow, prostrate, colon, and lung [ 3 , 4 ]. (oncotarget.com)
Both function as tumor suppressors, which means they keep cells from growing and dividing too rapidly or in an uncontrolled way. (medlineplus.gov)
Both proteins are also involved in stopping cell division in older cells (senescence). (medlineplus.gov)
The p14(ARF) and p53 proteins are often made in cells that are unable to undergo cell division. (medlineplus.gov)
Without p16(INK4A) to regulate cell growth and division (proliferation), cells can continue to grow and divide without control, which can lead to tumor formation. (medlineplus.gov)
Without one of these tumor suppressors, cells can grow and divide unchecked, leading to the development of cancer. (medlineplus.gov)
Initial exponential tumor growth is followed by a plateau phase when cell death nearly equals the rate of formation of daughter cells. (msdmanuals.com)
Small tumors have a greater percentage of actively dividing cells than do large tumors. (msdmanuals.com)
GEP analyses were performed on highly purified, flow-cytometry sorted tumor-cells from eight subgroups of BCLs. (lu.se)
This enabled identification of TFs that can be uniquely associated to the tumor cells of chronic lymphocytic leukemia (CLL), diffuse large B-cell lymphoma (DLBCL), follicular lymphoma (FL), hairy cell leukemia (HCL), and mantle cell lymphoma (MCL). (lu.se)

In case repair is not possible, p53 induces apoptosis. (nordiqc.org)
These CSCs, which were found to overexpress tumor promoter caveolin-1 (Cav-1), displayed aggressive cancer phenotypes of apoptosis resistance and enhanced cell invasion and migration compared with their non-CSC counterpart. (oncotarget.com)
The p53 protein is an important tumor suppressor that is essential for regulating cell division, senescence, and self-destruction (apoptosis). (medlineplus.gov)

HspA9 is located on chromosome 5, band q31, a region thatis often deleted in myeloid leukemias and myelodysplasia, making it a candidate tumor suppressor gene. (qedbio.com)
This region contains a candidate tumor suppressor gene, TP53, which has recently been implicated in the etiology of a broad array of human cancers. (nih.gov)

The biological role and underlying mechanism of action of zinc-finger protein 326 (ZNF326) in malignant tumors, including breast cancer, are still not clear. (cancerindex.org)
Head and neck cancer encompasses malignant tumors arising within the upper aerodigestive tract. (cancernetwork.com)
[ 4 , 5 ] ) Benign neoplasms occur more frequently in women than in men, but malignant tumors are distributed equally between the sexes. (medscape.com)

An increased tendency to acquire CHROMOSOME ABERRATIONS when various processes involved in chromosome replication, repair, or segregation are dysfunctional. (lookformedical.com)
Chromosome aberrations may result in CHROMOSOME DISORDERS. (lookformedical.com)
or other CHROMOSOME BREAKAGE related aberrations. (lookformedical.com)
Cytogenetic analysis of LOH mutants by chromosome painting indicated a mosaic of chromosomal aberrations involving chromosome 17, in which partial chromosome deletions, amplifications, and multiple translocations appeared heterogeneously in a single mutant. (soken.ac.jp)
We speculate that spontaneous DSBs trigger the breakage-fusion bridge cycle leading to such multiple chromosome aberrations. (soken.ac.jp)
To study the possible role of TP53 in astrocytoma development, 24 randomly chosen human astrocytic tumors were examined for genomic TP53 sequence aberrations using primer-directed DNA amplification in conjunction with direct sequencing. (nih.gov)

Six proto-oncogenes (K-ras, c-myc, c-fos, c-jun, c-sis, and erbB), as well as the p53 tumor suppressor, were investigated for gene amplification using differential polymerase chain reaction (PCR), while the expression of the proteins produced by these genes was evaluated by Western blot analysis. (cdc.gov)
Chromosome painting was performed to confirm that this amplification was not simply due to additional copies of the chromosomes carrying these oncogenes. (cdc.gov)
The review highlights the discovery of oncogenes and suppressor tumor genes, underlining the crucial role of these achievements in cancer diagnosis and therapies. (jcancer.org)
In addition, these alterations affect 3 principal categories of genes, as follows: proto-oncogenes, tumor suppressor genes, and DNA repair genes. (medscape.com)
This article briefly discusses tumor suppressor genes and then focuses on the role of proto-oncogenes in childhood cancer. (medscape.com)

HspA9 suppresses nuclear translocation, transcriptional activation, and control centrosome-duplication functions of p53. (qedbio.com)

MCT-1 oncoprotein accelerates p53 degradation by means of the ubiquitin-dependent proteolysis. (tmu.edu.tw)
This ARF product functions as a stabilizer of the tumor suppressor protein p53 as it can interact with, and sequester, the E3 ubiquitin-protein ligase MDM2, a protein responsible for the degradation of p53. (rc-crispr.com)
ATR-Chk1-mediated protein degradation of Cdc25A protein phosphatase is also a mechanism conferring intra-S-phase checkpoint activation. (kegg.jp)
MicroRNAs (miRNAs) are small, noncoding RNAs that bind to the 3' UTR of target mRNAs, and silence gene expression by inducing degradation of target mRNAs or inhibition of protein translation [ 10 ]. (cdc.gov)

The levels of p53 mRNA are comparatively reduced in a subset of cancer specimens, which highly present MCT-1 mRNA. (tmu.edu.tw)
Cancer has been in existence on Earth even before the appearance of man, as evidenced by paleontological findings of tumors in animals ( 1 , 2 ). (jcancer.org)
P53 helps regulate cell growth and repair, and its loss of function is associated with negative outcomes in cancer patients. (longevitywiki.org)
p16 INK4a is a candidate gene that could account for the cancer predisposition in p53 wild type LFS families. (bmj.com)
In view of the comparable biological and phenotypic features of p53 and p16 INK4a inactivation, we proposed that germline inactivation of the p16 INK4a gene could account for the predisposition to cancer development in a proportion of LFS families that harboured wild type p53 . (bmj.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)
Immunostimulatory cytokines can enhance anti-tumor immunity and are part of the therapeutic armamentarium for cancer treatment. (weeksmd.com)
The fact that XPO1 and other essential nucleo-cytoplasmatic transport proteins are over expressed in cancer, specifically in melanoma, offers the opportunity to treat cancer by modulating this transport system. (massgeneral.org)
Changes in the p53 gene is one of the most common genetic changes associated with cancer, being implicated in a wide range of tumour types. (nordiqc.org)
P53 is the strongest predictor of survival in high-risk primary breast cancer patients undergoing high-dose chemotherapy with autologous blood stem cell support. (nordiqc.org)
Bortezomib has been studied extensively in vitro and in vivo , and anticancer activity has been seen in cell and animal models for several solid tumor types, including prostate cancer. (aacrjournals.org)

18-20 p16 INK4a shares functional similarities with p53 in that it blocks progression through the cell cycle at G1/S by inhibiting CDK 4/6 mediated phosphorylation of Rb. (bmj.com)
In spite of the structural and functional differences, the CDK inhibitor isoforms and the ARF product encoded by this gene, through the regulatory roles of CDK4 and p53 in cell cycle G1 progression, share a common functionality in cell cycle G1 control. (rc-crispr.com)
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)
The availability of a sophisticated genetic tool box makes Drosophila an excellent genetic model well suited to studying the biology of Lunasin and its effect on tumor progression in an in vivo model organism. (weeksmd.com)
These CSCs are potential driving force of tumor initiation and progression due to their self-renewal and tumorigenic properties [ 5 , 6 ]. (oncotarget.com)

In this study, we demonstrate that the deficiency of wild-type p53 protein may allow unrepaired DSBs to initiate chromosomal instability. (soken.ac.jp)
p53 binding decreases its control with cell proliferation and increases genetic instability, leading to neoplastic transformation. (nordiqc.org)
Mutated p53 shows impaired DNA-binding and, consequently, release from cell cycle checkpoint control following DNA damage, thereby increasing genomic instability and promoting gene amplification. (nordiqc.org)
We demonstrate that replicative senescence, a tumor suppressor mechanism and guardian of genome stability, sometimes requires genomic instability to initiate its own action," the authors said. (genengnews.com)

p53 is called the guardian of the genome. (nordiqc.org)
Also unknown is why telomeric uncapping which is considered a DNA double stranded break does not stably activate the "guardian of the genome," a tumor suppressor protein called p53. (genengnews.com)

This gene is frequently mutated or deleted in a wide variety of tumors, and is known to be an important tumor suppressor gene. (rc-crispr.com)

A combination of genetic events that affects both alleles (e.g., deletion of one allele and point mutation of the other) causes loss of WT p53. (nordiqc.org)

This theory has been confirmed by genetic studies such as analysis of X-chromosome inactivation patterns, which indicated a clonal origin for both the epithelial and sarcomatoid components of CCRCCs with sarcomatoid differentiation. (medscape.com)
Inactivation of p53 by Human papillomavirus (HPV) 16/18 E6 plays a crucial role in cervical tumorigenesis. (molvis.org)
In this study, we further speculate that p53 inactivation may be linked with HPV infection in pterygium pathogenesis. (molvis.org)
To investigate the involvement of HPV 16/18 E6 in p53 inactivation in pterygium, the association between HPV 16 or HPV 18 infection, the HPV E6 oncoprotein, and p53 protein expression was analyzed in this study. (molvis.org)
HPV 16/18 E6 contributes to HPV-mediated pterygium pathogenesis as it is partly involved in p53 inactivation and is expressed in HPV DNA-positive pterygium. (molvis.org)
8 9 This lack of an absolute phenotype:genotype concordance could be attributed to incomplete screening of the p53 gene, inactivation of the p53 protein through interaction with other cellular proteins or viruses, or defects in other genes involved in p53 mediated cell cycle regulatory pathways. (bmj.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)

The viral E2 protein regulates transcription of E6 and E7 and thereby has an indirect effect on cell proliferation. (bris.ac.uk)
Abdul Hamid, N, Brown, C & Gaston, K 2009, ' The regulation of cell proliferation by the papillomavirus early proteins ', Cellular and Molecular Life Sciences , vol. 66 (10), pp. 1700 - 1717. (bris.ac.uk)
[1] Depending on the type of stress, p53 can either temporarily halt cell growth and initiate repair or permanently stop cell proliferation. (longevitywiki.org)
Background HspA9, a memer of the Hsp70 family, encodes a heat-shock cognate protein that is involved in the control of cell proliferation and acts as a chaperone. (qedbio.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)

Double-strand break (DSB) repair protein involved in response to DNA damage, telomere dynamics and class-switch recombination (CSR) during antibody genesis. (cusabio.com)

Genetic abnormalities commonly found in MEITL that do have potentially pro-malignant effects include: Losses on the short (i.e. "p") arm around position 21.3 on one of the two inherited chromosomes 9. (wikipedia.org)
p53 in nonneoplastic central nervous system lesions: an immunohistochemical and genetic sequencing study. (nordiqc.org)
Recent molecular genetic analyses of astrocytomas have demonstrated frequent chromosome 17 deletions involving the telomeric region of the short arm (17p12-pter). (nih.gov)

The p53 protein, encoded by TP53 gene, is a specific transcription factor consisting of 393 amino acids with 7 functional domains from N‐terminal to C‐terminal, transactivation domain (TAD)‐1, TAD‐2, proline‐rich domain (PRD), DNA‐binding domain (DBD), hinge domain (HD), oligomerization domain (OD), and C‐terminal regulatory domain (CTR). (longevitywiki.org)
[1] The human gene encoding the p53 protein is called TP53 (italics indicate that this is the name of a gene, not a protein), and includes 11 exons and 10 introns. (longevitywiki.org)
For example, the TP53 gene, located on chromosome 17, encodes a 53-kd nuclear protein that functions as a cell cycle checkpoint. (medscape.com)
[ 2 ] Targeted disruption of TP53 in the mouse leads to the development of various tumors (see image below). (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 Tax protein has pleiotropic effects on host-cell gene expression and activates several pathways such as the cyclic AMP responsive binding protein (CREB), the nuclear factor kappa-B (NF-κB), the cyclin-dependant kinases (CDKs), and the Akt pathways. (nih.gov)
The Tax protein has pleiotropic effects on host-cell gene expression and activates several pathways such as the cyclic AMP responsive binding protein (CREB), the nuclear factor kappa-B, the cyclin-dependant kinases (CDKs), and the Akt pathways. (nih.gov)
Protein transport between the nuclear and the cytoplasmic compartment is a key factor for cell viability and proliferation. (massgeneral.org)

HPV 16/18 infection was detected by nested-polymerase chain reaction (nested-PCR), the p53 mutation was detected by direct sequencing, and the p53 and the HPV 16/18 E6 proteins were studied using immunohistochemistry on 129 pterygial specimens and 20 normal conjunctivas. (molvis.org)
In addition, p53 protein negative expression in pterygium was correlated with HPV16/18 E6 oncoprotein expression but not with a p53 mutation. (molvis.org)
In this report, we analyzed p53 protein expression and gene mutation in pterygium in comparison with HPV 16/18 infection and E6 oncoprotein expression in pterygium tissues to understand whether the HPV infection was involved in pterygium pathogenesis. (molvis.org)
Abrogation of p53 function by E6 resulted in an increase in the spontaneous mutation frequencies at the heterozygous thymidine kinase (TK) locus but not at the hemizygous hypoxanthine phosphoribosyl transferase (HPRT) locus. (soken.ac.jp)

Targeting the p53 signaling pathway in cancers: Molecular mechanisms and clinical studies. (longevitywiki.org)

In humans, this gene is located on chromosome 17 (17p13.1). (longevitywiki.org)
The p53 gene is a tumour suppressor gene located on the short arm of chromosome 17 (17p13.1). (nordiqc.org)

It is located on chromosome 9p21 and its three exons encode a 156 amino acid, 15.8 kDa protein. (bmj.com)

p53 and its transcriptional targets play an important role in both G1 and G2 checkpoints. (kegg.jp)
p53 acts a two checkpoints in the cell cycle, between G1 and S, and between G2 and M, respectively. (nordiqc.org)

In HPV-induced tumours, misappropriate random integration of the viral genome into the host chromosome often leads to disruption of the E2 gene and the loss of E2 expression. (bris.ac.uk)

[ 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)
B-cell lymphomas (BCLs) constitute a diverse set of tially identify new functional, diagnostic, and therapeutic tumors, both morphologically and clinically, that are mainly targets. (lu.se)

MCT-1 counteracts mutually with p53 at transcriptional levels. (tmu.edu.tw)

Also the over-expression of mdm2 protein arrests the p53 turnover. (nordiqc.org)

Currently, the 2004 WHO classification of renal tumors recognizes this transformation as "sarcomatoid change" or "sarcomatoid features" arising within RCC, rather than as a separate histologic entity. (medscape.com)
One such study found an apparent association between the level of expression of transformation related protein 53 ( TRP53 ) mRNA and the normality of embryo morphology [ 1 ]. (biomedcentral.com)

Our results indicate that synergistic promotions of chromosomal imbalances and oncogenic potency as a result of MCT-1 expression and p53 loss play important roles in tumor development. (tmu.edu.tw)
Analysis of p53 in dysplastic and neoplastic states is a powerful tool to provide molecular information on the oncogenic process. (nordiqc.org)
Depending on the context and the cell is type they are expressed, one can view miRNA oncogenic or tumor suppressor activity. (bvsalud.org)

1 Neoplasms, or more commonly tumors, are the result of aberrant growth of tissue. (5dok.net)

It is a tumor suppressor that is coded by the most often mutated gene in human cancers. (longevitywiki.org)
In contrast to other Cetacea, Balaena mysticetus had a unique leucine substitution in the proline-rich region, corresponding to amino acid residue 77 in human p53. (longevitywiki.org)
The p53 protein from this species had additional serine and arginine residues in the core domain (corresponding to an insertion after amino acid L188 in human p53), which had a deleterious effect on p53 functionality. (longevitywiki.org)
These two species share a unique arrangement in the p53 DNA-binding region, with the insertion of seven amino acid residues in the central DNA-binding region (following amino acid 295 in the human p53 canonical sequence). (longevitywiki.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)
Astrocytomas, including the most malignant form, glioblastoma multiforme, are the most frequent and deadly primary tumors of the human nervous system. (nih.gov)

By binding to DNA, the normal p53 negatively regulates cell growth and division. (nordiqc.org)

At least three alternatively spliced variants encoding distinct proteins have been reported, two of which encode structurally related isoforms known to function as inhibitors of CDK4 kinase. (rc-crispr.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)
The p16(INK4A) protein attaches (binds) to two other proteins called CDK4 and CDK6. (medlineplus.gov)

Treatment of murine macrophages (J774A.1) with Mitsui-7 MWCNTsincreased the expression of Alox5 mRNA and protein in a concentration- and time-dependent manner. (cdc.gov)

In dysplastic lesions, e.g., in Barrett's esophagus, p53 expression increases the risk of carcinoma. (nordiqc.org)
That is, as the size of the gland decreases, the incidence of malignancy of a tumor in the gland increases in approximately these proportions. (medscape.com)

These proteins help regulate the cell cycle, which is the cell's way of replicating itself in an organized, step-by-step fashion. (medlineplus.gov)

In response to DNA damage, the checkpoint kinase ATM phosphorylates and activates Chk2, which in turn directly phosphorylates and activates p53 tumor suppressor protein. (kegg.jp)

Plays a key role in the repair of double-strand DNA breaks (DSBs) in response to DNA damage by promoting non-homologous end joining (NHEJ)-mediated repair of DSBs and specifically counteracting the function of the homologous recombination (HR) repair protein BRCA1. (cusabio.com)

p53 in senescence-it's a marathon, not a sprint. (longevitywiki.org)

Both p53 wild type and p53 mutant samples were included in the p16 INK4a analysis to determine whether germline alterations of one gene precluded the occurrence of alterations of the other. (bmj.com)

The multiple mechanisms that regulate p53 activity and cell fate. (longevitywiki.org)
In order to protect against itself, special cellular mechanisms of tumor suppression have formed in the body. (vechnayamolodost.ru)

1. According to the molecular weight of the target protein, prepare 0% separation gel. (elabscience.com)
Add the test sample to each well, and add 5 μL of Pre-stained Protein Marker ( Cat# E-BC-R273 )to a reserved well in order to verify the target molecular weight and the extent of membrane transfer. (elabscience.com)
1. Choose the PVDF Membrane (Cat# E-BC-R266 ) with a pore size of μm according to the molecular weight of the target protein. (elabscience.com)

6. Redwood AJ, Masters LL, Chan B, Leary S, Forbes C, Jonjić S, Juranić Lisnić V, Lisnić B, Smith LM: Repair of an attenuated low passage murine cytomegalovirus bacterial artificial chromosome identifies a novel spliced gene essential for salivary gland tropism. (com.hr)
Although researchers have learned much from the study of this diverse group of tumors over the years, the diagnosis and treatment of salivary gland neoplasms remain complex and challenging problems for the head and neck surgeon. (medscape.com)
Salivary gland neoplasms make up 6% of all head and neck tumors. (medscape.com)
In children and adolescents, salivary gland tumors make up 0.5% of all malignancies. (medscape.com)
Almost half of all submandibular gland neoplasms and most sublingual and minor salivary gland tumors are malignant. (medscape.com)
Successful diagnosis and treatment of patients with salivary gland tumors require a thorough understanding of tumor etiology, biologic behavior of each tumor type, and salivary gland anatomy. (medscape.com)

The most common tumor of the parotid gland is the pleomorphic adenoma , which represents about 60% of all parotid neoplasms, as seen in the table below. (medscape.com)

This recombinant protein was biotinylated in vivo by AviTag-BirA technology, which method is BriA catalyzes amide linkage between the biotin and the specific lysine of the AviTag. (cusabio.com)

In a normally diploid cell (DIPLOIDY) the loss of a chromosome pair is termed nullisomy (symbol: 2N-2), the loss of a single chromosome is MONOSOMY (symbol: 2N-1), the addition of a chromosome pair is tetrasomy (symbol: 2N+2), the addition of a single chromosome is TRISOMY (symbol: 2N+1). (lookformedical.com)

Often p53 positivity is correlated with high grade lesions (e.g., carcinoma of breast, prostate and bladder, malignant lymphoma) and poor prognosis. (nordiqc.org)
A few tumour types are characterised by strong p53 expression in most cases, e.g., uterine papillary serous carcinoma. (nordiqc.org)
In classification of uterine carcinoma, p53 should be included in the panel. (nordiqc.org)
p53 positivity is a parameter in the identification of tubal intraepithelial carcinoma associated with pelvic serous carcinoma. (nordiqc.org)

Is aging a payment for suppressing cancerous tumors? (vechnayamolodost.ru)
This type of cancerous tumor occurs in the moist lining of the mouth, nose, and throat. (medlineplus.gov)

NK activation was evaluated, and its tumoricidal activity was assessed using in vitro and in vivo tumor models. (weeksmd.com)

The abovementioned analysis and some other facts of long-lived organisms in various animal groups led to conclusion that the amino acid sequence of p53 is associated with organismal lifespan. (longevitywiki.org)

Consistent with M1 polarization, the MWCNTs induced the production and secretion of proinflammatory cytokines tumor necrosis factor- and interleukin-1, and proinflammatory LMs leukotriene B4 (LTB4) and prostaglandin E2 (PGE2). (cdc.gov)

10-12 However, in the remaining "classical" LFS families, and in most LFS-L families, no alterations in p53 have been found. (bmj.com)

Our current understanding of cellular aging rests upon the uncapping of the repetitive, non-protein-coding extremities of our linear chromosomes called telomeres. (genengnews.com)

Unlike blood tests that take a liquid sample, a biopsy takes a tissue sample from the tumor, lymph node, or bone marrow. (healthline.com)
However, most GEP studies have typically been performed on whole tissue samples, containing varying degrees of tumor cell content, which results in uncertainties in data analysis. (lu.se)

The role of truncated p53 isoforms in the DNA damage response. (longevitywiki.org)

Anatomy53

Organisms8

Diseases26

Chemicals and Drugs78

Analytical, Diagnostic and Therapeutic Techniques and Equipment25

Phenomena and Processes109

Disciplines and Occupations1

Information Science3

Health Care1

Mutations17

Cells49

Apoptosis3

Candidate tumor supp2

Malignant tumors3

Aberrations6

Oncogenes5

Translocation1

Degradation4

Cancer11

Progression5

Instability4

Guardian of the genome2

Important tumor1

Deletion1

Inactivation7

Cell proliferation4

Genes involved1

Telomere1

Genetic3

TP535

Nuclear3

Mutation4

Signaling pathway1

17p13.12

Exons1

Checkpoints2

Host chromosome1

Functional2

Transcriptional1

Mdm21

Transformation2

Oncogenic3

Aberrant1

Human6

Regulates1

CDK43

MRNA1

Increases2

Regulate the cell cycle1

Phosphorylates1

Recombination1

Senescence1

Germline1

Mechanisms2

Molecular3

Salivary gland6

Neoplasms1

Biotinylated in vivo1

Diploid1

Carcinoma4

Cancerous2

Vivo1

Amino acid1

Cytokines1

Alterations1

Telomeres1

Tissue2

Isoforms1