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Articoli di riviste sul tema "Suppressor cells Identification"

Autore: Grafiati

Pubblicato: 4 giugno 2021

Ultima modifica: 19 febbraio 2022

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1

Bardin, Sylvie D., Ralf T. Voegele, and Turlough M. Finan. "Phosphate Assimilation in Rhizobium(Sinorhizobium) meliloti: Identification of apit-Like Gene." Journal of Bacteriology 180, no. 16 (August 15, 1998): 4219–26. http://dx.doi.org/10.1128/jb.180.16.4219-4226.1998.

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ABSTRACT Rhizobium meliloti mutants defective in thephoCDET-encoded phosphate transport system form root nodules on alfalfa plants that fail to fix nitrogen (Fix−). We have previously reported that two classes of second-site mutations can suppress the Fix− phenotype ofphoCDET mutants to Fix+. Here we show that one of these suppressor loci (sfx1) contains two genes, orfA and pit, which appear to form an operon transcribed in the order orfA-pit. The Pit protein is homologous to various phosphate transporters, and we present evidence that three suppressor mutations arose from a single thymidine d

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2

Powers, Jason G., Tim L. Sit, Feng Qu, T. Jack Morris, Kook-Hyung Kim, and Steven A. Lommel. "A Versatile Assay for the Identification of RNA Silencing Suppressors Based on Complementation of Viral Movement." Molecular Plant-Microbe Interactions® 21, no. 7 (July 2008): 879–90. http://dx.doi.org/10.1094/mpmi-21-7-0879.

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The cell-to-cell movement of Turnip crinkle virus (TCV) in Nicotiana benthamiana requires the presence of its coat protein (CP), a known suppressor of RNA silencing. RNA transcripts of a TCV construct containing a reporter gene (green fluorescent protein) (TCV-sGFP) in place of the CP open reading frame generated foci of three to five cells. TCV CP delivered in trans by Agrobacterium tumefaciens infiltration potentiated movement of TCV-sGFP and increased foci diameter, on average, by a factor of four. Deletion of the TCV movement proteins in TCV-sGFP (construct TCVΔ92-sGFP) abolished the movem

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3

Bedke, Tanja, Sarah Lurati, Claudia Stuehler, Nina Khanna, Hermann Einsele, and Max S. Topp. "Identification and Characterization of Human Aspergillus Fumigatus-Specific Tr1-(Like) Cells." Blood 118, no. 21 (November 18, 2011): 181. http://dx.doi.org/10.1182/blood.v118.21.181.181.

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Abstract Abstract 181 Introduction: The ubiquitous mold Aspergillus fumigatus (A. fumigatus) induces two forms of pathogenesis: invasive aspergillosis in neutropenic patients and allergic aspergillosis in patients with chronic obstructive lung disease as well as in immunosuppressed patients. Mouse models of aspergillosis suggest that not only effector T cells (Teff) but also regulatory T cells (Treg) play a crucial role for the regulation of a protective T cell-mediated immunity to A. fumigatus. However, it is little-known about the involvement of Treg during A. fumigatus infection in humans.

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4

Benni, Mei Li, and Lenore Neigeborn. "Identification of a New Class of Negartive Regulators Affecting Sporulation-Specific Gene Expression in Yeast." Genetics 147, no. 3 (November 1, 1997): 1351–66. http://dx.doi.org/10.1093/genetics/147.3.1351.

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We characterized two yeast loci, MDS3 and PMD1, that negatively regulate sporulation. Initiation of sporulation is mediated by the meiotic activator IME1, which relies on MCK1 for maximal expression. We isolated the MDS3-1 allele (encoding a truncated form of Mds3p) as a suppressor that restores IME1 expression in mck1 mutants. mds3 null mutations confer similar suppression phenotypes as MDS3-1, indicating that Mds3p is a negative regulator of sporulation and the MDS3-1 allele confers a dominant-negative phenotype. PMD1 is predicted to encode a protein sharing significant similarity with Mds3p

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5

He, B., Y. Chiba, H. Li, S. de Vega, K. Tanaka, K. Yoshizaki, M. Ishijima, et al. "Identification of the Novel Tooth-Specific Transcription Factor AmeloD." Journal of Dental Research 98, no. 2 (November 14, 2018): 234–41. http://dx.doi.org/10.1177/0022034518808254.

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Basic-helix-loop-helix (bHLH) transcription factors play an important role in various organs’ development; however, a tooth-specific bHLH factor has not been reported. In this study, we identified a novel tooth-specific bHLH transcription factor, which we named AmeloD, by screening a tooth germ complementary DNA (cDNA) library using a yeast 2-hybrid system. AmeloD was mapped onto the mouse chromosome 1q32. Phylogenetic analysis showed that AmeloD belongs to the achaete-scute complex-like ( ASCL) gene family and is a homologue of ASCL5. AmeloD was uniquely expressed in the inner enamel epitheli

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6

Movahedi, Kiavash, Martin Guilliams, Jan Van den Bossche, Rafael Van den Bergh, Conny Gysemans, Alain Beschin, Patrick De Baetselier, and Jo A. Van Ginderachter. "Identification of discrete tumor-induced myeloid-derived suppressor cell subpopulations with distinct T cell–suppressive activity." Blood 111, no. 8 (April 15, 2008): 4233–44. http://dx.doi.org/10.1182/blood-2007-07-099226.

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Abstract The induction of CD11b+Gr-1+ myeloid-derived suppressor cells (MDSCs) is an important immune-evading mechanism used by tumors. However, the exact nature and function of MDSCs remain elusive, especially because they constitute a heterogeneous population that has not yet been clearly defined. Here, we identified 2 distinct MDSC subfractions with clear morphologic, molecular, and functional differences. These fractions consisted of either mononuclear cells (MO-MDSCs), resembling inflammatory monocytes, or low-density polymorphonuclear cells (PMN-MDSCs), akin to immature neutrophils. Inte

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7

Anger, Natalia, and Joanna Rossowska. "Myeloid-derived suppressor cells as a target for anticancer therapy." Postępy Higieny i Medycyny Doświadczalnej 72 (December 31, 2018): 1179–98. http://dx.doi.org/10.5604/01.3001.0012.8267.

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Myeloid-derived suppressor cells are heterogenic immature myeloid cells, which possess suppressor activity and play an important role in both, tumor progression and metastasis. The accumulation of MDSCs is induced primarily by factors that are secreted by the tumor microenvironment, which disturb myelopoiesis that occurs in the bone marrow and enables the migration of immature myeloid cells into the tumor. MDSCs promote tumor growth by inhibiting the activity of immunocompetent cells, as well as by activating non-immunological processes, such as tumor angiogenesis, the degradation of extracell

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8

Kansa, Geoffrey S., and Edgar G. Engleman. "Phenotypic identification of suppressor-effector, suppressor-amplifier and suppressor-inducer T cells of B cell differentiation in man." European Journal of Immunology 17, no. 4 (1987): 453–57. http://dx.doi.org/10.1002/eji.1830170403.

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9

Zimring, James C., and Judith A. Kapp. "Identification and Characterization of CD8⁺ Suppressor T Cells." Immunologic Research 29, no. 1-3 (2004): 303–12. http://dx.doi.org/10.1385/ir:29:1-3:303.

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10

Blanchard, Thomas G., Steven J. Czinn, Vivekjyoti Banerjee, Neha Sharda, Andrea C. Bafford, Fahad Mubariz, Dennis Morozov, Antonino Passaniti, Hafiz Ahmed, and Aditi Banerjee. "Identification of Cross Talk between FoxM1 and RASSF1A as a Therapeutic Target of Colon Cancer." Cancers 11, no. 2 (February 8, 2019): 199. http://dx.doi.org/10.3390/cancers11020199.

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Metastatic colorectal cancer (mCRC) is characterized by the expression of cellular oncogenes, the loss of tumor suppressor gene function. Therefore, identifying integrated signaling between onco-suppressor genes may facilitate the development of effective therapy for mCRC. To investigate these pathways we utilized cell lines and patient derived organoid models for analysis of gene/protein expression, gene silencing, overexpression, and immunohistochemical analyses. An inverse relationship in expression of oncogenic FoxM1 and tumor suppressor RASSF1A was observed in various stages of CRC. This

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11

Du, Quansheng, Dana Lehavi, Ouriel Faktor, Yipeng Qi, and Nor Chejanovsky. "Isolation of an Apoptosis Suppressor Gene of theSpodoptera littoralis Nucleopolyhedrovirus." Journal of Virology 73, no. 2 (February 1, 1999): 1278–85. http://dx.doi.org/10.1128/jvi.73.2.1278-1285.1999.

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ABSTRACT Spodoptera frugiperda SF9 cells infected with mutants of the Autographa californica nucleopolyhedrovirus (AcMNPV) which lack a functional p35 gene undergo apoptosis, aborting the viral infection. The Spodoptera littoralis nucleopolyhedrovirus (SlNPV) was able to suppress apoptosis triggered by vΔP35K/pol+, an AcMNPVp35 null mutant. To identify the putative apoptotic suppressor gene of SlNPV, overlapping cosmid clones representing the entire SlNPV genome were individually cotransfected along with genomic DNA of vΔP35K/pol+. Using this complementation assay, we isolated a SlNPV DNA frag

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12

Kawamata, Norihiko, Takayuki Saitoh, Sakura Sakajiri, and Phillip H. Koeffler. "Identification of Candidate Tumor Suppressor Genes Silenced Epigenetically in Mantle Cell Lymphoma." Blood 106, no. 11 (November 16, 2005): 3001. http://dx.doi.org/10.1182/blood.v106.11.3001.3001.

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Abstract Many tumor suppressor genes are silenced by epigenetic mechanisms in human cancers, including mantle cell lymphoma (MCL). In this study, we have used a variety of research tools to screen for genes that are epigenetically silenced in MCL. Changes in the global gene expression profile of the MCL cell line, Jeko1, were analyzed after treatment with the combination of the demethylating agent, 5-aza-2′-deoxycytidine, and the histone deacetylase inhibitor, suberoyl anilide bishydroxamide, by DNA microarray technique. By screening over 22,000 genes, we identified 26 candidate tumor suppress

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13

Kass, L. "Identification of lymphocyte subpopulations with a polymethine dye." Journal of Histochemistry & Cytochemistry 36, no. 7 (July 1988): 711–15. http://dx.doi.org/10.1177/36.7.2454984.

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Using the polymethine dye p-ethoxyphenyl-p-aminostyryl-1,3,3-trimethyl-3H-indolium chloride as an aqueous stain applied to specimens of peripheral blood or buffy coat fixed in FAA fixative, differential coloration of leukocytes was achieved using darkfield illumination. Neutrophils stained dark maroon and contained green granules, eosinophils contained bright blue granules, basophils revealed yellow and pink granules, and monocytes stained green with green and yellow vacuoles. In studies of purified lymphocyte subpopulations obtained in a cell sorter, T-helper cells stained red, T-suppressor c

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14

HALWANI, FAWAZ, RONALD D. GUTTMANN, HÉLÈNE STE.-CROIX, and GERALD J. PRUDʼHOMME. "IDENTIFICATION OF NATURAL SUPPRESSOR CELLS IN LONG-TERM RENAL ALLOGRAFT RECIPIENTS." Transplantation 54, no. 6 (December 1992): 973–77. http://dx.doi.org/10.1097/00007890-199212000-00006.

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15

James, P., and B. D. Hall. "ret1-1, a yeast mutant affecting transcription termination by RNA polymerase III." Genetics 125, no. 2 (June 1, 1990): 293–303. http://dx.doi.org/10.1093/genetics/125.2.293.

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Abstract In eukaryotes, extended tracts of T residues are known to signal the termination of RNA polymerase III transcription. However, it is not understood how the transcription complex interacts with this signal. We have developed a selection system in yeast that uses ochre suppressors weakened by altered transcription termination signals to identify mutations in the proteins involved in termination of transcription by RNA polymerase III. Over 7600 suppression-plus yeast mutants were selected and screened, leading to the identification of one whose effect is mediated transcriptionally. The r

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16

Bryant, Andrew, Borna Mehrad, Todd Brusko, James West, and Lyle Moldawer. "Myeloid-Derived Suppressor Cells and Pulmonary Hypertension." International Journal of Molecular Sciences 19, no. 8 (August 3, 2018): 2277. http://dx.doi.org/10.3390/ijms19082277.

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Myeloid–derived suppressor cells (MDSCs) comprised a heterogeneous subset of bone marrow–derived myeloid cells, best studied in cancer research, that are increasingly implicated in the pathogenesis of pulmonary vascular remodeling and the development of pulmonary hypertension. Stem cell transplantation represents one extreme interventional strategy for ablating the myeloid compartment but poses a number of translational challenges. There remains an outstanding need for additional therapeutic targets to impact MDSC function, including the potential to alter interactions with innate and adaptive

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17

Lee, Hansoo, Donghwa Kim, Han C. Dan, Eric L. Wu, Tatiana M. Gritsko, Chuanhai Cao, Santo V. Nicosia, et al. "Identification and Characterization of Putative Tumor Suppressor NGB, a GTP-Binding Protein That Interacts with the Neurofibromatosis 2 Protein." Molecular and Cellular Biology 27, no. 6 (January 8, 2007): 2103–19. http://dx.doi.org/10.1128/mcb.00572-06.

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ABSTRACT Mutations of the neurofibromatosis 2 (NF2) tumor suppressor gene have frequently been detected not only in schwannomas and other central nervous system tumors of NF2 patients but also in their sporadic counterparts and malignant tumors unrelated to the NF2 syndrome such as malignant mesothelioma, indicating a broader role for the NF2 gene in human tumorigenesis. However, the mechanisms by which the NF2 product, merlin or schwannomin, is regulated and controls cell proliferation remain elusive. Here, we identify a novel GTP-binding protein, dubbed NGB (referring to NF2-associated GTP b

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18

Sorensen, C. M., R. J. Hayashi, and C. W. Pierce. "Identification of Igh-C-linked determinants on suppressor T cell hybrids and factors specific for L-glutamic acid60-L-alanine30-L-tyrosine10 (GAT)." Journal of Experimental Medicine 162, no. 3 (September 1, 1985): 1044–59. http://dx.doi.org/10.1084/jem.162.3.1044.

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Hyperimmunization of BALB/c mice with concanavalin A-stimulated blasts from the Ig allotype-congenic strain, C.B20, results in the production of antibodies reactive with T cells in an allotype-restricted manner. Spleen cells from these hyperimmune BALB/c mice were used to generate a panel of hybridomas that secrete monoclonal antibodies, reactive, in an allotype-restricted manner, exclusively with T cells subpopulations, and in particular, reactive with suppressor T cell hybridomas and their secreted soluble factors. Two functional classes of antibodies were identified: those that react with s

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19

Bohana-Kashtan, Osnat, Hyam Levitsky, and Curt I. Civin. "Identification of New Alloantigen-Reactive CD8+ Cytotoxic and Suppressor T Cell Subpopulations." Blood 110, no. 11 (November 16, 2007): 3229. http://dx.doi.org/10.1182/blood.v110.11.3229.3229.

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We sought to develop a better understanding of the T cells involved in the human allogeneic immune response, in order to eventually engineer a donor graft with reduced GVHD-mediating potential, without ablating general immune competence. Prior studies reported that all the activated CD4+ T cells responding to a specific antigen challenge reside within the CD4high population expressing high levels of membrane CD4. We identified a new population of activated CD8+ T cells that developed during an in vitro allogeneic immune response, along with the allo-activated CD4high T cell population. Analogo

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20

Goulart, Michelle R., G. Elizabeth Pluhar, and John R. Ohlfest. "Identification of Myeloid Derived Suppressor Cells in Dogs with Naturally Occurring Cancer." PLoS ONE 7, no. 3 (March 13, 2012): e33274. http://dx.doi.org/10.1371/journal.pone.0033274.

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21

Vincent, Carr D., Benjamin A. Buscher, Jonathan R. Friedman, Lee Anne Williams, Patrick Bardill та Joseph P. Vogel. "Identification of Non-dot/icm Suppressors of the Legionella pneumophila ΔdotL Lethality Phenotype". Journal of Bacteriology 188, № 23 (22 вересня 2006): 8231–43. http://dx.doi.org/10.1128/jb.00937-06.

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ABSTRACT Legionella pneumophila, a causative agent of bacterial pneumonia, survives inside phagocytic cells by avoiding rapid targeting to the lysosome. This bacterium utilizes a type IVB secretion system, encoded by the dot/icm genes, to replicate inside host cells. DotL, a critical component of the Dot/Icm secretion apparatus, functions as the type IV coupling protein. In contrast to most dot/icm genes, which are dispensable for growth on bacteriological media, dotL is required for the viability of wild-type L. pneumophila. Previously we reported that ΔdotL lethality could be suppressed by i

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22

Gabrilovich, Dmitry I. "The Dawn of Myeloid-Derived Suppressor Cells: Identification of Arginase I as the Mechanism of Immune Suppression." Cancer Research 81, no. 15 (August 1, 2021): 3953–55. http://dx.doi.org/10.1158/0008-5472.can-21-1237.

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23

Choi, Jaebok, Julie Ritchey, and John F. DiPersio. "Generation of Treg-Like Cells from CD4+CD25- T Cells Occurs Via Both Foxp3 Dependent and Independent Pathways." Blood 112, no. 11 (November 16, 2008): 813. http://dx.doi.org/10.1182/blood.v112.11.813.813.

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Abstract Regulatory T cells (Treg) contribute to the maintenance of self-tolerance and have been demonstrated to both suppress autoimmune diseases and mitigate GvHD in mouse models. Major obstacles for their routine use in human clinical trials to reduce autoimmunity or GvHD include the low number of Treg found in the peripheral blood in the resting state (5–10% of CD4+ T cells), low yields and efficiencies of purification and severe limitations maintaining suppressor function after ex vivo expansion. The master gene responsible for the normal development and suppressor function of Treg is Fox

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24

Kaufmann, J., G. Pronk, K. Giese, and A. Klippel. "Identification of novel effectors of invasive cell growth downstream of phosphoinositide 3-kinase." Biochemical Society Transactions 32, no. 2 (April 1, 2004): 355–59. http://dx.doi.org/10.1042/bst0320355.

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Conventional approaches to identifying cancer targets are complicated by the chromosomal instability of tumour cells, and typically result in a large number of differentially expressed candidate genes with uncertain disease relevance. Here we present a novel approach which aims to elucidate the molecular changes that are induced after loss of tumour suppressor function. Using gene silencing tools, we mimic the loss of tumour suppressor function to identify key regulators of tumour initiation and progression. Loss of function of the tumour suppressor PTEN (phosphatase and tensin homologue delet

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Perez, Cristina, Cirino Botta, Aintzane Zabaleta, Noemi Puig, Maria-Teresa Cedena, Ibai Goicoechea, Daniel Alameda, et al. "Immunogenomic identification and characterization of granulocytic myeloid-derived suppressor cells in multiple myeloma." Blood 136, no. 2 (July 9, 2020): 199–209. http://dx.doi.org/10.1182/blood.2019004537.

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Abstract Granulocytic myeloid-derived suppressor cells (G-MDSCs) promote tumor growth and immunosuppression in multiple myeloma (MM). However, their phenotype is not well established for accurate monitoring or clinical translation. We aimed to provide the phenotypic profile of G-MDSCs based on their prognostic significance in MM, immunosuppressive potential, and molecular program. The preestablished phenotype of G-MDSCs was evaluated in bone marrow samples from controls and MM patients using multidimensional flow cytometry; surprisingly, we found that CD11b+CD14−CD15+CD33+HLADR− cells overlapp

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Schröder, Matthias, Simone Loos, Svenja Kerstin Naumann, Christopher Bachran, Marit Krötschel, Viktor Umansky, Laura Helming, and Lee Kim Swee. "Identification of inhibitors of myeloid-derived suppressor cells activity through phenotypic chemical screening." OncoImmunology 6, no. 1 (November 29, 2016): e1258503. http://dx.doi.org/10.1080/2162402x.2016.1258503.

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Yang, Bingfen, Xinjing Wang, Jing Jiang, Fei Zhai, and Xiaoxing Cheng. "Identification of CD244-expressing myeloid-derived suppressor cells in patients with active tuberculosis." Immunology Letters 158, no. 1-2 (March 2014): 66–72. http://dx.doi.org/10.1016/j.imlet.2013.12.003.

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Stanley, Robert F., Richard T. Piszczatowski, Boris Bartholdy, Kelly Mitchell, Wendy M. McKimpson, Swathi Narayanagari, Dagmar Walter, et al. "A myeloid tumor suppressor role for NOL3." Journal of Experimental Medicine 214, no. 3 (February 23, 2017): 753–71. http://dx.doi.org/10.1084/jem.20162089.

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Despite the identification of several oncogenic driver mutations leading to constitutive JAK–STAT activation, the cellular and molecular biology of myeloproliferative neoplasms (MPN) remains incompletely understood. Recent discoveries have identified underlying disease-modifying molecular aberrations contributing to disease initiation and progression. Here, we report that deletion of Nol3 (Nucleolar protein 3) in mice leads to an MPN resembling primary myelofibrosis (PMF). Nol3−/− MPN mice harbor an expanded Thy1+LSK stem cell population exhibiting increased cell cycling and a myelomonocytic d

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Gueller, Saskia, Martina Komor, Julian C. Desmond, Oliver G. Ottmann, Dieter Hoelzer, H. Phillip Koeffler, and Wolf-Karsten Hofmann. "Identification of Putative New Tumor Suppressor Genes in Highly Purified CD34+ Bone Marrow Cells from Patients with Myelodysplastic Syndromes." Blood 104, no. 11 (November 16, 2004): 204. http://dx.doi.org/10.1182/blood.v104.11.204.204.

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Abstract Activation of transcription of DNA by demethylation and hyperacetylation is known to cause hematologic improvement in patients with myelodysplastic syndromes (MDS). In this study we discriminated genes not expressed in CD34+ cells from untreated patients with MDS but activated by in vitro demethylation (2-aza-5-deoxycytidine, Decitabine) and hyperacetylation (suberoylanilide hydroxamic acid, SAHA). Highly purified CD34+ cells from normal individuals (n=3) and patients with low (n=3) and high (n=3) risk MDS were cultured with SCF (50 ng/ml), IL-3 (10 ng/ml) and GM-CSF (10 ng/ml). The c

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Khan, Shaheena, Jennifer L. Taylor, and Carrie W. Rinker-Schaeffer. "Disrupting Ovarian Cancer Metastatic Colonization: Insights from Metastasis Suppressor Studies." Journal of Oncology 2010 (2010): 1–7. http://dx.doi.org/10.1155/2010/286925.

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Ovarian cancer affects approximately 25,000 women in the United States each year and remains one of the most lethal female malignancies. A standard approach to therapy is surgical cytoreduction, after which the remaining microscopic residual disease is treated with chemotherapy. The vast majority of patients have disease recurrence, underscoring the crucial need for approaches to control the regrowth, or colonization, of tissues after local treatment. Improved therapies require mechanistic information about the process of metastatic colonization, the final step in metastasis, in which cancer c

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Kennah, Erin, Ashley Ringrose, Liang L. Zhou, Sharmin Esmailzadeh, Hong Qian, Ming-wan Su, Youwen Zhou, and Xiaoyan Jiang. "Identification of tyrosine kinase, HCK, and tumor suppressor, BIN1, as potential mediators of AHI-1 oncogene in primary and transformed CTCL cells." Blood 113, no. 19 (May 7, 2009): 4646–55. http://dx.doi.org/10.1182/blood-2008-08-174037.

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Abstract AHI-1 is an oncogene often targeted by provirus insertional mutagenesis in murine leukemias and lymphomas. Aberrant expression of human AHI-1 occurs in cutaneous T-cell lymphoma (CTCL) cells and in CD4+CD7− Sezary cells from patients with Sezary syndrome. Stable knockdown of AHI-1 using retroviral-mediated RNA interference in CTCL cells inhibits their transforming activity in vitro and in vivo. To identify genes involved in AHI-1–mediated transformation, microarray analysis was performed to identify differentially expressed genes in AHI-1–suppressed CTCL cells. Fifteen up-regulated an

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Hara, Hideo, Yusuke Nanri, Emi Tabata, Saori Mitsutake, and Takeshi Tabira. "Identification of astrocyte-derived immune suppressor factor that induces apoptosis of autoreactive T cells." Journal of Neuroimmunology 233, no. 1-2 (April 2011): 135–46. http://dx.doi.org/10.1016/j.jneuroim.2010.12.011.

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Castellano, L., J. Waxman, G. Giamas, C. Apostolopous, and J. Stebbing. "The identification of new tumour suppressor micrornas epigenetically silenced in drug resistant cancer cells." European Journal of Cancer Supplements 6, no. 9 (July 2008): 95. http://dx.doi.org/10.1016/s1359-6349(08)71541-6.

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Sherger, Matthew, William Kisseberth, Cheryl London, Susan Olivo-Marston, and Tracey L. Papenfuss. "Identification of myeloid derived suppressor cells in the peripheral blood of tumor bearing dogs." BMC Veterinary Research 8, no. 1 (2012): 209. http://dx.doi.org/10.1186/1746-6148-8-209.

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Rivera, Claudio Alberto, George A. Dominguez, Vesselin Tomov, Gary W. Falk, Gregory G. Ginsberg, Dmitry Gabrilovich, Anil K. Rustgi, and John P. Lynch. "Identification of Myeloid Derived Suppressor Cells in the Barrett’s Metaplasia to Esophageal Adenocarcinoma Sequence." Gastroenterology 152, no. 5 (April 2017): S234. http://dx.doi.org/10.1016/s0016-5085(17)31071-5.

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Wang, Ying, Peng Li, Bo Wang, Shuai Wang, and Pinan Liu. "Identification of myeloid-derived suppressor cells that have an immunosuppressive function in NF2 patients." Journal of Cancer Research and Clinical Oncology 145, no. 2 (January 2, 2019): 523–33. http://dx.doi.org/10.1007/s00432-018-02825-8.

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Schmidt, Eva, Jana Krosl, Jalila Chagraoui, Nadine Mayotte, Caroline Pabst, Tara McRae, and Guy Sauvageau. "Identification of Lats 1 As a Putative Tumor Suppressor in HoxA9/Meis Induced Leukemia." Blood 118, no. 21 (November 18, 2011): 2474. http://dx.doi.org/10.1182/blood.v118.21.2474.2474.

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Abstract Abstract 2474 Aberrant expression of Hox genes and their cofactors Pbx and Meis1 has been detected in approximately 50% of all human leukemias, and proteins interacting with these homeodomain factors could play a major role in leukemia development. Studies in drosophila showed that hth/MEIS directly interacts with YKI, a component of the Hippo signaling pathway (Peng HW et al., 2009). The core components of this pathway in the mammalian cells are the kinases MST 1 or 2 and LATS 1 or 2, and the downstream transcription cofactors WWTR1 and YAP (homologues of the drosophila Yki). The Hip

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38

Asou, Hiroya, Yuko Ozaki, Akiko Nagamachi, Daisuke Aki, Hirotaka Matsui, and Toshiya Inaba. "Identification of Two 7q Genes Encoding Centrosomal Proteins as Myeloid Tumor-Suppressor Candidates." Blood 112, no. 11 (November 16, 2008): 1793. http://dx.doi.org/10.1182/blood.v112.11.1793.1793.

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Abstract We previously reported a candidate myeloid tumor-suppressor gene Miki (mitotic kinetic regulator, LOC253012) isolated from a common microdeletion cluster in chromosome subband 7q21.2 that was identified by microarray-based CGH analyses of JMML (ASH Annual Meeting, 2006 and 2007). Deletion of one Miki gene was also detected in 28 % of adult MDS/AML patients by copy-number assessment using real-time quantitative PCR (qPCR). Miki encodes a centrosomal protein: downregulation of Miki by siRNA disturbs the maturation and positioning of centrosomes, as well as spindle formation in mitotic c

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39

Dieckmann, Detlef, Heidi Plottner, Susanne Berchtold, Thomas Berger, and Gerold Schuler. "Ex Vivo Isolation and Characterization of Cd4+Cd25+ T Cells with Regulatory Properties from Human Blood." Journal of Experimental Medicine 193, no. 11 (June 4, 2001): 1303–10. http://dx.doi.org/10.1084/jem.193.11.1303.

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It has been known for years that rodents harbor a unique population of CD4+CD25+ “professional” regulatory/suppressor T cells that is crucial for the prevention of spontaneous autoimmune diseases. Here we demonstrate that CD4+CD25+CD45RO+ T cells (mean 6% of CD4+ T cells) are present in the blood of adult healthy volunteers. In contrast to previous reports, these CD4+CD25+ T cells do not constitute conventional memory cells but rather regulatory cells exhibiting properties identical to their rodent counterparts. Cytotoxic T lymphocyte–associated antigen (CTLA)-4 (CD152), for example, which is

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40

Middleton, Melissa Kristine, Alicia Marie Zukas, Tanya Rubinstein, Michele Jacob, Peijuan Zhu, Liang Zhao, Ian Blair, and Ellen Puré. "Identification of 12/15-lipoxygenase as a suppressor of myeloproliferative disease." Journal of Experimental Medicine 203, no. 11 (October 16, 2006): 2529–40. http://dx.doi.org/10.1084/jem.20061444.

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Abstract (sommario):

Though Abl inhibitors are often successful therapies for the initial stages of chronic myelogenous leukemia (CML), refractory cases highlight the need for novel molecular insights. We demonstrate that mice deficient in the enzyme 12/15-lipoxygenase (12/15-LO) develop a myeloproliferative disorder (MPD) that progresses to transplantable leukemia. Although not associated with dysregulation of Abl, cells isolated from chronic stage 12/15-LO–deficient (Alox15) mice exhibit increased activation of the phosphatidylinositol 3–kinase (PI3-K) pathway, as indicated by enhanced phosphorylation of Akt. Fu

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41

Shen, John P., Rohith Srivas, Ana Bojorquez-Gomez, Katherine Licon, Jian Feng Li, Robert W. Sobol, and Trey Ideker. "Cross-species synthetic lethal interaction screening as a strategy for the identification of novel therapeutic targets in cancer." Journal of Clinical Oncology 31, no. 15_suppl (May 20, 2013): 11105. http://dx.doi.org/10.1200/jco.2013.31.15_suppl.11105.

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Abstract (sommario):

11105 Background: Mutation, deletion, or epigenetic silencing of tumor suppressor genes is a near universal feature of malignant cells. However, therapeutic strategies for restoring the function of mutated or deleted genes have proven difficult. Synthetic lethality, an event in which the simultaneous perturbation of two genes results in cellular death, has been proposed as a method to selectively target cancer cells. Identifying and pharmacologically inhibiting proteins encoded by genes that are synthetic lethal with known tumor suppressor mutations should result in selective toxicity to tumor

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42

Del Priore, V., C. A. Snay, A. Bahr, and C. N. Cole. "The product of the Saccharomyces cerevisiae RSS1 gene, identified as a high-copy suppressor of the rat7-1 temperature-sensitive allele of the RAT7/NUP159 nucleoporin, is required for efficient mRNA export." Molecular Biology of the Cell 7, no. 10 (October 1996): 1601–21. http://dx.doi.org/10.1091/mbc.7.10.1601.

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RAT7/NUP159 was identified previously in a screen for genes whose products are important for nucleocytoplasmic export of poly(A)+ RNA and encodes an essential nucleoporin. We report here the identification of RSS1 (Rat Seven Suppressor) as a high-copy extragenic suppressor of the rat7-1 temperature-sensitive allele. Rss1p encodes a novel essential protein of 538 amino acids, which contains an extended predicted coiled-coil domain and is located both at nuclear pore complexes (NPCs) and in the cytoplasm. RSS1 is the first reported high-copy extragenic suppressor of a mutant nucleoporin. Overexp

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43

Rosin, Flávia Cristina Perillo, Juliana Figueredo Pedregosa, Joaquim Soares de Almeida, and Valquiria Bueno. "Identification of myeloid-derived suppressor cells and T regulatory cells in lung microenvironment after Urethane-induced lung tumor." International Immunopharmacology 11, no. 7 (July 2011): 873–78. http://dx.doi.org/10.1016/j.intimp.2010.12.025.

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44

Desmond, J. C., S. D. Raynaud, L. C. Jones, W. K. Hofmann, T. Haferlach та H. Phillip Koeffler. "Identification of Epigenetically Silenced Tumor Suppressor Genes in Myeloid Disorders Leads to the Identification of α-Catenin as a Target Gene in 5q- Syndrome." Blood 104, № 11 (16 листопада 2004): 2565. http://dx.doi.org/10.1182/blood.v104.11.2565.2565.

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Abstract (sommario):

Abstract CpG islands in the 5′ regulatory regions of genes are generally protected from cytosine methylation as methylation in a promoter can result in transcriptional silencing of the associated gene. Failure of a cell to prevent methylation in the promoter regions of tumor suppressor genes contributes to the onset and progression of cancers. The demethylating agent 5-aza-2′deoxycytidine (DAC) and the histone deacetylase inhibitor suberoyl anilide bishydroxamide (SAHA) possess potent antitumorigenic properties against myeloid disorders. Understanding the alterations of the transcriptome media

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45

Horrigan, Stephen K., Zarema H. Arbieva, Hong Yan Xie, Jelena Kravarusic, Noreen C. Fulton, Haley Naik, Tiffany T. Le, and Carol A. Westbrook. "Delineation of a minimal interval and identification of 9 candidates for a tumor suppressor gene in malignant myeloid disorders on 5q31." Blood 95, no. 7 (April 1, 2000): 2372–77. http://dx.doi.org/10.1182/blood.v95.7.2372.

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Abstract (sommario):

Abstract Interstitial deletion or loss of chromosome 5 is frequent in malignant myeloid disorders, including myelodysplasia (MDS) and acute myeloid leukemia (AML), suggesting the presence of a tumor suppressor gene. Loss of heterozygosity (LOH) analysis was used to define a minimal deletion interval for this gene. Polymorphic markers on 5q31 were identified using a high-resolution physical and radiation hybrid breakpoint map and applied to a patient with AML with a subcytogenetic deletion of 5q. By comparing the DNA from leukemic cells to buccal mucosa cells, LOH was detected with markers D5S4

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46

Horrigan, Stephen K., Zarema H. Arbieva, Hong Yan Xie, Jelena Kravarusic, Noreen C. Fulton, Haley Naik, Tiffany T. Le, and Carol A. Westbrook. "Delineation of a minimal interval and identification of 9 candidates for a tumor suppressor gene in malignant myeloid disorders on 5q31." Blood 95, no. 7 (April 1, 2000): 2372–77. http://dx.doi.org/10.1182/blood.v95.7.2372.007k20_2372_2377.

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Abstract (sommario):

Interstitial deletion or loss of chromosome 5 is frequent in malignant myeloid disorders, including myelodysplasia (MDS) and acute myeloid leukemia (AML), suggesting the presence of a tumor suppressor gene. Loss of heterozygosity (LOH) analysis was used to define a minimal deletion interval for this gene. Polymorphic markers on 5q31 were identified using a high-resolution physical and radiation hybrid breakpoint map and applied to a patient with AML with a subcytogenetic deletion of 5q. By comparing the DNA from leukemic cells to buccal mucosa cells, LOH was detected with markers D5S476 and D5

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47

Porta, Giuseppe Della, Paolo Radice, and Marco A. Pierotti. "Onco-Suppressor Genes in Human Cancer." Tumori Journal 75, no. 4 (August 1989): 329–36. http://dx.doi.org/10.1177/030089168907500406.

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Abstract (sommario):

The analysis of the molecular mechanisms governing multistep carcinogenesis became experimentally approachable since the identification and characterization in tumor cells of altered or activated versions of cellular genes (oncogenes) that normally control cell growth and differentiation. The activating mutations confer new properties to the oncogene products and should therefore be considered as gain of function mutations. In addition, the oncogenes appear to act as dominant genetic traits since they act also in the presence of the homologous wild-type allele. However, the concept of a domina

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48

Liu, Yun, Rihua Zhang, Jing Xin, Yan Sun, Jie Li, Dong Wei, and Allan Z. Zhao. "Identification of S100A16 as a Novel Adipogenesis Promoting Factor in 3T3-L1 Cells." Endocrinology 152, no. 3 (March 1, 2011): 903–11. http://dx.doi.org/10.1210/en.2010-1059.

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Abstract (sommario):

S100A16 is a member of S100 protein super family that carries calcium-binding EF-hand motifs. Its expression is ubiquitous and elevated in various types of tumors. The functions of S100 proteins are still being defined, although many members of S100 protein family are traditionally considered as markers of tumor tissues. Using 3T3-L1 preadipocyte model, we investigated the expression and function of S100A16 during differentiation into adipocytes as well as the potential roles of S100A16 in the regulation of insulin sensitivity. We found that the expression of S100A16 was increased during diffe

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49

ROWDEN, G., D. DAVIS, D. LUCKETT та L. POULTER. "Identification of CD4+, 2H4 + (T8γ +) suppressor-inducer cells in normal human epidermis and superficial dermis". British Journal of Dermatology 119, № 2 (серпень 1988): 147–54. http://dx.doi.org/10.1111/j.1365-2133.1988.tb03195.x.

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50

Aichberger, Karl J., Karoline V. Gleixner, Irina Mirkina, Sabine Cerny-Reiterer, Barbara Peter, Veronika Ferenc, Michael Kneidinger, et al. "Identification of proapoptotic Bim as a tumor suppressor in neoplastic mast cells: role of KIT D816V and effects of various targeted drugs." Blood 114, no. 26 (December 17, 2009): 5342–51. http://dx.doi.org/10.1182/blood-2008-08-175190.

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Abstract (sommario):

Abstract Systemic mastocytosis (SM) is a myeloid neoplasm involving mast cells (MCs) and their progenitors. In most cases, neoplastic cells display the D816V-mutated variant of KIT. KIT D816V exhibits constitutive tyrosine kinase (TK) activity and has been implicated in increased survival and growth of neoplastic MCs. Recent data suggest that the proapoptotic BH3-only death regulator Bim plays a role as a tumor suppressor in various myeloid neoplasms. We found that KIT D816V suppresses expression of Bim in Ba/F3 cells. The KIT D816–induced down-regulation of Bim was rescued by the KIT-targetin

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