搜索结果: 'methocult media formulations for human hematopoietic cells serum containing'

Charafe-Jauffret E et al. (JAN 2010) Clinical cancer research : an official journal of the American Association for Cancer Research 16 1 45--55

Aldehyde dehydrogenase 1-positive cancer stem cells mediate metastasis and poor clinical outcome in inflammatory breast cancer.

PURPOSE: To examine the role of cancer stem cells (CSC) in mediating metastasis in inflammatory breast cancer (IBC) and the association of these cells with patient outcome in this aggressive type of breast cancer. EXPERIMENTAL DESIGN: CSCs were isolated from SUM149 and MARY-X,an IBC cell line and primary xenograft,by virtue of increased aldehyde dehydrogenase (ALDH) activity as assessed by the ALDEFLUOR assay. Invasion and metastasis of CSC populations were assessed by in vitro and mouse xenograft assays. Expression of ALDH1 was determined on a retrospective series of 109 IBC patients and this was correlated with histoclinical data. All statistical tests were two sided. Log-rank tests using Kaplan-Meier analysis were used to determine the correlation of ALDH1 expression with development of metastasis and patient outcome. RESULTS: Both in vitro and xenograft assays showed that invasion and metastasis in IBC are mediated by a cellular component that displays ALDH activity. Furthermore,expression of ALDH1 in IBC was an independent predictive factor for early metastasis and decreased survival in this patient population. CONCLUSIONS: These results suggest that the metastatic,aggressive behavior of IBC may be mediated by a CSC component that displays ALDH enzymatic activity. ALDH1 expression represents the first independent prognostic marker to predict metastasis and poor patient outcome in IBC. The results illustrate how stem cell research can translate into clinical practice in the IBC field. View Publication

产品类型：

产品号#：

01700

01705

01701

01702

产品名：

ALDEFLUOR™ 试剂盒

ALDEFLUOR™ DEAB试剂

ALDEFLUOR™测定缓冲液

Grudzien P et al. (OCT 2010) Anticancer research 30 10 3853--67

Inhibition of Notch signaling reduces the stem-like population of breast cancer cells and prevents mammosphere formation.

BACKGROUND: Cancer stem cells (CSCs) are believed to be responsible for breast cancer formation and recurrence; therefore,therapeutic strategies targeting CSCs must be developed. One approach may be targeting signaling pathways,like Notch,that are involved in stem cell self-renewal and survival. MATERIALS AND METHODS: Breast cancer stem-like cells derived from cell lines and patient samples were examined for Notch expression and activation. The effect of Notch inhibition on sphere formation,proliferation,and colony formation was determined. RESULTS: Breast cancer stem-like cells consistently expressed elevated Notch activation compared with bulk tumor cells. Blockade of Notch signaling using pharmacologic and genomic approaches prevented sphere formation,proliferation,and/or colony formation in soft agar. Interestingly,a gamma-secretase inhibitor,MRK003,induced apoptosis in these cells. CONCLUSION: Our findings support a crucial role for Notch signaling in maintenance of breast cancer stem-like cells,and suggest Notch inhibition may have clinical benefits in targeting CSCs. View Publication

产品类型：

产品号#：

01700

01705

产品名：

ALDEFLUOR™ 试剂盒

ALDEFLUOR™ DEAB试剂

Podar K et al. (FEB 2003) The Journal of biological chemistry 278 8 5794--801

Essential role of caveolae in interleukin-6- and insulin-like growth factor I-triggered Akt-1-mediated survival of multiple myeloma cells.

Caveolae,specialized flask-shaped lipid rafts on the cell surface,are composed of cholesterol,sphingolipids,and structural proteins termed caveolins; functionally,these plasma membrane microdomains have been implicated in signal transduction and transmembrane transport. In the present study,we examined the role of caveolin-1 in multiple myeloma cells. We show for the first time that caveolin-1,which is usually absent in blood cells,is expressed in multiple myeloma cells. Analysis of myeloma cell-derived plasma membrane fractions shows that caveolin-1 is co-localized with interleukin-6 receptor signal transducing chain gp130 and with insulin-like growth factor-I receptor. Cholesterol depletion by beta-cyclodextrin results in the loss of caveola structure in myeloma cells,as shown by transmission electron microscopy,and loss of caveolin-1 function. Interleukin-6 and insulin-like growth factor-I,growth and survival factors in multiple myeloma,induce caveolin-1 phosphorylation,which is abrogated by pre-treatment with beta-cyclodextrin. Importantly,inhibition of caveolin-1 phosphorylation blocks both interleukin-6-induced protein complex formation with caveolin-1 and downstream activation of the phosphatidylinositol 3-kinase/Akt-1 pathway. beta-Cyclodextrin also blocks insulin-like growth factor-I-induced tyrosine phosphorylation of insulin-responsive substrate-1 and downstream activation of the phosphatidylinositol 3-kinase/Akt-1 pathway. Therefore,cholesterol depletion by beta-cyclodextrin abrogates both interleukin-6- and insulin-like growth factor-I-triggered multiple myeloma cell survival via negative regulation of caveolin-1. Taken together,this study identifies caveolin-1 and other structural membrane components as potential new therapeutic targets in multiple myeloma. View Publication

产品类型：

产品号#：

15129

15169

产品名：

RosetteSep™人多发性骨髓瘤细胞富集抗体混合物

Castriconi R et al. (DEC 2004) Cancer research 64 24 9180--4

Natural killer cell-mediated killing of freshly isolated neuroblastoma cells: critical role of DNAX accessory molecule-1-poliovirus receptor interaction.

In the present study,we assessed the susceptibility of freshly isolated neuroblastoma cells to killing mediated by normal human natural killer (NK) cells and analyzed the receptor-ligand interactions that regulate this event. We show that killing of freshly isolated neuroblasts,similar to neuroblastoma cell lines,involves NKp46 and NKp30 (natural cytotoxicity receptors). However,freshly isolated neuroblasts were generally more resistant to NK-mediated lysis than conventional neuroblastoma cell lines. Moreover,a significant heterogeneity in susceptibility to lysis existed among neuroblastomas derived from different patients. Remarkably,susceptibility to lysis directly correlated with the surface expression,on neuroblasts,of poliovirus receptor [PVR (CD155)],a ligand for the DNAX accessory molecule-1 [DNAM-1 (CD226)] triggering receptor expressed by NK cells. Indeed,PVR-expressing neuroblastomas were efficiently killed by NK cells. Moreover,monoclonal antibody-mediated masking of either DNAM-1 (on NK cells) or PVR (on neuroblasts) resulted in strong inhibition of tumor cell lysis. Thus,assessment of the PVR surface levels may represent a novel useful criterion to predict the susceptibility/resistance of neuroblastomas to NK-mediated killing. View Publication

产品类型：

产品号#：

15122

15162

产品名：

RosetteSep™ 人CD45去除抗体混合物

RosetteSep™人CD45去除抗体混合物

Puissant A et al. (FEB 2010) Cancer research 70 3 1042--52

Resveratrol promotes autophagic cell death in chronic myelogenous leukemia cells via JNK-mediated p62/SQSTM1 expression and AMPK activation.

Autophagy that is induced by starvation or cellular stress can enable cancer cell survival by sustaining energy homeostasis and eliminating damaged organelles and proteins. In response to stress,cancer cells have been reported to accumulate the protein p62/SQSTM1 (p62),but its role in the regulation of autophagy is controversial. Here,we report that the plant phytoalexin resveratrol (RSV) triggers autophagy in imatinib-sensitive and imatinib-resistant chronic myelogenous leukemia (CML) cells via JNK-dependent accumulation of p62. JNK inhibition or p62 knockdown prevented RSV-mediated autophagy and antileukemic effects. RSV also stimulated AMPK,thereby inhibiting the mTOR pathway. AMPK knockdown or mTOR overexpression impaired RSV-induced autophagy but not JNK activation. Lastly,p62 expression and autophagy in CD34+ progenitors from patients with CML was induced by RSV,and disrupting autophagy protected CD34+ CML cells from RSV-mediated cell death. We concluded that RSV triggered autophagic cell death in CML cells via both JNK-mediated p62 overexpression and AMPK activation. Our findings show that the JNK and AMPK pathways can cooperate to eliminate CML cells via autophagy. View Publication

产品类型：

产品号#：

09600

09650

产品名：

StemSpan™ SFEM

Fuertes MB et al. (APR 2008) Journal of immunology (Baltimore,Md. : 1950) 180 7 4606--14

Intracellular retention of the NKG2D ligand MHC class I chain-related gene A in human melanomas confers immune privilege and prevents NK cell-mediated cytotoxicity.

Most tumors grow in immunocompetent hosts despite expressing NKG2D ligands (NKG2DLs) such as the MHC class I chain-related genes A and B (MICA/B). However,their participation in tumor cell evasion is still not completely understood. Here we demonstrate that several human melanomas (cell lines and freshly isolated metastases) do not express MICA on the cell surface but have intracellular deposits of this NKG2DL. Susceptibility to NK cell-mediated cytotoxicity correlated with the ratio of NKG2DLs to HLA class I molecules but not with the amounts of MICA on the cell surface of tumor cells. Transfection-mediated overexpression of MICA restored cell surface expression and resulted in an increased in vitro cytotoxicity and IFN-gamma secretion by human NK cells. In xenografted nude mice,these melanomas exhibited a delayed growth and extensive in vivo apoptosis. Retardation of tumor growth was due to NK cell-mediated antitumor activity against MICA-transfected tumors,given that this effect was not observed in NK cell-depleted mice. Also,mouse NK cells killed MICA-overexpressing melanomas in vitro. A mechanistic analysis revealed the retention of MICA in the endoplasmic reticulum,an effect that was associated with accumulation of endoH-sensitive (immature) forms of MICA,retrograde transport to the cytoplasm,and degradation by the proteasome. Our study identifies a novel strategy developed by melanoma cells to evade NK cell-mediated immune surveillance based on the intracellular sequestration of immature forms of MICA in the endoplasmic reticulum. Furthermore,this tumor immune escape strategy can be overcome by gene therapy approaches aimed at overexpressing MICA on tumor cells. View Publication

产品类型：

产品号#：

15025

15065

产品名：

RosetteSep™人NK细胞富集抗体混合物

Morrow M et al. (MAY 2004) Blood 103 10 3890--6

TEL-AML1 promotes development of specific hematopoietic lineages consistent with preleukemic activity.

The t(12;21)(p13;q22) translocation is the most common chromosomal abnormality yet identified in any pediatric leukemia and gives rise to the TEL-AML1 fusion product. To investigate the effects of TEL-AML1 on hematopoiesis,fetal liver hematopoietic progenitor cells (HPCs) were transduced with retroviral vectors expressing this fusion protein. We show that TEL-AML1 dramatically alters differentiation of HPCs in vitro,preferentially promoting B-lymphocyte development,enhancing self-renewal of B-cell precursors,and leading to the establishment of long-term growth factor-dependent pre-B-cell lines. However,it had no effect on myeloid development in vitro. Further experiments were performed to determine whether TEL-AML1 also demonstrates lineage-specific activity in vivo. TEL-AML1-expressing HPCs displayed a competitive advantage in reconstituting both B-cell and myeloid lineages in vivo but had no effect on reconstitution of the T-cell lineage. Despite promoting these alterations in hematopoiesis,TEL-AML1 did not induce leukemia in transplanted mice. Our study provides a unique insight into the role of TEL-AML1 in leukemia predisposition and a potential model to study the mechanism of leukemogenesis associated with this fusion. View Publication

产品类型：

产品号#：

03534

03231

产品名：

MethoCult™GF M3534

MethoCult™M3231

1:23

视频

Tools for Breast Cancer Research

发布日期: 1/25/10

产品手册

Reliable Antibodies for Your Research

产品类型：

品牌：

EasySep

产品号#：

60100

60100.1

60100AD

60100AD.1

60102

60102FI

60104

60104AD

60104AD.1

60104AZ

60104AZ.1

60104BT

60104BT.1

60104BT.2

60104FI

60104FI.1

60104PE

60104PE.1

60106

60106.1

60106AZ

60106AZ.1

60106BT

60106BT.1

60106FI

60106FI.1

60106PE

60106PE.1

60107

60107.1

601

产品名：

抗β-微管蛋白III抗体，克隆AA10

抗β-微管蛋白III抗体，克隆AA10，Alexa Fluor® 488

抗β-微管蛋白III抗体，clone AA10，Alexa Fluor® 488

抗小鼠TCR Gamma/Delta抗体，clone GL3

抗小鼠TCR Gamma/Delta抗体，clone GL3，Alexa Fluor® 488

抗小鼠TCR Gamma/Delta抗体，clone GL3，APC

抗小鼠TCR Gamma/Delta抗体，clone GL3，Biotin

抗小鼠TCR Gamma/Delta抗体，clone GL3，FITC

抗小鼠TCR Gamma/Delta抗体，clone GL3，PE

抗人CD71（转铁蛋白受体）抗体，clone OKT9

抗人CD71（转铁蛋白受体）抗体，clone OKT9，APC

抗人CD71（转铁蛋白受体）抗体，clone OKT9，Biotin

抗人CD71（转铁蛋白受体）抗体，clone OKT9，FITC

抗人CD71（转铁蛋白受体）抗体，clone OKT9，PE

Fenouille N et al. (DEC 2010) Cancer research 70 23 9659--70

Persistent activation of the Fyn/ERK kinase signaling axis mediates imatinib resistance in chronic myelogenous leukemia cells through upregulation of intracellular SPARC.

SPARC is an extracellular matrix protein that exerts pleiotropic effects on extracellular matrix organization,growth factor availability,cell adhesion,differentiation,and immunity in cancer. Chronic myelogenous leukemia (CML) cells resistant to the BCR-ABL inhibitor imatinib (IM-R cells) were found to overexpress SPARC mRNA. In this study,we show that imatinib triggers SPARC accumulation in a variety of tyrosine kinase inhibitor (TKI)-resistant CML cell lines. SPARC silencing in IM-R cells restored imatinib sensitivity,whereas enforced SPARC expression in imatinib-sensitive cells promoted viability as well as protection against imatinib-mediated apoptosis. Notably,we found that the protective effect of SPARC required intracellular retention inside cells. Accordingly,SPARC was not secreted into the culture medium of IM-R cells. Increased SPARC expression was intimately linked to persistent activation of the Fyn/ERK kinase signaling axis. Pharmacologic inhibition of this pathway or siRNA-mediated knockdown of Fyn kinase resensitized IM-R cells to imatinib. In support of our findings,increased levels of SPARC mRNA were documented in blood cells from CML patients after 1 year of imatinib therapy compared with initial diagnosis. Taken together,our results highlight an important role for the Fyn/ERK signaling pathway in imatinib-resistant cells that is driven by accumulation of intracellular SPARC. View Publication

产品类型：

产品号#：

04100

产品名：

MethoCult™ H4100

产品手册

Small Molecules for Cancer Research

产品类型：

产品号#：

72012

72014

72032

72034

72042

72044

72052

72054

72062

72064

72072

72074

72082

72092

72102

72112

72114

72122

72124

72132

72142

72144

72152

72154

72162

72164

72172

72174

72182

72184

72202

72204

72212

72214

72222

72232

72234

72242

72252

72254

72262

72264

722

产品名：

5-氮杂胞苷（5-Azacytidine）

BIO

BIX01294 (Trihydrochloride Hydrate)

CHIR99021

环状 Pifithrin-α（Cyclic Pifithrin-Alpha）

环状 Pifithrin-α (Hydrobromide)

环巴胺（Cyclopamine）

DAPT

地塞米松（Dexamethasone）

Dorsomorphin

Forskolin

IWP-2

抗坏血酸（Ascorbic Acid）

LY294002

PD173074

PD98059

PD0325901

Purmorphamine

RG108

SB203580 (Hydrochloride)

SB431542 (Hydrate)

SB431542（水合物）

丁酸钠（Sodium Butyrate）

Thiazovivin

All-Trans Retinoic Acid

全反式视黄酸

Lidonnici MR et al. (OCT 2010) Cancer research 70 20 7949--59

Expression of the transcriptional repressor Gfi-1 is regulated by C/EBPalpha and is involved in its proliferation and colony formation-inhibitory effects in p210BCR/ABL-expressing cells.

Ectopic expression of CAAT/enhancer binding protein α (C/EBPα) in p210BCR/ABL-expressing cells induces granulocytic differentiation,inhibits proliferation,and suppresses leukemogenesis. To dissect the molecular mechanisms underlying these biological effects,C/EBPα-regulated genes were identified by microarray analysis in 32D-p210BCR/ABL cells. One of the genes whose expression was activated by C/EBPα in a DNA binding-dependent manner in BCR/ABL-expressing cells is the transcriptional repressor Gfi-1. We show here that C/EBPα interacts with a functional C/EBP binding site in the Gfi-1 5'-flanking region and enhances the promoter activity of Gfi-1. Moreover,in K562 cells,RNA interference-mediated downregulation of Gfi-1 expression partially rescued the proliferation-inhibitory but not the differentiation-inducing effect of C/EBPα. Ectopic expression of wild-type Gfi-1,but not of a transcriptional repressor mutant (Gfi-1P2A),inhibited proliferation and markedly suppressed colony formation but did not induce granulocytic differentiation of BCR/ABL-expressing cells. By contrast,Gfi-1 short hairpin RNA-tranduced CD34(+) chronic myeloid leukemia cells were markedly more clonogenic than the scramble-transduced counterpart. Together,these studies indicate that Gfi-1 is a direct target of C/EBPα required for its proliferation and survival-inhibitory effects in BCR/ABL-expressing cells. View Publication

产品类型：

产品号#：

02690

09600

09650

产品名：

StemSpan™CC100

StemSpan™ SFEM

搜索结果: 'methocult media formulations for human hematopoietic cells serum containing'

Aldehyde dehydrogenase 1-positive cancer stem cells mediate metastasis and poor clinical outcome in inflammatory breast cancer.

Inhibition of Notch signaling reduces the stem-like population of breast cancer cells and prevents mammosphere formation.

Essential role of caveolae in interleukin-6- and insulin-like growth factor I-triggered Akt-1-mediated survival of multiple myeloma cells.

Natural killer cell-mediated killing of freshly isolated neuroblastoma cells: critical role of DNAX accessory molecule-1-poliovirus receptor interaction.

Resveratrol promotes autophagic cell death in chronic myelogenous leukemia cells via JNK-mediated p62/SQSTM1 expression and AMPK activation.

Intracellular retention of the NKG2D ligand MHC class I chain-related gene A in human melanomas confers immune privilege and prevents NK cell-mediated cytotoxicity.

TEL-AML1 promotes development of specific hematopoietic lineages consistent with preleukemic activity.

Persistent activation of the Fyn/ERK kinase signaling axis mediates imatinib resistance in chronic myelogenous leukemia cells through upregulation of intracellular SPARC.

Expression of the transcriptional repressor Gfi-1 is regulated by C/EBPalpha and is involved in its proliferation and colony formation-inhibitory effects in p210BCR/ABL-expressing cells.

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