Cancer Statistics, 2003

Jemal, Ahmedin; Murray, Taylor; Samuels, Alicia; Ghafoor, Asma; Ward, Elizabeth; Thun, Michael J.

doi:10.3322/canjclin.53.1.5

Cited by 3,254 publications

(1,641 citation statements)

References 7 publications

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“…Interleukin-6 is produced by MM cells and promotes myeloma cell proliferation in an autocrine manner (Klein et al, 1995;Chauhan et al, 1996;Jemal et al, 2003;Anderson, 2004) through phosphorylation of the signalling protein STAT3 (Kaptein et al, 1996;Hirano et al, 2000;Chatterjee et al, 2002). As Atiprimod inhibits NF-kB activity and, by doing so, suppresses IL-6 production, we wondered whether Atiprimod downregulates STAT3 phosphorylation.…”

Section: Atiprimod Downregulates Both Il-6-induced and Constitutive Smentioning

confidence: 99%

Atiprimod blocks STAT3 phosphorylation and induces apoptosis in multiple myeloma cells

et al. 2005

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Multiple myeloma (MM) accounts for 1 % of all cancer deaths. Although treated aggressively, almost all myelomas eventually recur and become resistant to treatment. Atiprimod 5] decane dimaleate) has exerted anti-inflammatory activities and inhibited oeteoclast-induced bone resorption in animal models and been well tolerated in patients with rheumatoid arthritis in phase I clinical trials. Therefore, we investigated its activity in MM cells and its mechanism of action. We found that Atiprimod inhibited proliferation of the myeloma cell lines U266-B1, OCI-MY5, MM-1, and MM-1R in a timeand dose-dependent manner. Atiprimod blocked U266-B1 myeloma cells in the G 0 /G 1 phase, preventing cell cycle progression. Furthermore, Atiprimod inhibited signal transducer and activator of transcription (STAT) 3 activation, blocking the signalling pathway of interleukin-6, which contributes to myeloma cell proliferation and survival, and downregulated the antiapoptotic proteins Bcl-2, Bcl-X L , and Mcl-1. Incubation of U266-B1 myeloma cells with Atiprimod induced apoptosis through the activation of caspase 3 and subsequent cleavage of the DNA repair enzyme poly(adenosine diphosphate-ribose) polymerase. Finally, Atiprimod suppressed myeloma colony-forming cell proliferation in fresh marrow cells from five patients with newly diagnosed MM in a dose-dependent fashion. These data suggest that Atiprimod has a role in future therapies for MM.

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Section: Atiprimod Downregulates Both Il-6-induced and Constitutive Smentioning

confidence: 99%

Atiprimod blocks STAT3 phosphorylation and induces apoptosis in multiple myeloma cells

et al. 2005

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“…Pancreatic ductal adenocarcinoma (PDAC) is the fourth leading cause of cancer-related deaths in the industrialized world (Jemal et al, 2003). This is due to both a paucity of diagnostic tools to detect early stages of the disease and a poor outcome following chemotherapy and radiation therapy even when combined with surgical excision of the tumour (DiMagno et al, 1999).…”

Section: Introductionmentioning

confidence: 99%

Periostin promotes invasiveness and resistance of pancreatic cancer cells to hypoxia-induced cell death: role of the β4 integrin and the PI3k pathway

Baril¹,

Gangeswaran²,

Mahon³

et al. 2006

Oncogene

257

244

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Pancreatic ductal adenocarcinoma is a devastating disease, characterized by a rapid progression and poor treatment response. Using gene expression profiling of pancreatic cancer tissues, we previously identified periostin as a potential diagnostic and therapeutic target. In this study, we report the overexpression of periostin in a larger set of pancreatic cancer tissues and show that although the periostin transcript is exclusively expressed in tumour cells, the protein product is only detected in the extracellular matrix adjacent to cancer cells. Using an enzyme-linked immunosorbent assay (ELISA) assay, we show significantly increased levels of periostin in the sera of pancreatic cancer patients compared to non-cancer controls. We demonstrate that periostin promotes the invasiveness of tumour cells by increasing the motility of cells without inducing expression of proteases, and enhances the survival of tumour cells exposed to hypoxic conditions. At the molecular level, we provide evidence that the a 6 b 4 integrin complex acts as the cell receptor of periostin in pancreatic cancer cells and that interaction promotes phosphorylation of focal adhesion kinase (FAK) and protein kinase B (AKT) though activation of the PI3 kinase pathway, but not the RAS/MEK/ERK pathway. These findings suggest an important role of periostin in pancreatic cancer and provide a rationale to study periostin for diagnostic and therapeutic applications.

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“…Prostate cancer is the most commonly diagnosed noncutaneous neoplasm among males in Western countries and is estimated to result in 28 900 deaths this year in the US alone (Jemal et al, 2003). Serum prostate specific antigen (PSA) level and clinico-pathological factors like Gleason score and pT-stage are accepted diagnostic and prognostic factors, which, however, often fail to predict accurately the clinical outcome in individual cases (Frydenberg et al, 1997).…”

mentioning

confidence: 99%

Expression analysis of imbalanced genes in prostate carcinoma using tissue microarrays

et al. 2006

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To identify candidate genes relevant for prostate tumour prognosis and progression, we performed an exhaustive gene search in seven previously described genomic-profiling studies of 161 prostate tumours, and four expression profiling studies of 61 tumours. From the resulting list of candidate genes, six were selected for protein-expression analysis based on the availability of antibodies applicable to paraffinised tissue: fatty acid synthase (FASN), MYC, b-adrenergic receptor kinase 1 (BARK1, GRK2) the catalytic subunits of protein phosphatases PP1a (PPP1CA) and PP2A (PPP2CB) and metastasis suppressor NM23-H1. These candidates were analysed by immunohistochemistry (IHC) on a tissue microarray containing 651 cores of primary prostate cancer samples and benign prostatic hyperplasias (BPH) from 175 patients. In univariate analysis, expression of PP1a (P ¼ 0.001) was found to strongly correlate with Gleason score. MYC immunostaining negatively correlated with both pT-stage and Gleason score (Po0.001 each) in univariate as well as in multivariate analysis. Furthermore, a subgroup of patients with high Gleason scores was characterised by a complete loss of BARK1 protein (P ¼ 0.023). In conclusion, our study revealed novel molecular markers of potential diagnostic and therapeutic relevance for prostate carcinoma.

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Cancer Statistics, 2003

Cited by 3,254 publications

References 7 publications

Atiprimod blocks STAT3 phosphorylation and induces apoptosis in multiple myeloma cells

Atiprimod blocks STAT3 phosphorylation and induces apoptosis in multiple myeloma cells

Periostin promotes invasiveness and resistance of pancreatic cancer cells to hypoxia-induced cell death: role of the β4 integrin and the PI3k pathway

Expression analysis of imbalanced genes in prostate carcinoma using tissue microarrays

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