Lung cancer

Hoffman, Philip C.; Mauer, Ann M.; Vokes, Everett E.

doi:10.1016/s0140-6736(00)82038-3

Cited by 613 publications

(435 citation statements)

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“…The current treatment strategies for advanced lung cancer include surgical resection, radiation, cytotoxic chemotherapy, and photodynamic therapy (5). In almost two thirds of cases, the cancer has already spread beyond localized disease at the time of diagnosis, limiting therapeutic options (23,24). Therefore, the exploration and development of more effective chemopreventive/chemotherapeutic agents and therapies that can target the molecules associated with tumor proliferation, angiogenesis, and apoptosis resistance will lead to improved outcomes in patients with lung cancer.…”

Section: Introductionmentioning

confidence: 99%

Proanthocyanidins Inhibit In vitro and In vivo Growth of Human Non–Small Cell Lung Cancer Cells by Inhibiting the Prostaglandin E2 and Prostaglandin E2 Receptors

Sharma

Meeran

Katiyar

2010

Molecular Cancer Therapeutics

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Overexpression of cyclooxygenase-2 (COX-2) and prostaglandins (PG) is linked to a wide variety of human cancers. Here, we assessed whether the chemotherapeutic effect of grape seed proanthocyanidins (GSP) on non-small cell lung cancer (NSCLC) cells is mediated through the inhibition of COX-2 and PGE 2 /PGE 2 receptor expression. The effects of GSPs on human NSCLC cell lines in terms of proliferation, apoptosis, and expression of COX-2, PGE 2 , and PGE 2 receptors were determined using Western blotting, fluorescence-activated cell sorting analysis, and reverse transcription-PCR. In vitro treatment of NSCLC cells (A549, H1299, H460, H226, and H157) with GSPs resulted in significant growth inhibition and induction of apoptosis, which were associated with the inhibitory effects of GSPs on the overexpression of COX-2, PGE 2 , and PGE 2 receptors (EP1 and EP4) in these cells. Treatment of cells with indomethacin, a pan-COX inhibitor, or transient transfection of cells with COX-2 small interfering RNA, also inhibited cell growth and induced cell death. The effects of a GSP-supplemented AIN76A control diet fed to nude mice bearing tumor xenografts on the expression of COX-2, PGE 2 , and PGE 2 receptors in the xenografts were also evaluated. The growth-inhibitory effect of dietary GSPs (0.5%, w/w) on the NSCLC xenograft tumors was associated with the inhibition of COX-2, PGE 2 , and PGE 2 receptors (EP1, EP3, and EP4) in tumors. This preclinical study provides evidence that the chemotherapeutic effect of GSPs on lung cancer cells in vitro and in vivo is mediated, at least in part, through the inhibition of COX-2 expression and subsequently the inhibition of PGE 2 and PGE 2 receptors.Mol Cancer Ther; 9(3); 569-80. ©2010 AACR.

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Section: Introductionmentioning

confidence: 99%

Proanthocyanidins Inhibit In vitro and In vivo Growth of Human Non–Small Cell Lung Cancer Cells by Inhibiting the Prostaglandin E2 and Prostaglandin E2 Receptors

Sharma

Meeran

Katiyar

2010

Molecular Cancer Therapeutics

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“…Novel chemotherapeutic agents have been shown in some studies to increase survival of stage IIIB/ IV patients. However, these patients were cured rarely, if ever, by current chemotherapeutic agents (Hoffman et al, 2000). On the other hand, several phase III studies have shown that cisplatincontaining induction chemotherapy may increase survival rate in stage IIIA or IIIB locally advanced non-small cell lung cancer (LAD-NSCLC) patients.…”

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confidence: 99%

Gemcitabine and cisplatin in a multimodality treatment for locally advanced non-small cell lung cancer

et al. 2002

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The role of new cytotoxic agents like gemcitabine has not yet been proven in the neoadjuvant settings. We designed a phase II study to test the feasibility of using gemcitabine and cisplatin before local treatment for stage III non-small cell lung cancer patients. Patients received three cycles of induction chemotherapy of gemcitabine (1000 mg m 72 , days 1, 8, 15) and cisplatin (90 mg m 72 , day 15) every 4 weeks before evaluation for operability. Operable patients underwent radical resection. Inoperable patients and patients who had incomplete resection received concurrent chemoradiotherapy with daily low dose cisplatin. All patients who did not progress after local treatment received three more cycles of adjuvant chemotherapy of gemcitabine and cisplatin. Fifty-two patients received induction treatment. Two patients had complete response and 31 patients had partial response (response rate 63.5%) after induction chemotherapy. Thirty-six patients (69%) were operable. Eighteen patients (35%) had their tumours completely resected. Two patients had pathological complete response. Median overall survival was 19.1 months, projected 1-year survival was 66% and 2-year survival was 34%. Three cycles of gemcitabine and cisplatin is effective and can be used as induction treatment before surgery for locally advanced non-small cell lung cancer patients.

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“…In the leukocytes, pStat1 increased modestly (\1.5-fold) with IFN-c treatment (data was not shown). The clinico-pathologic characteristics of Patients A and B were listed in Table 1 Different Patterns of Stat1 Activation in Cancer Cells from MPE had Different Sensitivities to Cisplatin Cisplatin was the main agent for treating advanced lung cancer (10). Because Stat1 activation might contribute to drug resistance of cancer cells (16,17), the relationship between Stat1 activation after IFN-c stimulation and cell sensitivity to cisplatin in cancer cells from MPEs was investigated.…”

Section: Scpfc and Western Blot Analysis Of Ifn-c-induced Stat1 Phospmentioning

confidence: 99%

“…Lung cancer is frequently complicated by malignant pleural effusion (MPE) (10). Clinically, MPE is easily recurrent and difficult to manage (11,12).…”

mentioning

confidence: 99%

Single cell phospho‐specific flow cytometry can detect dynamic changes of phospho‐Stat1 level in lung cancer cells

Lin

Huang

et al. 2010

Cytometry Pt A

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Single cell phospho-specific flow cytometry (SCPFC) enables the investigation of signaling network interactions and the categorization of disease outcome. While this method has been successfully used to study hematologic disorders, its application on solid tumors has not been examined. This study aimed to demonstrate the ability of SCPFC to detect dynamic changes of Tyrosine phospho-Stat1 (pStat1) in solid tumor models and in human tumor samples. In the human lung cancer cell line PC14PE6/ AS2, the fluorescence intensity changes of pStat1 after IFN-c stimulation were compatible to results obtained by Western blot analysis. In metastatic animal models, cancer cells from subcutaneous tumors, malignant ascites, and peritoneal tumors responded to IFN-c. The pStat1 was activated in these cells after IFN-c stimulation, with a 1.5-to 2.5-fold increase in fluorescence intensity compared to the unstimulated control. To examine the potential clinical application of SCPFC, cancer cells were collected from malignant pleural effusions (MPEs) of lung cancer patients to observe the activation of pStat1 after IFN-c stimulation. Cell apoptosis after cisplatin treatment was evaluated by Annexin V staining, which showed that MPE cancer cells with higher pStat1 changes after IFN-c stimulation were more resistant to cisplatin. In conclusion, there is a preliminary application of SCPFC to solid tumors and links to drug sensitivity are promising. ' 2010 International Society for Advancement of Cytometry Key terms flow cytometry; phospho-Stat1; lung cancer; malignant pleural effusion MOST human neoplasms have aberrant signal transduction elements. Understanding the structure and regulation of these elements will provide more insights into cancer treatment. Among these signaling networks, phospho-protein members of signaling cascades govern the initiation and regulation of proliferative signals within cells. It is proposed that the phosphorylation of key signaling molecules in response to particular stimuli correlates with certain mutations and the body's response to cancer treatment.Using multi-parameter flow cytometry, single cell phospho-specific flow cytometry (SCPFC) has revealed that potentiated phospho-proteins in leukemia cells like Stats, p38, and Erk respond to several key stimuli, including IL-3, IFN-c, GCSF, GM-CSF, and FL (flt3 ligand) (1). By recording the basal patterns and changes in activity of phospho-proteins, expression profiles have been correlated with a mutant form of Flt3 (fms-like tyrosine kinase 3) and with disease outcome. Unfortunately, although SCPFC is well demonstrated in hematologic oncology (2-4), its application in solid tumors has not been fully examined.The signal transducer and activator of transcription (Stat) proteins are a family of transcription factors that mediate normal cell differentiation, tumor cell proliferation, and apoptosis. Previous studies have identified a suppression effect of Stat1 on

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Lung cancer

Cited by 613 publications

References 40 publications

Proanthocyanidins Inhibit In vitro and In vivo Growth of Human Non–Small Cell Lung Cancer Cells by Inhibiting the Prostaglandin E2 and Prostaglandin E2 Receptors

Proanthocyanidins Inhibit In vitro and In vivo Growth of Human Non–Small Cell Lung Cancer Cells by Inhibiting the Prostaglandin E2 and Prostaglandin E2 Receptors

Gemcitabine and cisplatin in a multimodality treatment for locally advanced non-small cell lung cancer

Single cell phospho‐specific flow cytometry can detect dynamic changes of phospho‐Stat1 level in lung cancer cells

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