Jay M Lee

University of California, Los Angeles, Los Angeles, CA, United States

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Publications (31)76.3 Total impact

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    ABSTRACT: Our objective was to identify risk factors associated with survival in patients who underwent pulmonary metastasectomy for soft tissue or bone sarcoma and to create a risk stratification model.
    The Journal of thoracic and cardiovascular surgery. 09/2014;
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    ABSTRACT: Purpose Patients with stage I NSCLC treated with SBRT do not undergo a staging mediastinoscopy, yet reported mediastinal recurrence rates appear lower than in those undergoing surgical resection. We determined incidental SBRT doses to assess whether this could account for the low rates of recurrence. Methods Between March 2009 and September 2012, patients with inoperable lung tumors (n=136) treated with SBRT at our institution were reviewed. SBRT regimen was 54Gy in 3 fractions with PETCT staging. Incidental doses to mediastinal lymph node stations (MLNS), primary tumor control (LC), locoregional (LR), distant control (DC) and overall survival (OS) rates were determined. Results 46 patients with stage I NSCLC met the inclusion criteria. The calculated median incidental SBRT dose to all MLNS was < 5 Gy for the majority of patients (75%). At a median follow up of 16.8 months (0.6–38.9 months), the 1 & 2 year LC, LR, OS and DC rates were 100%&95.5%, 97.4%&81.7%, 88.1%&81% and 96.9%&86.9%, respectively. Only 2 patients (4.9%) had mediastinal recurrences with incidental SBRT doses to MLNS that were similar to the rest of patients (p>0.05). Conclusions Low mediastinal recurrence in stage I NSCLC treated with SBRT validates omission of staging mediastinoscopy. The low incidental dose to MLNS does not seem to explain the low mediastinal recurrence in the majority of patients. Our findings also confirm that prophylactic radiation to the mediastinum is not necessary, and support a hypothesis that local ablation of the primary lesion could indirectly affect subclinical nodal disease through unknown mechanisms.
    Clinical Lung Cancer 07/2014; · 2.04 Impact Factor
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    ABSTRACT: Interleukin-27 signaling is mediated by the JAK-STAT pathway via activation of STAT1 and STAT3, which have tumor suppressive and oncogenic activities, respectively. Epithelial--mesenchymal transition (EMT) and angiogenesis are key processes in carcinogenesis. Although IL-27 has been shown to have potent anti-tumor activity in various cancer models, the role of IL-27 in EMT and angiogenesis is poorly understood. In this study, we investigated the role of IL-27 in regulating EMT and angiogenesis through modulation of the STAT pathways in human non-small cell lung carcinoma (NSCLC) cells. STAT activation following IL-27 exposure was measured in human NSCLC cell lines. Expression of epithelial (E-cadherin, gamma-catenin) and mesenchymal (N-cadherin, vimentin) markers were assessed by Western blot analysis. Production of pro-angiogenic factors (VEGF, IL-8/CXCL8, CXCL5) were examined by ELISA. Cell motility was examined by an in vitro scratch and transwell migration assays. Selective inhibitors of STAT1 (STAT1 siRNAs) and STAT3 (Stattic) were used to determine whether both STAT1 and STAT3 are required for IL-27 mediated inhibition of EMT and secretion of angiogenic factors. Our results demonstrate that IL-27 stimulation in NSCLC resulted in 1) STAT1 and STAT3 activation in a JAK-dependent manner, 2) development of epithelial phenotypes, including a decrease in the expression of a transcriptional repressor for E-cadherin (SNAIL), and mesenchymal marker (vimentin) with a reciprocal increase in the expression of epithelial markers, 3) inhibition of cell migration, and 4) reduced production of pro-angiogenic factors. STAT1 inhibition in IL-27--treated cells reversed the IL-27 effect with resultant increased expression of Snail, vimentin and the pro-angiogenic factors. The inhibition of STAT3 activation had no effect on the development of the epithelial phenotype. IL-27 induces mesenchymal to epithelial transition and inhibits the production of pro-angiogenic factors in a STAT1--dominant pathway. These findings highlight the importance of STAT1 in repressing lung carcinogenesis and describe a new anti-tumor mechanism of IL-27.
    Journal of Experimental & Clinical Cancer Research 11/2013; 32(1):97. · 3.07 Impact Factor
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    ABSTRACT: Although tumor growth leads to inflammatory responses, the immune system develops tolerance to cancer. One way to break host tolerance to tumors is to activate key immune effector activities. Toward this end, various adjuvants are under investigation in an effort to harness the immune system to overcome tolerance to tumor-associated self-antigens. There is enthusiasm for the use of specific ligands for toll-like receptor 3 (TLR3) that play a key role in the innate immune system. TLR3 agonists serve as immune adjuvants because they potently induce innate immune responses by activating dendritic cell (DC) maturation and inflammatory cytokine secretion. These activities facilitate the bridge between the innate and adaptive immune systems promoting the expansion of cytotoxic T lymphocytes (CTL) that destroy cancer cells. TLR3 agonists either alone or in combination with tumor antigens have shown success in terms of enhancing immune responses and eliciting antitumor activity in preclinical models. However, TLR3 agonists can also impact regulatory cells that dampen immune responses. Thus, immune strategies that utilize TLR3 agonists should consider the relative induction of suppressive as well as beneficial antitumor immune activities. Herein, we summarize the TLR3 agonists that will hopefully come to clinical fruition.
    Expert Opinion on Therapeutic Targets 03/2013; · 4.90 Impact Factor
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    ABSTRACT: 10  Abstract— Lung cancer remains a challenging health problem with more than 1.1 million deaths worldwide annually. With current therapy, the long term survival for the majority of lung cancer patients remains low, thus new therapeutic strategies are needed. One such strategy would be to develop immune therapy for lung cancer. Immune approaches remain attractive because although surgery, chemotherapy, and radiotherapy alone or in combination produce response rates in all histological types of lung cancer, relapse is frequent. Strategies that harness the immune system to react against tumors can be integrated with existing forms of therapy for optimal responses toward this devastating disease. Both antigen presenting cell (APC) and T cell activities are reduced in the lung tumor microenvironment. In this review we discuss our experience with efforts to restore host APC and T cell activities in the lung cancer microenvironment by intratumoral administration of dendritic cells (DC) expressing the CCR7 receptor ligand CCL21 (secondary lymphoid chemokine, SLC). Based on the results demonstrating that CCL21 is an effective anti cancer agent in the pre-clinical lung tumor model systems, a phase I clinical trial was initiated using intratumoral injection of CCL21 gene modified autologous DC in lung cancer. Results from the trial thus far indicate tolerability, immune enhancement and tumor shrinkage via this approach.
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    ABSTRACT: Lung cancer remains a challenging health problem with more than 1.1 million deaths worldwide annually. With current therapy, the long term survival for the majority of lung cancer patients remains low, thus new therapeutic strategies are needed. One such strategy would be to develop immune therapy for lung cancer. Immune approaches remain attractive because although surgery, chemotherapy, and radiotherapy alone or in combination produce response rates in all histological types of lung cancer, relapse is frequent. Strategies that harness the immune system to react against tumors can be integrated with existing forms of therapy for optimal responses toward this devastating disease. Both antigen presenting cell (APC) and T cell activities are reduced in the lung tumor microenvironment. In this review we discuss our experience with efforts to restore host APC and T cell activities in the lung cancer microenvironment by intratumoral administration of dendritic cells (DC) expressing the CCR7 receptor ligand CCL21 (secondary lymphoid chemokine, SLC). Based on the results demonstrating that CCL21 is an effective anti cancer agent in the pre-clinical lung tumor model systems, a phase I clinical trial was initiated using intratumoral injection of CCL21 gene modified autologous DC in lung cancer. Results from the trial thus far indicate tolerability, immune enhancement and tumor shrinkage via this approach.
    International trends in immunity. 01/2013; 1(1):10-15.
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    ABSTRACT: The EGFR tyrosine kinase inhibitors (TKIs) demonstrate efficacy in NSCLC patients whose tumors harbor activating EGFR mutations. However, patients who initially respond to EGFR TKI treatment invariably develop resistance to the drugs. Known mechanisms account for approximately 70% of native and acquired EGFR TKI resistance. In the current study we investigated a novel mechanism of NSCLC resistance to erlotinib. Experimental Design: The mechanisms of acquired erlotinib resistance were evaluated by microarray analysis in thirteen NSCLC cell lines and in vivo in mice. Correlations between plasma neutrophil gelatinase associated lipocalin (NGAL) levels, erlotinib response and the EGFR mutational status were assessed in advanced stage NSCLC patients treated with erlotinib. In 5 of 13 NSCLC cell lines NGAL was significantly upregulated. NGAL knockdown in erlotinib-resistant cells increased erlotinib sensitivity in vitro and in vivo. NGAL overexpression in erlotinib-sensitive cells augmented apoptosis resistance. This was mediated by NGAL-dependent modulation of the pro-apoptotic protein Bim levels. Evaluation of the plasma NGAL levels in NSCLC patients that received erlotinib revealed that patients with lower baseline NGAL demonstrated a better erlotinib response. Compared to patients with wild type EGFR, patients with activating EGFR mutations had lower plasma NGAL at baseline and weeks 4 and 8. Our studies uncover a novel mechanism of NGAL-mediated modulation of Bim levels in NSCLC that might contribute to TKI resistance in lung cancer patients. These findings provide the rationale for the further investigations of the utility of NGAL as a potential therapeutic target or diagnostic biomarker.
    American Journal of Translational Research 01/2013; 5(5):481-96.
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    ABSTRACT: Introduction. Patients with high-grade sarcoma (HGS) frequently develop metastatic disease thus limiting their long-term survival. Lung metastases (LM) have historically been treated with surgical resection (metastasectomy). A potential alternative for controlling LM could be stereotactic body radiation therapy (SBRT). We evaluated the outcomes from our institutional experience utilizing SBRT. Methods. Sixteen consecutive patients with LM from HGS were treated with SBRT between 2009 and 2011. Routine radiographic and clinical follow-up was performed. Local failure was defined as CT progression on 2 consecutive scans or growth after initial shrinkage. Radiation pneumonitis and radiation esophagitis were scored using Common Toxicity Criteria (CTC) version 3.0. Results. All 16 patients received chemotherapy, and a subset (38%) also underwent prior pulmonary metastasectomy. Median patient age was 56 (12-85), and median follow-up time was 20 months (range 3-43). A total of 25 lesions were treated and evaluable for this analysis. Most common histologies were leiomyosarcoma (28%), synovial sarcoma (20%), and osteosarcoma (16%). Median SBRT prescription dose was 54 Gy (36-54) in 3-4 fractions. At 43 months, local control was 94%. No patient experienced G2-4 radiation pneumonitis, and no patient experienced radiation esophagitis. Conclusions. Our retrospective experience suggests that SBRT for LM from HGS provides excellent local control and minimal toxicity.
    Sarcoma 01/2013; 2013:360214.
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    ABSTRACT: Myeloid derived suppressor cells (MDSC) are important regulators of immune responses. We evaluated the mechanistic role of MDSC depletion on antigen presenting cell (APC), NK, T cell activities and therapeutic vaccination responses in murine models of lung cancer. Individual antibody mediated depletion of MDSC (anti-Gr1 or anti-Ly6G) enhanced the antitumor activity against lung cancer. In comparison to controls, MDSC depletion enhanced the APC activity and increased the frequency and activity of the NK and T cell effectors in the tumor. Compared to controls, the anti-Gr1 or anti-Ly6G treatment led to increased: (i) CD8 T cells, (ii) NK cells, (iii) CD8 T or NK intracytoplasmic expression of IFNγ, perforin and granzyme (iv) CD3 T cells expressing the activation marker CD107a and CXCR3, (v) reduced CD8 T cell IL-10 production in the tumors (vi) reduced tumor angiogenic (VEGF, CXCL2, CXCL5, and Angiopoietin1&2) but enhanced anti-angiogenic (CXCL9 and CXCL10) expression and (vii) reduced tumor staining of endothelial marker Meca 32. Immunocytochemistry of tumor sections showed reduced Gr1 expressing cells with increased CD3 T cell infiltrates in the anti-Gr1 or anti-Ly6G groups. MDSC depletion led to a marked inhibition in tumor growth, enhanced tumor cell apoptosis and reduced migration of the tumors from the primary site to the lung compared to controls. Therapeutic vaccination responses were enhanced in vivo following MDSC depletion with 50% of treated mice completely eradicating established tumors. Treated mice that rejected their primary tumors acquired immunological memory against a secondary tumor challenge. The remaining 50% of mice in this group had 20 fold reductions in tumor burden compared to controls. Our data demonstrate that targeting MDSC can improve antitumor immune responses suggesting a broad applicability of combined immune based approaches against cancer. This multifaceted approach may prove useful against tumors where MDSC play a role in tumor immune evasion.
    PLoS ONE 10/2012; 7(7):e40677. · 3.53 Impact Factor
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    ABSTRACT: Lung cancer evades host immune surveillance by dysregulating inflammation. Tumors and their surrounding stromata produce growth factors, cytokines, and chemokines that recruit, expand, and/or activate myeloid-derived suppressor cells (MDSCs). MDSCs regulate immune responses and are frequently found in malignancy. In this review the authors discuss tumor-MDSC interactions that suppress host antitumor activities and the authors' recent findings regarding MDSC depletion that led to improved therapeutic vaccination responses against lung cancer. Despite the identification of a repertoire of tumor antigens, hurdles persist for immune-based anticancer therapies. It is likely that combined therapies that address the multiple immune deficits in cancer patients will be required for effective therapy. MDSCs play a major role in the suppression of T-cell activation and they sustain tumor growth, proliferation, and metastases. Regulation of MDSC recruitment, differentiation or expansion, and inhibition of the MDSC suppressive function with pharmacologic agents will be useful in the control of cancer growth and progression. Pharmacologic agents that regulate MDSCs may be more effective when combined with immunotherapies. Optimization of combined approaches that simultaneously downregulate MDSC suppressor pathways, restore APC immune-stimulating activity, and expand tumor-reactive T cells will be useful in improving therapy.
    ImmunoTargets and therapy. 10/2012; 2012(1):7-12.
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    ABSTRACT: Lung cancer is the leading cause of cancer death for both men and women worldwide. Since most of the symptoms found for lung cancer are nonspecific, diagnosis is mostly done at late and progressed stage with the consecutive poor therapy outcome. Effective early detection techniques are sorely needed. The emerging field of salivary diagnostics could provide scientifically credible, easy-to-use, non-invasive and cost-effective detection methods. Recent advances have allowed us to develop discriminatory salivary biomarkers for a variety of diseases from oral to systematic diseases. In this study, salivary transcriptomes of lung cancer patients were profiled and led to the discovery and pre-validation of seven highly discriminatory transcriptomic salivary biomarkers (BRAF, CCNI, EGRF, FGF19, FRS2, GREB1, and LZTS1). The logistic regression model combining five of the mRNA biomarkers (CCNI, EGFR, FGF19, FRS2, and GREB1) could differentiate lung cancer patients from normal control subjects, yielding AUC value of 0.925 with 93.75 % sensitivity and 82.81 % specificity in the pre-validation sample set. These salivary mRNA biomarkers possess the discriminatory power for the detection of lung cancer. This report provides the proof of concept of salivary biomarkers for the non-invasive detection of the systematic disease. These results poised the salivary biomarkers for the initiation of a multi-center validation in a definitive clinical context.
    Cellular and Molecular Life Sciences CMLS 06/2012; 69(19):3341-50. · 5.62 Impact Factor
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    Tumor Microenvironment and Myelomonocytic Cells, 03/2012; , ISBN: 978-953-51-0439-1
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    ABSTRACT: Primary chest wall sarcomas are rare mesenchymal tumors and their mainstay of therapy is wide surgical resection. We report our single-institution, multidisciplinary experience with full-thickness resection for primary chest wall sarcomas. A retrospective review of our prospectively maintained databases revealed that 51 patients were referred for primary chest wall sarcomas from 1990 to 2009. All patients required resections that included rib and/or sternum. Twenty-nine patients (57%) had extended resections beyond the chest wall. Forty-two patients (82%) required prosthetic reconstruction and 17 patients (33%) had muscle flap coverage. Overall, 51% (26/51) of patients received neoadjuvant therapy. Seventy-three percent (11/15) of high-grade soft tissue sarcomas, 77% (10/13) of high-risk bony sarcomas, and 67% (4/6) of desmoid tumors were treated with induction therapy. Negative margins were obtained in 46 patients (90%). There were no perioperative mortalities. Eight patients (16%) experienced complications. Local recurrence and metastasis was detected in 14 and 23%. Five-year overall and disease-free survivals were 66% and 47%, respectively. Favorable prognostic variables for survival included age ≤50 years, tumor volume ≤200 cm, desmoid tumor, bony tumor, chondrosarcoma, and low-grade soft tissue sarcoma. We report our multidisciplinary experience with primary chest wall sarcomas that included induction therapy in the majority of high-risk soft tissue and bony sarcomas and desmoid tumors. Despite aggressive preoperative treatments, acceptable surgical results with low morbidity and mortality can be achieved. Neoadjuvant systemic therapy may reduce local and distant recurrence and improve overall survival.
    Journal of thoracic oncology: official publication of the International Association for the Study of Lung Cancer 03/2012; 7(3):552-8. · 4.55 Impact Factor
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    ABSTRACT: Many tumors, including lung cancers, promote immune tolerance to escape host immune surveillance and facilitate tumor growth. Tumors utilize numerous pathways to inhibit immune responses, including the elaboration of immune-suppressive mediators such as PGE2, TGF-β, IL-10, VEGF, GM-CSF, IL-6, S100A8/A9 and SCF, which recruit and/or activate myeloid-derived suppressor cells (MDSCs). MDSCs, a subset of heterogeneous bone marrow-derived hematopoietic cells, are found in the peripheral blood of cancer patients and positively correlate to malignancy. Solid tumors contain MDSCs that maintain an immune-suppressive network in the tumor microenvironment. This review will focus on the interaction of tumors with MDSCs that lead to dysregulation of antigen presentation and T-cell activities in murine tumor models. Specific genetic signatures in lung cancer modulate the activities of MDSCs and impact tumor progression. Targeting MDSCs may have a long-term antitumor benefit and is at the forefront of anticancer therapeutic strategies.
    Immunotherapy 03/2012; 4(3):291-304. · 2.39 Impact Factor
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    ABSTRACT: Lung cancer is often asymptomatic or causes only nonspecific symptoms in its early stages. Early detection represents one of the most promising approaches to reduce the growing lung cancer burden. Human saliva is an attractive diagnostic fluid because its collection is less invasive than that of tissue or blood. Profiling of proteins in saliva over the course of disease progression could reveal potential biomarkers indicative of oral or systematic diseases, which may be used extensively in future medical diagnostics. There were 72 subjects enrolled in this study for saliva sample collection according to the approved protocol. Two-dimensional difference gel electrophoresis combined with MS was the platform for salivary proteome separation, quantification, and identification from two pooled samples. Candidate proteomic biomarkers were verified and prevalidated by using immunoassay methods. There were 16 candidate protein biomarkers discovered by two-dimensional difference gel electrophoresis and MS. Three proteins were further verified in the discovery sample set, prevalidation sample set, and lung cancer cell lines. The discriminatory power of these candidate biomarkers in lung cancer patients and healthy control subjects can reach 88.5% sensitivity and 92.3% specificity with AUC = 0.90. This preliminary data report demonstrates that proteomic biomarkers are present in human saliva when people develop lung cancer. The discriminatory power of these candidate biomarkers indicate that a simple saliva test might be established for lung cancer clinical screening and detection.
    Molecular &amp Cellular Proteomics 11/2011; 11(2):M111.012112. · 7.25 Impact Factor
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    ABSTRACT: Sarcomas are rare mesenchymal malignancies. Accurate preoperative diagnosis is a prerequisite in considering investigational or institutional management algorithms that include neoadjuvant treatment. We reviewed our experience using core needle biopsy for chest wall sarcomas. A retrospective review of our sarcoma databases revealed that 40 core needle biopsies and 35 tumor resections were performed in 34 patients, with chest wall musculoskeletal tumors, referred to the University of California, Los Angeles from 1991 to 2010. Primary, metastatic, or recurrent sarcomas involving the sternum, ribs, and soft tissues of the chest wall were evaluated for (1) adequacy of tissue from image-guided core needle biopsies and (2) accuracy in determining malignancy, histological subtype, and sarcoma grade. Twenty-eight of the 40 needle biopsy samples (70%) were adequate for histopathological analysis. Forty-two percent of nondiagnostic findings occurred due to insufficient tissue, whereas the remainder had sufficient tissue, but the pathologist was unable to determine specific histology. Excluding the nondiagnostic samples, the accuracy in determining malignancy, histological subtype, and grade in sarcomas was 100, 92, and 87%, respectively. The sensitivity and specificity of determining malignancy and high-grade sarcomas were 100, 100, 77, and 100%, respectively. There were no complications from the image-guided biopsies. We demonstrated that image-guided core needle biopsy when performed and reviewed by experienced radiologists and musculoskeletal pathologists is a safe and accurate diagnostic technique for chest wall sarcomas. Core needle biopsy should be considered in the multidisciplinary approach to chest wall musculoskeletal tumors, especially when induction therapy is considered.
    Journal of thoracic oncology: official publication of the International Association for the Study of Lung Cancer 09/2011; 7(1):151-6. · 4.55 Impact Factor
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    ABSTRACT: Despite advances in treatments, lung cancer has been the leading cause of cancer-related deaths in the United States for the past several decades. Recent findings from the National Lung Screening Trial reveal that low-dose helical computed tomography (CT) scan screening of high-risk individuals reduces lung cancer mortality. This suggests that early detection is of key importance to improving patient outcome. However, of those screened with CT scans, 25% had positive scans that require further follow-up studies which often involve more radiation exposure and invasive tests to reduce false positive results. The purpose of this study was to identify candidate plasma biomarkers to aid in diagnosis of lung cancer in at-risk individuals. We found increased expression of the CXC chemokine connective tissue-activating peptide (CTAP)-III from plasma specimens of lung cancer patients compared to at-risk control subjects. Identification of the peptide was confirmed by the addition of an anti-NAP-2 antibody that recognizes CTAP-III and NAP-2. We also quantified and verified the increased levels of plasma CTAP-III with ELISA in patients with lung cancer (mean ± SD, 1859 ± 1219 ng/mL) compared to controls (698 ± 434 ng/mL; P<0.001). Our findings demonstrate elevated plasma levels of CTAP-III occur in lung cancer patients. Further studies are required to determine if this chemokine could be utilized in a blood-based biomarker panel for the diagnosis of lung cancer.
    American Journal of Translational Research 05/2011; 3(3):226-33.
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    ABSTRACT: Solitary fibrous tumors of the pleura are rare neoplasms with both benign and malignant behaviors that are not reliably predicted by histologic findings. We report the case of a 55-year-old woman with recurrent pneumonias whose left mainstem bronchus was occluded by a 2.1- x 1.4-cm endobronchial mass that extended extraluminally into the subcarina. The mass was tissue diagnosed to be a solitary fibrous tumor preoperatively, and was completely resected by sleeve resection of the left mainstem bronchus with lung preservation. This report describes the challenging surgical management of an infrequently encountered tumor in a unique location.
    The Annals of thoracic surgery 08/2010; 90(2):659-61. · 3.45 Impact Factor
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    ABSTRACT: While genetic changes are critical for the malignant transformation of epithelial cells, the microenvironment in which the cells reside also governs carcinogenesis. Most tumors arise within a cellular microenvironment characterized by suppressed host immunity, dysregulated inflammation, and increased production of cellular growth and survival factors that induce angiogenesis and inhibit apoptosis. The studies highlighted in this chapter indicate that the lung tumor and its microenvironment interact, together informing the process of carcinogenesis. Understanding the molecular mechanisms driving the contributions of the tumor microenvironment to lung carcinogenesis may afford us the opportunity to develop new drugs that target these reversible nonmutational events in the prevention and treatment of lung cancer. Findings from recent microenvironment-related clinical studies have implications for understanding the immunopathobiology of lung cancer, for targeting surgery and adjuvant therapy, and for designing future trials of adjuvant therapy. If the field is to progress and promising leads in the laboratory are to translate into anticancer therapeutics, future trials targeting the tumor microenvironment must incorporate improved patient risk assessment and selection, in addition to the continued evaluation of combination therapies using the optimal biological dose of each compound being tested. Appropriately targeting the tumor microenvironment in a highly selected patient population is a newly emerging strategy that holds unique potential for advancing the current state of lung cancer prevention and treatment. KeywordsTumor microenvironment-NSCLC prognosis-Mast cells-Macrophage-Dendritic cells-Ectopic lymph nodes-T regulatory cells-MMP-COX-2-PGE2-PPARγ-15-PGDH-Inflammation-EMT-NF-κB-HGF-c-MET-Angiogenesis-Molecular signatures
    03/2010: pages 27-69;
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    ABSTRACT: Chemokines (ie, chemoattractant cytokines) are a family of small secreted molecules that mediate leukocyte migration. It is becoming increasingly more evident that chemokines play an integral role in the initiation of a specific immune response. With respect to cancer, chemokines are being studied for both their role in tumor biology and as promising immunotherapy candidates. We review several areas of chemokine importance in tumor immunity and discuss the experimental evidence that is leading to the clinical use of this cytokine family in new treatment approaches for patients with cancer.
    The Cancer Journal 01/2010; 16(4):325-35. · 3.66 Impact Factor

Publication Stats

344 Citations
76.30 Total Impact Points

Institutions

  • 2007–2013
    • University of California, Los Angeles
      • • Department of Medicine
      • • Department of Surgery
      • • Division of Pulmonary and Critical Care
      • • Division of Cardiothoracic Surgery
      Los Angeles, CA, United States
  • 2009–2012
    • Comprehensive Cancer Centers of Nevada
      Las Vegas, Nevada, United States
  • 2010
    • Moffitt Cancer Center
      Tampa, Florida, United States