Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0178874 (tumor progression)
 40,807 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Interferon-alpha (IFN-alpha) is well established in the treatment of neuroendocrine carcinomas (NEC). Treatment is accompanied by fatigue and flu-like symptoms. In patients with chronic hepatitis C, pegylated IFN (PEGIFN) leads to improved antiviral efficacy and good tolerability. Our aim was to assess the efficacy and tolerability of PEG-IFN on the management of patients with well-differentiated NEC of the gastroenteropancreatic system. In 17 patients, the effect of PEG-IFN-alpha2b was studied. After first-line octreotide treatment, IFN-alpha was added at the time of tumor progression. Six patients were switched from conventional IFN-alpha, and 11 patients were IFN naive. Inhibition of tumor growth, including stabilization of disease, occurred in 13 of 17 patients, and biochemical and symptomatic responses were seen in 7 of 10 patients with functionally active tumors. Tolerability of PEG-IFN-alpha2b was much better than that of IFN-alpha. Fatigue occurred in 59% of all patients but was mild in severity. Eleven of thirteen patients who had a benefit remained on therapy for a median time of 20 months (range 6-30 months). PEG-IFN-alpha2b provides symptomatic and antiproliferative efficacy in patients with NEC. Better tolerability of PEG-IFN-alpha2b improved patients' compliance, justifying its use in patients who do not tolerate conventional IFN-alpha treatment.
J Interferon Cytokine Res 2006 Jan
PMID:Efficacy and tolerability of pegylated IFN-alpha in patients with neuroendocrine gastroenteropancreatic carcinomas. 1642 43

Matrix metalloproteinase-8 (MMP-8), also known as collagenase-2 or neutrophil collagenase, was long thought to be expressed solely by maturing neutrophils, and functionally restricted to ECM breakdown. Recent experiments, however, have revealed that this protease can be expressed by a wide variety of cell types and that it plays an important regulatory role in both acute and chronic inflammation. This review intends to give the reader an overview of the most interesting recent findings concerning the role of MMP-8 in inflammation and in cancer progression.
Cytokine Growth Factor Rev 2006 Aug
PMID:Matrix metalloproteinase-8: cleavage can be decisive. 1682 Mar 17

Hormonal cancers such as breast and prostate cancer arise from steroid hormone-regulated tissues. In addition to breast and prostate cancer hormonal regulation has also a role in endometrial, ovarian, testis and thyroid carcinomas. The effects of estrogens, androgens and progestagens on tumor growth are largely mediated by paracrine and autocrine target molecules which include growth factors and growth factor receptors. During cancer progression the hormonal growth regulation is often lost or overcome by an inappropriate activation of growth factor signaling cascades. One of the growth factors which have been associated with the regulation of growth and progression of hormonal cancer is fibroblast growth factor 8 (FGF8) which has also been recognized as an oncogene. FGF8 is widely expressed during embryonic development. It has been shown to mediate embryonic epithelial-mesenchymal transition and to have a crucial role in gastrulation and early organization and differentiation of midbrain/hindbrain, pharyngeal, cardiac, urogenital and limb structures. During adulthood FGF8 expression is much more restricted but in hormonal cancers it becomes frequently activated. High level of FGF8 expression in tumors is associated with a poor prognosis at least in prostate cancer. In experimental models FGF8 induces and facilitates prostate tumorigenesis and increases growth and angiogenesis of tumors. Several lines of evidence for autocrine and paracrine loops in the growth regulation of breast, prostate and ovarian cancer by FGF8 have been suggested.
Cytokine Growth Factor Rev
PMID:Role of fibroblast growth factor 8 in growth and progression of hormonal cancer. 1751 40

Angiogenesis plays an important role in many types of cancer. Interleukin-8 (IL-8) is known to be a pro-inflammatory and pro-angiogenic cytokine, and IL-8 has been reported to be associated with tumor progression, prognosis and survival in several types of cancers. However, the role of IL-8 in non-Hodgkin's lymphoma (NHL) has not been fully determined. Here, we evaluated the usefulness of measuring serum and urine IL-8 levels in patients with NHL. We developed reference intervals for serum and urine IL-8 level in 131 control individuals. We measured serum IL-8 and urine IL-8 levels in patients with NHL, and we compared the concentrations with those of control individuals. The reference intervals for serum IL-8 and urine IL-8 corrected by creatinine (Cr) were 15.9-430.3 pg/mL and 0.0-28.4 pg/mg Cr, respectively. The concentrations of urine IL-8/Cr were significantly higher in patients than in controls (48.9+/-194.4 vs. 5.2+/-13.8 pg/mg Cr, P<0.001). However, there were no significant differences in serum IL-8 concentrations between NHL patients and controls (159.2+/-40.4 vs. 99.6+/-107.1 pg/mL; P=0.099). Receiver operating characteristic (ROC) analysis gave 0.83 and 0.43 ROC area values for urine IL-8/Cr and serum IL-8, respectively. There was no correlation between the serum and urine concentrations of IL-8 and clinical variables, the only exception being the international prognostic index (IPI), which showed a marginal correlation with urine IL-8/Cr levels (P=0.07). This study indicated that urine IL-8/Cr levels might be useful as a diagnostic marker of NHL.
Cytokine 2008 Jul
PMID:Serum and urine levels of interleukin-8 in patients with non-Hodgkin's lymphoma. 1850 45

Bone remodelling is regulated by osteogenic cells which act individually through cellular and molecular interaction. These interactions can be established either through a cell-cell contact, involving molecules of the integrin family, or by the release of many polypeptidic factors and/or their soluble receptor chains. Proteolytic shedding of membrane-associated proteins regulates the physiological activity of numerous proteins. Proteases located on the plasma membrane, either as transmembrane proteins or anchored to cell-surface molecules, serve as activators or inhibitors of different cellular and physiological processes. This review will focus on the role of the proteases implicated in bone remodelling either through the proteolytic degradation of the extracellular matrix or through their relations with osteogenic factors. Their implication in bone tumor progression will be also considered.
Cytokine Growth Factor Rev 2009 Feb
PMID:Proteases and bone remodelling. 1904 Dec 77

Studies in mice and humans have demonstrated a role for the immune system in preventing the growth of tumors. Deciphering the mechanisms involved in the immune response to tumors is essential to our understanding of immune recognition and cancer progression. Here we report an innate immune response to tumors in Drosophila melanogaster. We found that circulating blood cells, termed hemocytes, adhere to tumors upon detection of basement membrane disruption, and subsequently counter their growth. Basement membrane components are remarkably conserved throughout the animal kingdom, providing a unique structure for the immune system to sense tissue integrity. Further, we show that tissue damage activates JNK signaling in both tumors and aseptic wounds, causing expression of JAK/STAT-activating cytokines. Cytokine secretion from the injured tissue is amplified into a systemic response through the induction of additional cytokine expression in the hemocytes and the fat body, resulting in hemocyte proliferation. Our findings reveal common mechanisms in the response to tumors and wounds in flies. A similar innate reaction may underlie the response to tumors and tissue damage in vertebrates and humans.
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PMID:An innate immune response of blood cells to tumors and tissue damage in Drosophila. 1904 77

Epidemiological and experimental data demonstrate, that inflammation contributes significantly to pancreatic carcinogenesis. IL1beta, a pleiotropic cytokine produced by inflammatory cells and tumor cells, promotes cancer progression. Single nucleotide polymorphisms (SNPs) of the IL1beta promoter were found to be associated with an increased risk for certain cancers. In this case-control study we determined IL1beta promoter SNPs in 73 patients with pancreatic cancer and 235 controls. We found that the IL1beta -511CT/-31TC genotype was significantly associated with an increased risk for pancreatic cancer (OR 1.42, p=0.0456). Among pancreatic cancer cases, patients with the -511CT/-31TC genotype had less frequently resectable disease than patients with other IL1beta -511/-31 genotypes (p=0.0323). Furthermore, the IL1beta -511CT/-31TC genotype was more frequent observed in UICC stage IV (p=0.039) and undifferentiated tumors (G3) (p=0.019). In addition, we found that the proinflammatory IL1beta -511CT/-31TC alleles define an IL1beta secretory phenotype in pancreatic cancer cell lines in vitro. These findings provide a first evidence for an association of the IL1beta gene promoter SNPs with risk for pancreatic cancer.
Cytokine 2009 May
PMID:Interleukin 1 beta gene promoter SNPs are associated with risk of pancreatic cancer. 1925 36

The significance of circulating levels of TNF-alpha and its soluble receptors (sTNF-Rs) in the plasma of patients with epithelial ovarian cancer (EOC) has not been fully elucidated. The present study was to investigate the relationship of pretreatment plasma levels of TNF-alpha, sTNFR-1 and sTNFR-2 with outcome in 126 patients with EOC. Concentrations of TNF-alpha and sTNF-Rs were determined by enzyme-linked immunosorbent assay (ELISA). Median TNF-alpha and sTNF-Rs levels were significantly higher in EOC patients than in healthy controls. High plasma levels of TNF-alpha and sTNF-Rs were correlated with tumor stage and with reduced mean survival time (MST). The results of the present study suggested that preoperative plasma TNF-alpha and sTNF-Rs levels in EOC patients correlated with the highest risk of cancer progression. Thus, the clinical value of an activated TNF system in EOC needs to be further investigated.
Eur Cytokine Netw 2009 Sep
PMID:Circulating levels of TNF-alpha and its soluble receptors in the plasma of patients with epithelial ovarian cancer. 1982 22

Chemokines are a key component of cancer-related inflammation. Chemokines and chemokine receptors are downstream of genetic events that cause neoplastic transformation and are components of chronic inflammatory conditions, which predispose to cancer. Components of the chemokine system affect in a cell autonomous or non-autonomous way multiple pathways of tumor progression, including: leukocyte recruitment and function; cellular senescence; tumor cell proliferation and survival; invasion and metastasis. Available information in preclinical and clinical settings suggests that the chemokine system represents a valuable target for the development of innovative therapeutic strategies.
Cytokine Growth Factor Rev 2010 Feb
PMID:The chemokine system in cancer biology and therapy. 2000 31

CCL2 is a chemokine known to recruit monocytes and macrophages to sites of inflammation. A growing body of research suggests CCL2 is progressively overexpressed in tumor beds and may play a role in the clinical progression of solid tumors. Cancer cells derived from several solid tumor types demonstrate functional receptors for CCL2, suggesting this chemokine may achieve tumorigenicity through direct effects on malignant cells; however, a variety of normal host cells that co-exist with cancer in the tumor microenvironment also respond to CCL2. These cells include macrophages, osteoclasts, endothelial cells, T-lymphocytes, and myeloid-derived immune suppressor cells (MDSCs). CCL2 mediated interactions between normal and malignant cells in the tumor microenvironment and plays a multi-faceted role in tumor progression.
Cytokine Growth Factor Rev 2010 Feb
PMID:CC chemokine ligand 2 (CCL2) promotes prostate cancer tumorigenesis and metastasis. 2000 49


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