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)

Invasive thymoma recently has been shown to be sensitive to combination chemotherapy and in some cases to be relatively indolent. Two cases of extensive thymoma which responded to primary treatment with a combination of a platinum compound (carboplatin or cisplatin), doxorubicin (Adriamycin), and cyclophosphamide (or PAC) are described. Tumor progression occurred 14 (case 1) and 60 months (case 2) after completion of initial PAC therapy and was treated with the same regimen resulting in a second remission, which lasted 6 months in case 1 and is continuing at 8 months in case 2. Similar reports of secondary responses using the same chemotherapy have been described in breast, lung, and ovarian cancers, as well as in Hodgkin's lymphomas. Our observations suggest that retreatment with the same platinum-based regimen should be considered in patients who have progressive thymomas following a previous chemotherapeutic response and a disease-free interval of greater than 12 months.
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PMID:Retreatment of recurrent invasive thymoma with platinum, doxorubicin, and cyclophosphamide. 926 13

The modifying effects of dietary administration of protocatechuic acid (PCA) during the progression phase of tongue carcinogenesis initiated with 4-nitroquinoline 1-oxide (4-NQO) were investigated in male F344 rats. For tumor progression we developed a new animal model, where rats initiated by 4-week treatment of 20 ppm 4-NQO in drinking water, received four cycles of 20 ppm 4-NQO to induce advanced tongue cancer (one cycle: 2 weeks of 4-NQO followed by 2 weeks of tap water), starting at 14 weeks after the initiation. In this model, metastasis of tongue cancer occurred in lungs. Starting two weeks before the cycle treatment with 4-NQO, animals were fed the 2000 ppm PCA containing diet and continued on this diet until the end of the study. At the termination of the experiment (week 32), the incidences of tongue neoplasms and preneoplastic lesions, polyamine levels in the tongue tissue, and cell proliferation activity estimated by morphometric analysis of silver-stained nucleolar organizer regions protein were compared among the groups. Feeding with PCA containing diet during the progression phase significantly decreased the occurrence of advanced tongue squamous cell carcinoma with metastasis (P<0.05) and preneoplasia (hyperplasia and dysplasia) (P<0.001). In addition, PCA exposure decreased polyamine levels in the tongue tissue (P<0.001) during progression phase. Our results suggest that dietary PCA inhibits progression of 4-NQO-induced oral carcinogenesis, and such inhibition might be related to suppression of cell proliferation by PCA.
Asian Pac J Cancer Prev
PMID:Dietary protocatechuic acid during the progression phase exerts chemopreventive effects on chemically induced rat tongue carcinogenesis. 1472 90

Disturbances of the ratio between angiogenic inducers and inhibitors in tumor microenvironment are the driving force behind angiogenic switch critical for tumor progression. Angiogenic inhibitors may vary depending on organismal age and the tissue of origin. We showed that alpha(1)-antitrypsin (AAT), a serine protease inhibitor (serpin) is an inhibitor of angiogenesis, which induced apoptosis and inhibited chemotaxis of endothelial cells. S- and Z-type mutations that cause abnormal folding and defective serpin activity abrogated AAT antiangiogenic activity. Removal of the C-terminal reactive site loop had no effect on its angiostatic activity. Both native AAT and AAT truncated on C-terminus (AATDelta) inhibited neovascularization in the rat cornea and delayed the growth of subcutaneous tumors in mice. Treatment with native AAT and truncated AATDelta, but not control vehicle reduced tumor microvessel density, while increasing apoptosis within tumor endothelium. Comparative analysis of the human tumors and normal tissues of origin showed correlation between reduced local alpha(1)-antitrypsin expression and more aggressive tumor growth.
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PMID:Alpha1-antitrypsin inhibits angiogenesis and tumor growth. 1531 42

There is a growing body of evidence that the occurrence of neuroendocrine (NE) differentiation in prostate carcinoma correlates with poor prognosis, tumor progression, and androgen-independence. In the present study, the expression of common NE markers, i.e., chromogranin A (ChGA), serotonin (5HT), neuron-specific enolase (NSE) and adrenomedullin (AM), was retrospectively examined in formalin-fixed, paraffin-embedded prostate tissue samples obtained from patients with adenocarcinoma and from patients with nodular hyperplasia of the prostatic gland (NHPG) (33 and 28, respectively). The statistical analysis of the results (tested the equality of matched pairs of observations using the Wilcoxon matched-pairs signed ranks test) revealed a more prominent expression of ChGA in benign epithelial cells adjacent to adenocarcinomatic lesions (Peri-PAC) than in the adenocarcinoma (PAC) (p = 0.0049). A similar pattern of expression was detected for 5HT (p = 0.000). When comparing the expression of ChGA and 5HT in tissue samples originating in cancer patients with those obtained from NHPG samples, more ChGA and 5HT were expressed in Peri-PAC than in NHPG (p = 0.0004 and 0.002, respectively). The results obtained raise the possibility that adenocarcinoma cells urge some adjacent benign epithelial cells to differentiate into NE cells, which, in turn, may promote tumor growth and invasion.
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PMID:Augmented expression of chromogranin A and serotonin in peri-malignant benign prostate epithelium as compared to adenocarcinoma. 1546 96

Studies of the angiotensin converting enzyme (ACE) I/D polymorphism have provided evidence that the D/D genotype is associated with gastric tumor progression and numbers of lymph node metastases, but not with the overall risk of gastric cancer. The highest levels of circulating and tissue ACE activity were found in carriers of the D/D genotype. Here, we further investigated the association using 454 Japanese subjects undergoing a health checkup and 202 gastric cancer patients. The ACE polymorphism was not found to be linked with H. pylori seropositivity or gastric atrophy. However, among H. pylori seropositive subjects with atrophy, those with the I/D genotype had an increased risk of gastric cancer (OR=1.59; 95% CI, 1.02-2.48). We also established that the polymorphism did not lower the age at diagnosis of gastric cancer. Confirmation of the association between ACE polymorphisms and development of gastric cancer requires much larger studies, and the biological role also needs to be fully elucidated.
Asian Pac J Cancer Prev
PMID:The ACE gene polymorphism is associated with the incidence of gastric cancer among H. pylori seropositive subjects with atrophic gastritis. 1643 92

Breast cancer is the most common malignancy in women in the world. High incidence and poor clinical outcomes underly the need for a better understanding of its tumor biology and how to effectively inhibit tumor progression. In the present study the question of whether NDRG2 might be a useful target for breast cancer therapy was addressed. With the increase or decrease of NDRG2 levels in MCF-7 and Bcap-37 cells by adenovirus-NDRG2 infection or NDRG2 siRNA transfection, CD24 expression was significantly decreased or increased, respectively. Furthermore, NDRG2 overexpression suppressed breast cancer cell adhesion and invasion, whereas knockdown of NDRG2 promoted these events. In conclusion, the data from the current study indicated that NDRG2, the product of a tumor suppressor gene, can regulate CD24 expression to decrease the metastatic potential of breast cancer cells.
Asian Pac J Cancer Prev 2010
PMID:NDRG2 expression regulates CD24 and metastatic potential of breast cancer cells. 2133 39

Advanced hepatocellular carcinoma (HCC) is an important cause of cancer mortality. Epithelial-mesenchymal transition (EMT) has been shown to be an important biological process in cancer progression and metastasis. We have focused on elucidating factors that induce EMT to promote carcinogenesis and subsequent metastasis in HCC using the BNL CL.2 (BNL) and BNL 1ME A. 7R.1 (1MEA) cell lines. BNL cells are normal hepatocytes whereas the 1MEA cells are HCC cells derived from chemical transformation of the BNL cells. Their morphological characteristics were examined. Expression levels of hepatocyte growth factor (HGF), markers of EMT and mediators of HGF signaling were determined and functional characteristics were compared. BNL cells were treated with HGF and effects on EMT-marker and mediators of HGF signaling were analyzed. BNL cells display characteristic epithelial morphology whereas 1MEA cells display mesenchymal characteristics. 1MEA cells express and secrete more HGF than BNL cells. There was significantly decreased expression of E-cadherin, albumin, AAT and increased expression of fibronectin, collagen-1, vimentin, snail and slug in 1MEA cells. There was also increased expression of cyclooxygenase-2 (COX-2), Akt and phosphorylated Akt (pAkt) in 1MEA cells. Moreover, 1MEA cells had increased migratory capacity inhibited by inhibition of COX-2 and Akt but not extracellular signal regulated kinase (ERK). Molecular mesenchymal characteristics of 1MEA cells were reversed by inhibition of COX-2, Akt and ERK. Treatment of BNL cells with HGF led to decreased expression of E-cadherin and increased expression of fibronectin, vimentin, snail, slug, COX-2, Akt, pAkt and increased migration, invasiveness and clonogenicity. We conclude that development of HCC is associated with upregulation of HGF which promotes EMT and carcinogenesis via upregulation of COX-2 and Akt. Consequently, HGF signaling may be targeted for therapy in advanced and metastatic HCC.
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PMID:Hepatocyte growth factor upregulation promotes carcinogenesis and epithelial-mesenchymal transition in hepatocellular carcinoma via Akt and COX-2 pathways. 2174 57

The transcription factor, Forkhead Box M1 (FoxM1), has a specific expression pattern during the cell cycle. It also plays an important role in cellular developmental pathways and in the maintenance of homeostasis between cell proliferation and apoptosis. However, the precise role and molecular mechanisms associated with FoxM1 in laryngeal squamous carcinoma remain unclear. Therefore, laryngeal squamous carcinoma cells were transfected with FoxM1-targeted small interfering RNA (siRNA) and compared with cells transfected with a control siRNA. Assays of these two treatment groups detected a decrease in cell viability associated with down-regulation of FoxM1 expression, and resulted in an inhibition of cell proliferation, migration, and invasion. These phenotypes were also associated changes in expression of VEGF and MMP-2, a decrease in expression of cyclin B, and an increase in expression of p27. These findings suggest that deregulation of FoxM1 protein signaling is sufficient to affect tumorigenesis and cancer progression. These results also indicate that inhibition of FoxM1 represents an attractive target for cancer therapy.
Asian Pac J Cancer Prev 2011
PMID:Deletion of Forkhead Box M1 transcription factor reduces malignancy in laryngeal squamous carcinoma cells. 2212 65

The zinc-finger factor Snai1 plays an important role in the down-regulation of E-cadherin expression and in the induction of epithelial-mesenchymal transition (EMT) during cancer progression. In gastric cancer tissues, we noted that Snail is abnormally high expressed and is remarkably associated with the lymph node metastasis. Using a plasmid containing newly synthesized artificial microRNA (amiRNA), we transfected gastric cancer cells to block Snail expression. Both Snail protein and mRNA levels were significantly decreased in stably transfected cells, while protein and mRNA expression of E-cadherin was up-regulated. In addition, migration and invasion potential were significantly decreased after knockdown of Snail.
Asian Pac J Cancer Prev 2011
PMID:Inhibition of invasion and metastasis of gastric cancer cells through snail targeting artificial microRNA interference. 2247 93

Patients with non-small cell lung cancer (NSCLC) who have activating epidermal growth factor receptor (EGFR) mutations derive clinical benefit from treatment with EGFR-tyrosine kinase inhibitors ((EGFR-TKIs)- namely gefitinib and erlotinib. However, these patients eventually develop resistance to EGFR-TKIs. Despite the fact that this acquired resistance may be the result of a secondary mutation in the EGFR gene, such as T790M or amplification of the MET proto-oncogene, there are other mechanisms which need to be explored. MicroRNAs (miRs) are a class of small non-coding RNAs that play pivotal roles in tumorigenesis, tumor progression and chemo-resistance. In this study, we firstly successfully established a gefitinib resistant cell line-HCC827/GR, by exposing normal HCC827 cells (an NSCLC cell line with a 746E-750A in-frame deletion of EGFR gene) to increasing concentrations of gefitinib. Then, we found that miR-214 was significantly up-regulated in HCC827/ GR. We also showed that miR-214 and PTEN were inversely expressed in HCC827/GR. Knockdown of miR-214 altered the expression of PTEN and p-AKT and re-sensitized HCC827/GR to gefitinib. Taken together, miR-214 may regulate the acquired resistance to gefitinib in HCC827 via PTEN/AKT signaling pathway. Suppression of miR-214 may thus reverse the acquired resistance to EGFR-TKIs therapy.
Asian Pac J Cancer Prev 2012
PMID:MicroRNA-214 regulates the acquired resistance to gefitinib via the PTEN/AKT pathway in EGFR-mutant cell lines. 2250 80


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