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      1. Author :
        Ale, A.; Ermolayev, V.; Herzog, E.; Cohrs, C.; de Angelis, M. H.; Ntziachristos, V.
      2. Title :
        FMT-XCT: in vivo animal studies with hybrid fluorescence molecular tomography-X-ray computed tomography
      3. Type :
        Journal Article
      4. Year :
        2012
      5. Publication :
        Nat Methods
      6. Products :

        OsteoSense

      7. Volume :
        9
      8. Issue :
        N/A
      9. Page Numbers :
        N/A
      10. Research Area :
        N/A
      11. Keywords :
        OsteoSense, Animals; Bone Remodeling; Disease Models, Animal; Equipment Design; Female; Fluorescence; Head and Neck Neoplasms/pathology/radiography; Image Processing, Computer-Assisted/*methods; Lung Neoplasms/pathology/radiography; Mammary Neoplasms, Experimental/pathology/radiography; Mice; Osteogenesis Imperfecta/pathology/radiography; Tomography, Optical/*methods; Tomography, X-Ray Computed/*methods
      12. Abstract :
        The development of hybrid optical tomography methods to improve imaging performance has been suggested over a decade ago and has been experimentally demonstrated in animals and humans. Here we examined in vivo performance of a camera-based hybrid fluorescence molecular tomography (FMT) system for 360 degrees imaging combined with X-ray computed tomography (XCT). Offering an accurately co-registered, information-rich hybrid data set, FMT-XCT has new imaging possibilities compared to stand-alone FMT and XCT. We applied FMT-XCT to a subcutaneous 4T1 tumor mouse model, an Aga2 osteogenesis imperfecta model and a Kras lung cancer mouse model, using XCT information during FMT inversion. We validated in vivo imaging results against post-mortem planar fluorescence images of cryoslices and histology data. Besides offering concurrent anatomical and functional information, FMT-XCT resulted in the most accurate FMT performance to date. These findings indicate that addition of FMT optics into the XCT gantry may be a potent upgrade for small-animal XCT systems.
      13. URL :
        http://www.ncbi.nlm.nih.gov/pubmed/22561987
      14. Call Number :
        PKI @ kd.modi @ 12
      15. Serial :
        10468
      1. Author :
        Derwall, M.; Malhotra, R.; Lai, C. S.; Beppu, Y.; Aikawa, E.; Seehra, J. S.; Zapol, W. M.; Bloch, K. D.; Yu, P. B.
      2. Title :
        Inhibition of bone morphogenetic protein signaling reduces vascular calcification and atherosclerosis
      3. Type :
        Journal Article
      4. Year :
        2012
      5. Publication :
        Arterioscler Thromb Vasc Biol
      6. Products :

        OsteoSense

      7. Volume :
        32
      8. Issue :
        N/A
      9. Page Numbers :
        N/A
      10. Research Area :
        N/A
      11. Keywords :
        OsteoSense, Animals; Anti-Inflammatory Agents/pharmacology; Antioxidants/pharmacology; Atherosclerosis/etiology/genetics/metabolism/pathology/*prevention & control; Bone Morphogenetic Protein Receptors, Type I/metabolism; Bone Morphogenetic Proteins/*antagonists & inhibitors/metabolism; Cardiovascular Agents/*pharmacology; Cholesterol, LDL/blood; Diet, High-Fat; Disease Models, Animal; Endothelial Cells/drug effects/metabolism; Fatty Liver/etiology/metabolism/prevention & control; Female; Hep G2 Cells; Humans; Lipoproteins, LDL/metabolism; Liver/drug effects/metabolism; Mice; Mice, Inbred C57BL; Mice, Knockout; Pyrazoles/*pharmacology; Pyrimidines/*pharmacology; Reactive Oxygen Species/metabolism; Receptors, LDL/deficiency/genetics; Recombinant Fusion Proteins/metabolism; Signal Transduction/*drug effects; Time Factors; Vascular Calcification/etiology/genetics/metabolism/pathology/*prevention &; control
      12. Abstract :
        OBJECTIVE: The expression of bone morphogenetic proteins (BMPs) is enhanced in human atherosclerotic and calcific vascular lesions. Although genetic gain- and loss-of-function experiments in mice have supported a causal role of BMP signaling in atherosclerosis and vascular calcification, it remains uncertain whether BMP signaling might be targeted pharmacologically to ameliorate both of these processes. METHODS AND RESULTS: We tested the impact of pharmacological BMP inhibition on atherosclerosis and calcification in LDL receptor-deficient (LDLR-/-) mice. LDLR-/- mice fed a high-fat diet developed abundant vascular calcification within 20 weeks. Prolonged treatment of LDLR-/- mice with the small molecule BMP inhibitor LDN-193189 was well-tolerated and potently inhibited development of atheroma, as well as associated vascular inflammation, osteogenic activity, and calcification. Administration of recombinant BMP antagonist ALK3-Fc replicated the antiatherosclerotic and anti-inflammatory effects of LDN-193189. Treatment of human aortic endothelial cells with LDN-193189 or ALK3-Fc abrogated the production of reactive oxygen species induced by oxidized LDL, a known early event in atherogenesis. Unexpectedly, treatment of mice with LDN-193189 lowered LDL serum cholesterol by 35% and markedly decreased hepatosteatosis without inhibiting HMG-CoA reductase activity. Treatment with BMP2 increased, whereas LDN-193189 or ALK3-Fc inhibited apolipoprotein B100 secretion in HepG2 cells, suggesting that BMP signaling contributes to the regulation of cholesterol biosynthesis. CONCLUSION: These results definitively implicate BMP signaling in atherosclerosis and calcification, while uncovering a previously unidentified role for BMP signaling in LDL cholesterol metabolism. BMP inhibition may be helpful in the treatment of atherosclerosis and associated vascular calcification.
      13. URL :
        http://www.ncbi.nlm.nih.gov/pubmed/22223731
      14. Call Number :
        PKI @ kd.modi @ 5
      15. Serial :
        10469
      1. Author :
        Sabbagh, Y.; Graciolli, F. G.; O'Brien, S.; Tang, W.; dos Reis, L. M.; Ryan, S.; Phillips, L.; Boulanger, J.; Song, W.; Bracken, C.; Liu, S.; Ledbetter, S.; Dechow, P.; Canziani, M. E.; Carvalho, A. B.; Jorgetti, V.; Moyses, R. M.; Schiavi, S. C.
      2. Title :
        Repression of osteocyte Wnt/beta-catenin signaling is an early event in the progression of renal osteodystrophy
      3. Type :
        Journal Article
      4. Year :
        2012
      5. Publication :
        J Bone Miner Res
      6. Products :

        OsteoSense

      7. Volume :
        27
      8. Issue :
        N/A
      9. Page Numbers :
        N/A
      10. Research Area :
        N/A
      11. Keywords :
        OsteoSense, Animals; Biopsy; Bone Remodeling; Bone and Bones/metabolism/pathology; Calcification, Physiologic; Cardiovascular Abnormalities/blood/complications/pathology/physiopathology; *Disease Progression; Female; Gene Expression Profiling; Gene Expression Regulation; Glycoproteins/metabolism; Humans; Kidney Failure, Chronic/blood/complications/pathology/physiopathology; Male; Mice; Mice, Inbred C57BL; Middle Aged; Mutation/genetics; Osteoclasts/metabolism/pathology; Osteocytes/*metabolism/*pathology; Protein-Serine-Threonine Kinases/genetics; Renal Osteodystrophy/blood/*metabolism/*pathology/physiopathology; Vascular Calcification; *Wnt Signaling Pathway/genetics
      12. Abstract :
        Chronic kidney disease-mineral bone disorder (CKD-MBD) is defined by abnormalities in mineral and hormone metabolism, bone histomorphometric changes, and/or the presence of soft-tissue calcification. Emerging evidence suggests that features of CKD-MBD may occur early in disease progression and are associated with changes in osteocyte function. To identify early changes in bone, we utilized the jck mouse, a genetic model of polycystic kidney disease that exhibits progressive renal disease. At 6 weeks of age, jck mice have normal renal function and no evidence of bone disease but exhibit continual decline in renal function and death by 20 weeks of age, when approximately 40% to 60% of them have vascular calcification. Temporal changes in serum parameters were identified in jck relative to wild-type mice from 6 through 18 weeks of age and were subsequently shown to largely mirror serum changes commonly associated with clinical CKD-MBD. Bone histomorphometry revealed progressive changes associated with increased osteoclast activity and elevated bone formation relative to wild-type mice. To capture the early molecular and cellular events in the progression of CKD-MBD we examined cell-specific pathways associated with bone remodeling at the protein and/or gene expression level. Importantly, a steady increase in the number of cells expressing phosphor-Ser33/37-beta-catenin was observed both in mouse and human bones. Overall repression of Wnt/beta-catenin signaling within osteocytes occurred in conjunction with increased expression of Wnt antagonists (SOST and sFRP4) and genes associated with osteoclast activity, including receptor activator of NF-kappaB ligand (RANKL). The resulting increase in the RANKL/osteoprotegerin (OPG) ratio correlated with increased osteoclast activity. In late-stage disease, an apparent repression of genes associated with osteoblast function was observed. These data confirm that jck mice develop progressive biochemical changes in CKD-MBD and suggest that repression of the Wnt/beta-catenin pathway is involved in the pathogenesis of renal osteodystrophy.
      13. URL :
        http://www.ncbi.nlm.nih.gov/pubmed/22492547
      14. Call Number :
        PKI @ kd.modi @ 10
      15. Serial :
        10475
      1. Author :
        van der Horst, G.; van der Pluijm, G.
      2. Title :
        Preclinical imaging of the cellular and molecular events in the multistep process of bone metastasis
      3. Type :
        Journal Article
      4. Year :
        2012
      5. Publication :
        Future Oncol
      6. Products :

        OsteoSense

      7. Volume :
        8
      8. Issue :
        N/A
      9. Page Numbers :
        N/A
      10. Research Area :
        N/A
      11. Keywords :
        OsteoSense, Animals; Bone Neoplasms/*diagnosis/*secondary; Diagnostic Imaging/*methods; Disease Models, Animal; Disease Progression; Humans; Molecular Imaging/methods; Neoplasm Metastasis/diagnosis
      12. Abstract :
        Bone metastasis is a complex process that ultimately leads to devastating metastatic bone disease. It is therefore of key interest to unravel the mechanisms underlying the multistep process of skeletal metastasis and cancer-induced bone disease, and to develop better treatment and management of patients with this devastating disease. Fortunately, novel technologies are rapidly emerging that allow real-time imaging of molecules, pathogenic processes, drug delivery and drug response in preclinical in vivo models. The outcome of these experimental studies will facilitate clinical cancer research by improving the detection of cancer cell invasion, metastasis and therapy response.
      13. URL :
        http://www.ncbi.nlm.nih.gov/pubmed/22515445
      14. Call Number :
        PKI @ kd.modi @ 16
      15. Serial :
        10478
      1. Author :
        Liao, A. H.; Li, Y. K.; Lee, W. J.; Wu, M. F.; Liu, H. L.; Kuo, M. L.
      2. Title :
        Estimating the delivery efficiency of drug-loaded microbubbles in cancer cells with ultrasound and bioluminescence imaging
      3. Type :
        Journal Article
      4. Year :
        2012
      5. Publication :
        Ultrasound Med Biol
      6. Products :

        Bioware cell linesIVIS Imaging Systems

      7. Volume :
        38
      8. Issue :
        N/A
      9. Page Numbers :
        N/A
      10. Research Area :
        N/A
      11. Keywords :
        4T1-luc2, IVIS, Bioluminescence
      12. Abstract :
        The application of drug-loaded microbubbles (MBs) in combination with ultrasound (US), which results in an increase in capillary permeability at the site of US-sonication-induced MB destruction, may be an efficient method of localized drug delivery. This study investigated the mechanism underlying the US-mediated release of luciferin-loaded MBs through the blood vessels to targeted cells using an in vivo bioluminescence imaging (BLI) system. The luciferin-loaded MBs comprised an albumin shell with a diameter of 1234 +/- 394 nm (mean +/- SD) and contained 2.48 x 10(9) bubbles/mL; within each MB, the concentration of encapsulated luciferin was 1.48 x 10(-)(1)(0) mg/bubble. The loading efficiency of luciferin in MBs was only about 19.8%, while maintaining both the bioluminescence and acoustic properties. In vitro and in vivo BLI experiments were performed to evaluate the US-mediated release of luciferin-loaded MBs. For in vitro results, the increase in light emission of luciferin-loaded albumin-shelled MBs after destruction via US sonication (6.24 +/- 0.72 x 10(7) photons/s) was significantly higher than that in the luciferin-loaded albumin-shelled MBs (3.11 +/- 0.33 x 10(7) photons/s) (p < 0.05). The efficiency of the US-mediated release of luciferin-loaded MBs in 4T1-luc2 tumor-bearing mice was also estimated. The signal intensity of the tumor with US destruction at 3 W/cm(2) for 30 s was significantly higher than without US destruction at 3 (p = 0.025), 5 (p = 0.013), 7 (p = 0.012) and 10 (p = 0.032) min after injecting luciferin-loaded albumin-shelled MBs. The delivery efficiency was, thus, improved with US-mediated release, allowing reduction of the total injection dose of luciferin.
      13. URL :
        http://www.ncbi.nlm.nih.gov/pubmed/22929655
      14. Call Number :
        PKI @ kd.modi @ 8
      15. Serial :
        10481
      1. Author :
        von Schwarzenberg, K.; Wiedmann, R. M.; Oak, P.; Schulz, S.; Zischka, H.; Wanner, G.; Efferth, T.; Trauner, D.; Vollmar, A. M.
      2. Title :
        Mode of cell death induction by pharmacological vacuolar H+-ATPase (V-ATPase) inhibition
      3. Type :
        Journal Article
      4. Year :
        2012
      5. Publication :
        J Biol Chem
      6. Products :

        Bioware cell linesIVIS Imaging Systems

      7. Volume :
        N/A
      8. Issue :
        N/A
      9. Page Numbers :
        N/A
      10. Research Area :
        N/A
      11. Keywords :
        4T1-luc2, IVIS, Bioluminescence
      12. Abstract :
        The vacuolar H+-ATPase (V-ATPase), a multisubunit proton pump, has come into focus as an attractive target in cancer invasion. However little is known about the role of V-ATPase in cell death and especially the underlying mechanisms remain mostly unknown. We used the myxobacterial macrolide archazolid B, a potent inhibitor of the V-ATPase, as an experimental drug as well as a chemical tool to decipher V-ATPase related cell death signaling. We found that archazolid induced apoptosis in highly invasive tumor cells at nanomolar concentrations which was executed by the mitochondrial pathway. Prior to apoptosis induction archazolid lead to the activation of a cellular stress response including activation of the hypoxia-inducible factor-1 alpha (HIF1alpha) and autophagy. Autophagy was induced at low concentrations of archazolid that do not alter pH in lysosomes and was shown by degradation of p62 or fusion of autophagosomes with lysosomes. HIF1alpha was induced due to energy stress shown by a decline of the ATP level and followed by a shut down of energy consuming processes. As silencing HIF1alpha increases apoptosis, the cellular stress response was suggested to be a survival mechanism. We conclude that archazolid leads to energy stress which activates adaptive mechanisms like autophagy mediated by HIF1alpha and finally leads to apoptosis. We propose V-ATPase as a promising drugable target in cancer therapy caught up at the interplay of apoptosis, autophagy and cellular/metabolic stress.
      13. URL :
        http://www.ncbi.nlm.nih.gov/pubmed/23168408
      14. Call Number :
        PKI @ kd.modi @ 9
      15. Serial :
        10480
      1. Author :
        Zhang, Z.; Hu, Z.; Gupta, J.; Krimmel, J. D.; Gerseny, H. M.; Berg, A. F.; Robbins, J. S.; Du, H.; Prabhakar, B.; Seth, P.
      2. Title :
        Intravenous administration of adenoviruses targeting transforming growth factor beta signaling inhibits established bone metastases in 4T1 mouse mammary tumor model in an immunocompetent syngeneic host
      3. Type :
        Journal Article
      4. Year :
        2012
      5. Publication :
        Cancer Gene Ther
      6. Products :

        Bioware cell linesIVIS Imaging Systems

      7. Volume :
        19
      8. Issue :
        N/A
      9. Page Numbers :
        N/A
      10. Research Area :
        N/A
      11. Keywords :
        4T1-luc2, IVIS, Bioluminescence, Adenoviridae/genetics/*metabolism/physiology; Administration, Intravenous; Animals; Bone Neoplasms/secondary/*therapy; Cell Line, Tumor; Female; Humans; Immunocompetence; Luminescent Measurements/methods; Mammary Neoplasms, Experimental/pathology/*therapy; Mice; Mice, Inbred BALB C; Oncolytic Virotherapy/methods; Oncolytic Viruses/genetics/metabolism/physiology; Phosphorylation; Promoter Regions, Genetic; Protein-Serine-Threonine Kinases/genetics/*metabolism; Receptors, Transforming Growth Factor beta/genetics/*metabolism; Signal Transduction; Smad2 Protein/genetics/metabolism; Telomerase/genetics; Transforming Growth Factor beta1/genetics/metabolism; Transplantation, Isogeneic/methods; Tumor Stem Cell Assay/methods; Virus Replication
      12. Abstract :
        We have examined the effect of adenoviruses expressing soluble transforming growth factor receptorII-Fc (sTGFbetaRIIFc) in a 4T1 mouse mammary tumor bone metastasis model using syngeneic BALB/c mice. Infection of 4T1 cells with a non-replicating adenovirus, Ad(E1-).sTbetaRFc, or with two oncolytic adenoviruses, Ad.sTbetaRFc and TAd.sTbetaRFc, expressing sTGFbetaRIIFc (the human TERT promoter drives viral replication in TAd.sTbetaRFc) produced sTGFbetaRIIFc protein. Oncolytic adenoviruses produced viral replication and induced cytotoxicity in 4T1 cells. 4T1 cells were resistant to the cytotoxic effects of TGFbeta-1 (up to 10 ng ml(-1)). However, TGFbeta-1 induced the phosphorylation of SMAD2 and SMAD3, which were inhibited by co-incubation with sTGFbetaRIIFc protein. TGFbeta-1 also induced interleukin-11, a well-known osteolytic factor. Intracardiac injection of 4T1-luc2 cells produced bone metastases by day 4. Intravenous injection of Ad.sTbetaRFc (on days 5 and 7) followed by bioluminescence imaging (BLI) of mice on days 7, 11 and 14 in tumor-bearing mice indicated inhibition of bone metastasis progression (P<0.05). X-ray radiography of mice on day 14 showed a significant reduction of the lesion size by Ad.sTbetaRFc (P<0.01) and TAd.sTbetaRFc (P<0.05). Replication-deficient virus Ad(E1-).sTbetaRFc expressing sTGFbetaRIIFc showed some inhibition of bone metastasis, whereas Ad(E1-).Null was not effective in inhibiting bone metastases. Thus, systemic administration of Ad.sTbetaRFc and TAd.sTbetaRFc can inhibit bone metastasis in the 4T1 mouse mammary tumor model, and can be developed as potential anti-tumor agents for breast cancer.
      13. URL :
        http://www.ncbi.nlm.nih.gov/pubmed/22744210
      14. Call Number :
        PKI @ kd.modi @ 7
      15. Serial :
        10479
      1. Author :
        Albanesi, M.; Mancardi, D. A.; Macdonald, L. E.; Iannascoli, B.; Zitvogel, L.; Murphy, A. J.; Leusen, J. H.; Bruhns, P.
      2. Title :
        Cutting Edge: FcgammaRIII (CD16) and FcgammaRI (CD64) Are Responsible for Anti-Glycoprotein 75 Monoclonal Antibody TA99 Therapy for Experimental Metastatic B16 Melanoma
      3. Type :
        Journal Article
      4. Year :
        2012
      5. Publication :
        J Immunol
      6. Products :

        Bioware cell linesIVIS Imaging Systems

      7. Volume :
        189
      8. Issue :
        N/A
      9. Page Numbers :
        N/A
      10. Research Area :
        N/A
      11. Keywords :
        B16-F10-luc2, B16F10-luc2, IVIS
      12. Abstract :
        mAb therapy for experimental metastatic melanoma relies on activating receptors for the Fc portion of IgG (FcgammaR). Opposing results on the respective contribution of mouse FcgammaRI, FcgammaRIII, and FcgammaRIV have been reported using the gp75-expressing B16 melanoma and the protective anti-gp75 mAb TA99. We analyzed the contribution of FcgammaRs to this therapy model using bioluminescent measurement of lung metastases loads, novel mouse strains, and anti-FcgammaR blocking mAbs. We found that the TA99 mAb-mediated effects in a combination therapy using cyclophosphamide relied on activating FcgammaRs. The combination therapy, however, was not more efficient than mAb therapy alone. We demonstrate that FcgammaRI and, unexpectedly, FcgammaRIII contributed to TA99 mAb therapeutic effects, whereas FcgammaRIV did not. Therefore, FcgammaRIII and FcgammaRI are, together, responsible for anti-gp75 mAb therapy of B16 lung metastases. Our finding that mouse FcgammaRIII contributes to Ab-induced tumor reduction correlates with clinical data on its human functional equivalent human FcgammaRIIIA (CD16A).
      13. URL :
        http://www.ncbi.nlm.nih.gov/pubmed/23150715
      14. Call Number :
        PKI @ kd.modi @ 8
      15. Serial :
        10482
      1. Author :
        Danussi, C.; Petrucco, A.; Wassermann, B.; Modica, T. M.; Pivetta, E.; Del Bel Belluz, L.; Colombatti, A.; Spessotto, P.
      2. Title :
        An EMILIN1-negative microenvironment promotes tumor cell proliferation and lymph node invasion
      3. Type :
        Journal Article
      4. Year :
        2012
      5. Publication :
        Cancer Prev Res (Phila)
      6. Products :

        Bioware cell linesIVIS Imaging Systems

      7. Volume :
        5
      8. Issue :
        N/A
      9. Page Numbers :
        N/A
      10. Research Area :
        N/A
      11. Keywords :
        B16-F10-luc2, B16F10-luc2, IVIS
      12. Abstract :
        The evidence that EMILIN1 (Elastic Microfibril Interface Located proteIN) deficiency in Emilin1(-/-) mice caused dermal and epidermal hyperproliferation and an abnormal lymphatic phenotype prompted us to hypothesize the involvement of this extracellular matrix component in tumor development and in lymphatic metastasis. Using the 12-dimethylbenz(alpha)anthracene/12-O-tetradecanoylphorbol-13-acetate (DMBA/TPA) two-stage model of skin carcinogenesis, we found that Emilin1(-/-) mice presented an accelerated formation, a higher incidence, and the development of a larger number of tumors compared with their wild-type littermates. EMILIN1-negative tumors showed more Ki67-positive proliferating cells and higher levels of pErk1/2. In these tumors, PTEN expression was lower. Emilin1(-/-) mice displayed enhanced lymphangiogenesis both in the tumor and in the sentinel lymph nodes. Accordingly, tumor growth and lymph node metastasis of transplanted syngenic tumors were also increased in Emilin1(-/-) mice. In vitro transmigration assays through lymphatic endothelial cells showed that EMILIN1 deficiency greatly facilitated tumor cell trafficking. Overall, these data established that EMILIN1 exerts a protective role in tumor growth, in tumor lymphatic vessel formation, as well as in metastatic spread to lymph nodes and reinforced the importance of its presence in the microenvironment to determine the tumor phenotype.
      13. URL :
        http://www.ncbi.nlm.nih.gov/pubmed/22827975
      14. Call Number :
        PKI @ kd.modi @ 9
      15. Serial :
        10483
      1. Author :
        Subbarayan, P. R.; Sarkar, M.; Nagaraja Rao, S.; Philip, S.; Kumar, P.; Altman, N.; Reis, I.; Ahmed, M.; Ardalan, B.; Lokeshwar, B. L.
      2. Title :
        Achyranthes aspera (Apamarg) leaf extract inhibits human pancreatic tumor growth in athymic mice by apoptosis
      3. Type :
        Journal Article
      4. Year :
        2012
      5. Publication :
        J Ethnopharmacol
      6. Products :

        Bioware cell linesIVIS Imaging Systems

      7. Volume :
        142
      8. Issue :
        N/A
      9. Page Numbers :
        523-30
      10. Research Area :
        N/A
      11. Keywords :
        BxPC-3, BxPC-3-luc2, IVIS, Achyranthes; Animals; Antineoplastic Agents, Phytogenic/pharmacology/*therapeutic use; Apoptosis/*drug effects; Caspase 3/genetics/metabolism; Gene Expression/drug effects; Humans; Injections, Intraperitoneal; Medicine, Ayurvedic; Mice; Mice, Nude; Pancreatic Neoplasms/*drug therapy/genetics/metabolism; Phosphorylation; *Phytotherapy; Plant Extracts/pharmacology/*therapeutic use; Plant Leaves; Proto-Oncogene Proteins c-akt/metabolism; RNA, Messenger/metabolism; Xenograft Model Antitumor Assays
      12. Abstract :
        ETHNOPHARMACOLOGICAL RELEVANCE: Achyranthes aspera (Family Amaranthacea) is used for cancer therapy by ayurvedic medical practitioners in India. However, due to the non formal nature of its use, there are no systematic studies validating its medicinal properties. Thus, it's utility as an anti cancer agent remains anecdotal. Earlier, we demonstrated A. aspera to exhibit time and dose-dependent preferential cytotoxicity to cultured human pancreatic cancer cells. In this report we validate in vivo anti tumor properties of A. aspera. MATERIALS AND METHODS: The in vivo anti tumor activity of leaf extract (LE) was tested by intraperitoneal (IP) injections into athymic mice harboring human pancreatic tumor subcutaneous xenograft. Toxicity was monitored by recording changes in behavioral, histological, hematological and body weight parameters. RESULTS: Dosing LE to athymic mice by I.P. injection for 32 days showed no adverse reactions in treated mice. Compared to the control set, IP administration of LE to tumor bearing mice significantly reduced both tumor weight and volume. Gene expression analysis using Real time PCR methods revealed that LE significantly induced caspase-3 mRNA (p<0.001) and suppressed expression of the pro survival kinase Akt-1 (p<0.05). TUNEL assay and immunohistochemistry confirmed apoptosis induction by activation of caspase-3 and inhibiting Akt phosphorylation in treated sets. These results are in agreement with RT PCR data. CONCLUSION: Taken together, these data suggest A. aspera to have potent anti cancer property.
      13. URL :
        http://www.ncbi.nlm.nih.gov/pubmed/22640722
      14. Call Number :
        PKI @ kd.modi @ 1
      15. Serial :
        10484
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