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  • American Association for Cancer Research (AACR)  (11)
  • 1
    Online Resource
    Online Resource
    American Association for Cancer Research (AACR) ; 2020
    In:  Clinical Cancer Research Vol. 26, No. 12_Supplement_2 ( 2020-06-15), p. A30-A30
    In: Clinical Cancer Research, American Association for Cancer Research (AACR), Vol. 26, No. 12_Supplement_2 ( 2020-06-15), p. A30-A30
    Abstract: Background: Tobacco and alcohol exposure are the dominant risk factors for the development of squamous cell cancer of the head and neck (SCCHN) worldwide. While human papilloma virus (HPV) is strongly associated with oropharyngeal SCCHN, much less is known about the role of obesity. Body mass index (BMI) has been implicated as a potential risk factor for SCCHN, yet the data available so far have demonstrated mixed results. Therefore, we conducted the largest case-control study to date to examine the potential association of risk of SCCHN with pretreatment BMI. Methods: BMI, clinical, and patient-reported epidemiologic information at diagnosis were collected among 2,310 SCCHN cases and 1,915 cancer-free controls from October 2001 to May 2013. Cases included cancers of the oral cavity, oropharynx, and hypopharynx/larynx. Logistic regression analysis was used to assess odds ratios (OR) with 95% confidence intervals (95% CIs). Multivariable-adjusted models were used to evaluate the association between BMI and SCCN risk, and further stratified analysis was performed. Results: At diagnosis, 1.9% of the cases (patients) were underweight (BMI & lt;18.5), 25.7% were normal weight (BMI 18.5- & lt;25), 38.4% were overweight (BMI 25- & lt;30), and 34% were obese (BMI ≥30). Pretreatment BMI was significantly associated with increased risk of SCCHN in patients who were underweight (OR, 2.61; 95%CI, 1.46-4.66) and reduced risk of SCCHN in patients who were overweight (OR, 0.69; 95%CI, 0.59-0.8) or obese (OR, 0.77; 95%CI, 0.65-0.91), respectively. The observed increased risk associated with underweight patients was most pronounced among alcohol drinkers (OR, 3.55; 95% CI, 1.49 -8.47), smokers (OR, 2.52; 95% CI, 1.16 -5.45), oral cavity cancer patients (OR, 2.57; 95% CI, 1.33-4.96), oropharyngeal cancer patients (OR, 2.76; 95% CI, 1.39-5.47), and hypopharyngeal/laryngeal cancer patients (OR, 3.21; 95% CI, 1.35-7.62). For obese patients, a significantly protective effect was found among smokers (OR, 0.59; 95% CI, 0.47 -0.74), alcohol drinkers (OR, 0.68; 95% CI, 0.55-0.84), oral cavity cancer patients (OR, 0.61; 95% CI, 0.48-0.76), oropharyngeal cancer patients (OR, 0.87; 95% CI, 0.71-1.07), and hypopharyngeal/laryngeal cancer patients (OR, 0.63; 95% CI, 0.47-0.86). Conclusion: The present findings suggest that pretreatment BMI is a significant independent risk factor for SCCHN. Increased BMI at diagnosis confers reduced risk while decreased BMI has increased risk for SCCHN. The mechanism for the inverse association between pretreatment BMI and risk of SCCHN has yet to be elucidated. Citation Format: Anshu Khanna, Eric Sturgis, Li Xu, Qingyi Wei, Guojun Li, Neil Gross. Association of pretreatment BMI with risk of head and neck cancer: A large-scale single-center study [abstract]. In: Proceedings of the AACR-AHNS Head and Neck Cancer Conference: Optimizing Survival and Quality of Life through Basic, Clinical, and Translational Research; 2019 Apr 29-30; Austin, TX. Philadelphia (PA): AACR; Clin Cancer Res 2020;26(12_Suppl_2):Abstract nr A30.
    Type of Medium: Online Resource
    ISSN: 1078-0432 , 1557-3265
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    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2020
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  • 2
    In: Cancer Research, American Association for Cancer Research (AACR), Vol. 68, No. 15 ( 2008-08-01), p. 6232-6240
    Abstract: Clinical studies have shown that decreased tamoxifen effectiveness correlates with elevated levels of vascular endothelial growth factor (VEGF)-A165 in biopsy samples of breast cancers. To investigate the mechanisms underlying tamoxifen resistance and metastasis, we engineered the estrogen receptor (ER)–positive MCF-7 human breast cancer cell line to express VEGF to clinically relevant levels in a doxycycline-regulated manner. Induction of VEGF expression in orthotopically implanted xenografts that were initially tamoxifen responsive and noninvasive resulted in tamoxifen-resistant tumor growth and metastasis to the lungs. Lung metastases were also observed in a VEGF-dependent manner following tail vein injection of tumor cells. At both primary and metastatic sites, VEGF-overexpressing tumors exhibited extensive fibroblastic stromal content, a clinical feature called desmoplasia. VEGF-induced metastatic colonies were surrounded by densely packed stromal cells before detectable angiogenesis, suggesting that VEGF is involved in the initiation of desmoplasia. Because expression of VEGF receptors R1 and R2 was undetectable in these tumor cells, the observed VEGF effects on reduction of tamoxifen efficacy and metastatic colonization are most likely mediated by paracrine signaling that enhances tumor/stromal cell interactions and increases the level of desmoplasia. This study reveals new roles for VEGF in breast cancer progression and suggests that combination of antiestrogens and VEGF inhibitors may prolong tamoxifen sensitivity and prevent metastasis in patients with ER-positive tumors. [Cancer Res 2008;68(15):6232–40]
    Type of Medium: Online Resource
    ISSN: 0008-5472 , 1538-7445
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    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2008
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  • 3
    Online Resource
    Online Resource
    American Association for Cancer Research (AACR) ; 2010
    In:  Cancer Research Vol. 70, No. 8_Supplement ( 2010-04-15), p. 563-563
    In: Cancer Research, American Association for Cancer Research (AACR), Vol. 70, No. 8_Supplement ( 2010-04-15), p. 563-563
    Abstract: Human breast cancers contain high levels of fibroblastic stroma as a critical feature of desmoplasia. The complex interactions between tumor and stromal cells play important roles in tumor growth, metastasis and resistance to anticancer treatments. Our previous in vivo studies showed that increased levels of tumor-released VEGF were associated with increased desmoplastic responses and resulted in a hormonal resistance phenotype of ER+ breast tumor. Based on our findings, a clinical trial conducted at UAB with a new combinational treatment targeting both ER and VEGF signalings has achieved significant objective response in ER+ breast cancer patients. In our current studies, we further studied the role of VEGF in mediating tumor-stromal interactions and initiation of desmoplasia. Our results have shown that tumor released VEGF interacts with stromal fibroblasts which express VEGF receptors R1, R2 and Neuropilin-1 (NRP1), thereby stimulating their infiltration to promote desmoplastic response. Down regulation of NRP1 expression by siRNA significantly abolished the fibroblast chemo-attractive motility towards VEGF, while the VEGFR1 and VEGFR2 blocking antibodies had no effects on their migration mobility, suggesting that NRP1 expressed in fibroblast is involved in tumor-stroma cell interactions in breast cancer. Our studies using breast cancer xenograft mouse model with regulated tumor VEGF expression revealed that tumor VEGF expression was positively correlated with expression of NRP1 and alpha smooth muscle actin (α-SMA, a transformed/myo fibroblast marker) in the tumor stroma. In addition, levels of tumor VEGF, stromal NRP1 and α-SMA were all positively correlated with level of tumor stromal content and tumor growth. Blocking tumor VEGF with a neutralizing antibody (Avastin) as a treatment modality in xenograft mice reversed the VEGF increased desmoplasia. Our study results reveal a novel role of VEGF and NRP1 in tumor-stromal interactions and desmoplasia, indicating NRP1 can be a therapeutic target for breast cancer treatment. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 101st Annual Meeting of the American Association for Cancer Research; 2010 Apr 17-21; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2010;70(8 Suppl):Abstract nr 563.
    Type of Medium: Online Resource
    ISSN: 0008-5472 , 1538-7445
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    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2010
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  • 4
    Online Resource
    Online Resource
    American Association for Cancer Research (AACR) ; 2010
    In:  Cancer Research Vol. 70, No. 8_Supplement ( 2010-04-15), p. 2390-2390
    In: Cancer Research, American Association for Cancer Research (AACR), Vol. 70, No. 8_Supplement ( 2010-04-15), p. 2390-2390
    Abstract: Angiogenesis is a highly regulated biological complex process, which consist of endothelial cells proliferation, migration, and tubulogenesis as key cellular steps to form new blood capillaries from preexisting vessels. Imbalance in angiogenesis contributes to a variety of human diseases. Tumor growth depends on angiogenesis and antiangiogenic agents have been developed as effective anti-cancer medicine. Recently, we have demonstrated that serotonin (5-HT), a well-recognized neurotransmitter, has a promoting effect on endothelial cells proliferation, migration and tubulogenesis, suggesting serotonin plays a role in regulation of angiogenesis. To study the role of serotonin in angiogenesis, we examined the expression of serotonin receptor isoforms in human endothelial cells. Real time PCR studies have showed that, serotonin receptor 1B (HTR1B), 1D (HTR1D), 1A (HTR1A) and 2B (HTR2B) are expressed in primary human endothelial cell lines. Blocking serotonin 1B receptor had significant inhibitory effect on endothelial cells proliferation and tubulogenesis. We have further explored the 1B-mediated signal transduction in endothelial cells. The results have revealed that the serotonin 1B receptor as a G protein-coupled receptor (GPCR) is coupled to Gi protein and decreased intracellular cAMP level upon its receptor binding. Both serotonin and 1B receptor agonist were able to activate ERK, p38, Akt, RhoA, Rac1 and PYK2/FAK signaling in endothelial cells. In contrast, a selective antagonist for serotonin 1B receptor blocks the serotonin-stimulated Akt and PYK2/FAK activation. Experiments with pertussis toxin (general Gi blocker) further demonstrated that heterotrimeric Gi-protein is required for the activation of Akt and PYK2/FAK by serotonin. These findings suggest that Akt and PYK2/FAK are involved in signaling transduction in serotonin-activated endothelial cells. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 101st Annual Meeting of the American Association for Cancer Research; 2010 Apr 17-21; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2010;70(8 Suppl):Abstract nr 2390.
    Type of Medium: Online Resource
    ISSN: 0008-5472 , 1538-7445
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    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2010
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  • 5
    In: Cancer Research, American Association for Cancer Research (AACR), Vol. 71, No. 19 ( 2011-10-01), p. 6122-6131
    Abstract: Deficiencies in immune function that accumulate during cancer immunoediting lead to a progressive escape from host immunosurveillance. Therapies that correct or overcome these defects could have a powerful impact on cancer management, but current knowledge of the types and mechanisms of immune escape is still incomplete. Here, we report a novel mechanism of escape from T-cell immunity that is caused by reduction in levels of the Delta family Notch ligands DLL1 and DLL4 in hematopoietic microenvironments. An important mediator of this effect was an elevation in the levels of circulating VEGF. Selective activation of the DLL1-Notch signaling pathway in bone marrow precursors enhanced T-cell activation and inhibited tumor growth. Conversely, tumor growth led to inhibition of Delta family ligand signaling through Notch in the hematopoietic environment, resulting in suppressed T-cell function. Overall, our findings uncover a novel mechanism of tumoral immune escape and suggest that a soluble multivalent form of DLL1 may offer a generalized therapeutic intervention to stimulate T-cell immunity and suppress tumor growth. Cancer Res; 71(19); 6122–31. ©2011 AACR.
    Type of Medium: Online Resource
    ISSN: 0008-5472 , 1538-7445
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    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2011
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  • 6
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    Online Resource
    American Association for Cancer Research (AACR) ; 2011
    In:  Cancer Research Vol. 71, No. 8_Supplement ( 2011-04-15), p. 5154-5154
    In: Cancer Research, American Association for Cancer Research (AACR), Vol. 71, No. 8_Supplement ( 2011-04-15), p. 5154-5154
    Abstract: Angiogenesis is a well-controlled process that is regulated by multiple factors that are secreted by the cancer cells as well as other cells within the tumor microenvironment. Angiogenesis inhibitors are showing therapeutic efficacy in an increasing number of human cancers. However, in both preclinical and clinical settings, the benefits are transitory and are followed by resistance and a restoration of tumor growth and progression. Therefore, novel anti-angiogenic strategies with complementary mechanisms are needed to maximize efficacy and minimize resistance to current angiogenesis inhibitors. Activation of platelets and blood coagulation frequently occurs in cancer patients. Apart from VEGF, platelets contain several other angiogenic growth factors and inhibitors that are released upon activation and promote tumor neoangiogenesis. Although considerable attention has been focused on platelet peptide growth factors, little is known about the mitogenic effects of nonpeptide platelet products such s serotonin (5-HT), considering that 99% of 5-HT in blood is found in platelets and is released at blood clotting sites. In previous studies, we have shown that endothelial cells express 5-HT receptors and 5-HT has growth stimulatory effcts on multiple types of endothelial cells. We have also demonstrated that 5-HT binds to inhibitory type of G-protein coupled receptors and stimulates the phosphorylation of PYK2/PI3K/AKT/mTOR signaling pathway, the same signaling pathway, which has been activated by most angiogenic factors, including VEGF. In our recent studies, we explored angiogenic promoting activity of 5-HT in the mouse matrigel plug assay (in vivo angiogenesis model system) and antiangiogenic potential of antagonists against 5-HT receptors in xenograft-CAM assay (ex vivo tumor angiogenesis model system). The most importantly, an antagonist against a specific 5-HT receptor demonstrated the synergistic effect in blocking tumor-induced new blood vessel formation when it was applied in combination with Sutent, a FDA approved antiangiogenic drug against VEGF receptor. The results of this study suggest that 5-HT signaling pathway constitute a novel target of tumor angiogenesis in anticancer therapeutic development. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 102nd Annual Meeting of the American Association for Cancer Research; 2011 Apr 2-6; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2011;71(8 Suppl):Abstract nr 5154. doi:10.1158/1538-7445.AM2011-5154
    Type of Medium: Online Resource
    ISSN: 0008-5472 , 1538-7445
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    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2011
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  • 7
    Online Resource
    Online Resource
    American Association for Cancer Research (AACR) ; 2011
    In:  Cancer Research Vol. 71, No. 8_Supplement ( 2011-04-15), p. 4265-4265
    In: Cancer Research, American Association for Cancer Research (AACR), Vol. 71, No. 8_Supplement ( 2011-04-15), p. 4265-4265
    Abstract: Tumor progression depends on angiogenesis. The clinical successes in recent years have demonstrated that antiangiogenic agents can be developed as effective treatment for cancer patients. However, the resistance to the current FDA approved antiangiogenic therapies is emerging, which presents challenges in cancer research and urgent needs for novel angiogenesis inhibitors with different mechanisms of drug actions to overcome the resistance. In our previous studies, we have identified a small molecule bithionol as a potential antiangiogenic agent through a chemical diversity library screening with a cell-based angiogenesis assay. Bithionol is a FDA approved and current clinically used anthelmintics, which has been found to directly inhibit activity of autotaxin, a secreted enzyme that catalyzes lysophosphatidic acid (LPA) production. LPA, as a lipid signaling molecule, is a potent angiogenic and cancer cell motility stimulating factor. Therefore, autotaxin plays important role in tumor angiogenesis and metastasis and has been recently identified as an attractive angiogenesis and cancer target. Our recent studies have shown that autotaxin is expressed at high levels in human endothelial and number of human cancer cell lines. Bithionol has demonstrated inhibitory activities against human endothelial cell proliferation, migration, and tube-formation as the three key cellular steps in angiogenesis process. The effect of bithionol on inhibition of tumor angiogenesis was also evaluated with an ex vivo xenograft chicken embryo chorioallantoic membrane (xenograft-CAM) model system. Bithionol is able to inhibit tumor-induced new blood vessel formation in a dose dependent manner and has demonstrated an additive inhibitory activity when it is applied in combination with Sutent, a current clinically used antiangiogenic drug. The results of this research suggest that bithionol provide a unique promising opportunity in developing new combinational treatment to increase the anticancer efficacy and minimize the resistance in cancer patients. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 102nd Annual Meeting of the American Association for Cancer Research; 2011 Apr 2-6; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2011;71(8 Suppl):Abstract nr 4265. doi:10.1158/1538-7445.AM2011-4265
    Type of Medium: Online Resource
    ISSN: 0008-5472 , 1538-7445
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    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2011
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  • 8
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    Online Resource
    American Association for Cancer Research (AACR) ; 2006
    In:  Molecular Cancer Therapeutics Vol. 5, No. 9 ( 2006-09-01), p. 2218-2224
    In: Molecular Cancer Therapeutics, American Association for Cancer Research (AACR), Vol. 5, No. 9 ( 2006-09-01), p. 2218-2224
    Abstract: 4′-Thio-β-d-arabinofuranosylcytosine (T-araC), a new-generation deoxycytidine nucleoside analogue, showed significant efficacy against numerous solid tumors in preclinical studies and entered clinical development for cancer therapy. It is a structural analogue of cytarabine (araC), a clinically used drug in the treatment of acute myelogenous leukemia, which has no or very limited efficacy against solid tumors. In comparison with araC, the excellent in vivo activity of T-araC against solid tumors suggests that, in addition to inhibition of DNA synthesis, T-araC may target cellular signaling pathways, such as angiogenesis, in solid tumors. We studied T-araC and araC for their antiangiogenic activities in vitro and in vivo. Both compounds inhibited human endothelial cell proliferation with similar IC50s. However, only T-araC inhibited endothelial cell migration and differentiation into capillary tubules. T-araC also abrogated endothelial cell extracellular signal-regulated kinase (ERK) 1/2 phosphorylation, a key signaling molecule involved in cellular processes of angiogenesis. Results from chick chorioallantoic membrane angiogenesis assays revealed that T-araC significantly inhibited the development of new blood vessels in vivo, whereas araC showed much less effect. The findings of this study show a role of T-araC in antiangiogenesis and suggest that T-araC combines antiproliferative and antiangiogenic activity in one molecule for a dual mechanism of drug action to achieve the excellent in vivo efficacy against several solid tumors. This study also provides important information for optimizing dosage and sequence of T-araC administration in clinical investigations by considering T-araC as both an antiproliferative and an antiangiogenic agent. [Mol Cancer Ther 2006;5(9):2218–24]
    Type of Medium: Online Resource
    ISSN: 1535-7163 , 1538-8514
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2006
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  • 9
    Online Resource
    Online Resource
    American Association for Cancer Research (AACR) ; 2012
    In:  Cancer Research Vol. 72, No. 8_Supplement ( 2012-04-15), p. 2333-2333
    In: Cancer Research, American Association for Cancer Research (AACR), Vol. 72, No. 8_Supplement ( 2012-04-15), p. 2333-2333
    Abstract: Platelet aggregation leads to significant serotonin release from its major storage and results in increasing of serotonin levels at injury site and thrombotic tumor environment. Many studies have shown that platelet activation plays a crucial role in tumor progression; however, the role of serotonin in angiogenesis and tumor progression has not been well studied. In this study, we have tested the hypothesis that 5-HT promotes angiogenesis, and antagonizing 5-HT activity has anti-angiogenic benefit in controlling tumor growth. Real time PCR and western blot studies showed that endothelial cell expressed 5-HT receptor 1B (HTR1B) in higher level than other 5-HT receptors. Endothelial cell proliferation and tube formation were significantly affected by blocking HTR1B and the cAMP and IP1 assays have revealed the HTR1B as the inhibitory type of GPCR. Stimulation of endothelial cell with 5-HT or HTR1B agonist has led to activation of two individual signaling pathways: ERK and Akt / mTOR. In further studies, p70S6K was recognized as the merging point of these signaling. These kinases have been also activated by known angiogenic factors (VEGF and FGF) but the mechanism of activation was different from serotonin and it was through their tyrosine kinase receptors. In contrast, pretreatment of endothelial cell with a selective HTR1B antagonist have led to blockade of the 5-HT induced kinases’ activation. We also demonstrated angiogenic promoting activity of 5-HT with a mouse Matrigel plug (in vivo angiogenesis model system) and antiangiogenic potential of antagonists against HTR1B with an ex vivo tumor angiogenesis model (xenograft CAM assay) and xenograft mice model of human ovary cancer (SKOV-3). Selective HTR1B antagonist displayed the synergistic effect (combination index analysis) in blocking tumor-induced new blood vessel formation when it was applied in combination with Sutent (VEGFR2 antagonist). HTR1B antagonist also showed preclinical efficacy in the xenograft model of human ovary cancer by reducing over 50% in tumor size and blood vessel density marker.The results of this study enhanced our understanding of the serotonin-signaling pathway in human endothelial cells during angiogenesis. This research also revealed the potential of 5-HT signaling as the new target for antiangiogenic development. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 103rd Annual Meeting of the American Association for Cancer Research; 2012 Mar 31-Apr 4; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2012;72(8 Suppl):Abstract nr 2333. doi:1538-7445.AM2012-2333
    Type of Medium: Online Resource
    ISSN: 0008-5472 , 1538-7445
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    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2012
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  • 10
    Online Resource
    Online Resource
    American Association for Cancer Research (AACR) ; 2010
    In:  Cancer Research Vol. 70, No. 8_Supplement ( 2010-04-15), p. 5474-5474
    In: Cancer Research, American Association for Cancer Research (AACR), Vol. 70, No. 8_Supplement ( 2010-04-15), p. 5474-5474
    Abstract: The clinical successes of VEGF-targeted agents in recent years have demonstrated that antiangiogenic therapy can be developed as effective anti-cancer treatment. However, the field of oncology is facing a new challenge of overcoming the resistance to VEGF-targeted therapy; therefore, novel angiogenesis inhibitors are required for new therapeutic development. During the growth of new blood capillaries, following proliferation and migration, endothelial cells undergo morphological changes and adhere to each other forming tubular structures as a process of tubulogenesis, which presents a unique target for inhibitory action of antiangiogenic agents. Southern Research angiogenesis research team has identified a structurally related series of heterocyclic compounds SRI-24637 and its analogs as a new class of antiangiogenic agents. SRI-24637 demonstrated selective potent inhibition of endothelial tube-formation and significant activity in blocking tumor-induced blood vessel formation using an ex vivo human cancer xenograft-CAM assay model system. The mechanism of action of SRI-24637 is different from the clinical VEGF-targeted drugs; therefore, it may provide a complementary mechanism to overcome the resistance to VEGF-targeted therapies. Bioavailability studies showed that SRI-24637 dosed at 40 mg/kg in DMSO/PEG400 reached systemic concentration levels much higher than the IC50 concentration for in vitro endothelial tube-formation. Comparing with the clinical VEGF-targeted drug Sunitinib, the cytotoxic activities of SRI-24637 against normal human fibroblast and epithelial cells suggest that the toxic side effects of SRI-24637 may be within a tolerable range. Ongoing preclinical efficacy studies with animal tumor models will aid in the development of SRI-24637 as an anti-cancer drug. Based on the outcome of these studies, further lead optimization will be done if required, before entering it into the clinical Phase I and II trials using protocols similar to those employed for Sunitinib and Sorafenib, or other investigational small molecules targeting tumor angiogenesis. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 101st Annual Meeting of the American Association for Cancer Research; 2010 Apr 17-21; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2010;70(8 Suppl):Abstract nr 5474.
    Type of Medium: Online Resource
    ISSN: 0008-5472 , 1538-7445
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    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2010
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