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  • 1
    Online Resource
    Online Resource
    Next Generation of Cancer Drug Repurposing: Therapeutic Combination of Aspirin and Oseltamivir Phosphate Potentiates Gemcitabine to Disable Key Survival Pathways Critical for Pancreatic Cancer Progression
    MDPI AG ; 2022
    In:  Cancers Vol. 14, No. 6 ( 2022-03-08), p. 1374-
    Details
    In: Cancers, MDPI AG, Vol. 14, No. 6 ( 2022-03-08), p. 1374-
    Abstract: Resistance to chemotherapeutics and high metastatic rates contribute to the abysmal survival rate in patients with pancreatic cancer. An alternate approach for treating human pancreatic cancer involves repurposing the anti-inflammatory drug, aspirin (ASA), with oseltamivir phosphate (OP) in combination with the standard chemotherapeutic agent, gemcitabine (GEM). The question is whether treatment with ASA and OP can sensitize cancer cells to the cytotoxicity induced by GEM and limit the development of chemoresistance. To assess the key survival pathways critical for pancreatic cancer progression, we used the AlamarBlue cytotoxicity assay to determine the cell viability and combination index for the drug combinations, flow cytometric analysis of annexin V apoptosis assay to detect apoptotic and necrotic cells, fluorometric QCM™ chemotaxis migration assay to assess cellular migration, fluorometric extracellular matrix (ECM) cell adhesion array kit to assess the expression of the ECM proteins, scratch wound assay using the 96-well WoundMaker™, and the methylcellulose clonogenic assay to assess clonogenic potential. The combination of ASA and OP with GEM significantly upended MiaPaCa-2 and PANC-1 pancreatic cancer cell viability, clonogenic potential, expression of critical extracellular matrix proteins, migration, and promoted apoptosis. ASA in combination with OP significantly improves the effectiveness of GEM in the treatment of pancreatic cancer and disables key survival pathways critical to disease progression.
    Type of Medium: Online Resource
    ISSN: 2072-6694
    URL: Article
    DOI: 10.3390/cancers14061374
    Language: English
    Publisher: MDPI AG
    Publication Date: 2022
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  • 2
    Online Resource
    Online Resource
    Erratum to: The role of Sulforaphane in cancer chemoprevention and health benefits: a mini-review
    Springer Science and Business Media LLC ; 2018
    In:  Journal of Cell Communication and Signaling Vol. 12, No. 2 ( 2018-6), p. 503-503
    Details
    In: Journal of Cell Communication and Signaling, Springer Science and Business Media LLC, Vol. 12, No. 2 ( 2018-6), p. 503-503
    Type of Medium: Online Resource
    ISSN: 1873-9601 , 1873-961X
    URL: Article
    DOI: 10.1007/s12079-017-0408-4
    Language: English
    Publisher: Springer Science and Business Media LLC
    Publication Date: 2018
    detail.hit.zdb_id: 2299380-0
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  • 3
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    Online Resource
    Metronomic Oral Topotecan with Pazopanib Is an Active Antiangiogenic Regimen in Mouse Models of Aggressive Pediatric Solid Tumor
    American Association for Cancer Research (AACR) ; 2011
    In:  Clinical Cancer Research Vol. 17, No. 17 ( 2011-09-01), p. 5656-5667
    Details
    In: Clinical Cancer Research, American Association for Cancer Research (AACR), Vol. 17, No. 17 ( 2011-09-01), p. 5656-5667
    Abstract: Purpose: Low dose metronomic (LDM) chemotherapy, combined with VEGF signaling pathway inhibitors, is a highly effective strategy to coordinately inhibit angiogenesis and tumor growth in many adult preclinical cancer models. We have tested the efficacies of daily oral LDM topotecan alone and in combination with pazopanib, a VEGF receptor inhibitor, in three pediatric extracranial solid tumor mouse models. Experimental Design: In vitro dose–response study of topotecan and pazopanib was conducted on several neuroblastoma, osteosarcoma, and rhabdomyosarcoma cell lines. In vivo antitumor efficacies of the LDM topotecan and pazopanib as single agents and in combination were tested on 4 subcutaneous xenograft models and on 2 neuroblastoma metastatic models. Circulating angiogenic factors such as circulating endothelial cells (CEC), circulating endothelial pro genitor cells (CEP), and microvessel densities were used as surrogate biomarker markers of antiangiogenic activity. Results: In vitro, topotecan caused a dose-dependent decrease in viabilities of all cell lines, while pazopanib did not. In vivo, combination of topotecan + pazopanib (TP + PZ) showed significant antitumor activity and significant enhancement in survival compared with the respective single agents in all models. Reductions in viable CEP and/or CEC levels and tumor microvessel density were correlated with tumor response and therefore confirmed the antiangiogenic activity of the regimens. Pharmacokinetic studies of both drugs did not reveal any drug–drug interaction. Conclusion: Metronomic administration of TP + PZ showed a statistically significant antitumor activity compared with respective single agents in pediatric tumor mouse models and represent a valid option as a maintenance therapy in aggressive pediatric solid tumors. Clin Cancer Res; 17(17); 5656–67. ©2011 AACR.
    Type of Medium: Online Resource
    ISSN: 1078-0432 , 1557-3265
    URL: Article
    DOI: 10.1158/1078-0432.CCR-11-0078
    RVK:
    XA 36791
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2011
    detail.hit.zdb_id: 1225457-5
    detail.hit.zdb_id: 2036787-9
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  • 4
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    Abstract B48: Cancer Stem Cells: characteristics, roles in metastatic disease and targeting therapy for the medically underserved
    American Association for Cancer Research (AACR) ; 2017
    In:  Cancer Epidemiology, Biomarkers & Prevention Vol. 26, No. 2_Supplement ( 2017-02-01), p. B48-B48
    Details
    In: Cancer Epidemiology, Biomarkers & Prevention, American Association for Cancer Research (AACR), Vol. 26, No. 2_Supplement ( 2017-02-01), p. B48-B48
    Abstract: Cancer stem cells have been observed to lead to the proliferation and relapse of cancers. While they share many properties with normal stem cells, CSCs are distinguished by their incredibly high survivability, drug resistance, and the ability to facilitate tumor progression. In this review, we discuss the origin, major properties used to identify and characterize CSCs, and also how they behave and are regulated with tumor progression and metastasis. In addition, we discuss multiple therapeutic strategies that were developed to target CSCs. Amongst these we review several natural compounds that in recent studies have shown great potential for preventing tumorigenesis and in the treatment of cancer cells by interacting with CSCs. Natural compounds are being widely researched for efficacy as cancer and CSC targeting agents. Natural drugs consume much less funding to produce. Also, as dietary compounds, they are less stigmatized by patients than artificially synthesized drugs, and they are inexpensive and available to even the medically underserved. Finally, we discuss several strategies that are used to maximize the effect of therapeutic strategies on the CSC fraction and further directions for this field of tumor biology. Note: This abstract was not presented at the conference. Citation Format: Zhenya Morgatskaya, Reza Bayat Mokhtari, Albina Tyker, Parandis Kazemi, Tina Homayouni, Narges Baluch, Sara Dhalla, Shreya Rekhi, Sushil Kumar, Herman Yeger. Cancer Stem Cells: characteristics, roles in metastatic disease and targeting therapy for the medically underserved. [abstract]. In: Proceedings of the Ninth AACR Conference on the Science of Cancer Health Disparities in Racial/Ethnic Minorities and the Medically Underserved; 2016 Sep 25-28; Fort Lauderdale, FL. Philadelphia (PA): AACR; Cancer Epidemiol Biomarkers Prev 2017;26(2 Suppl):Abstract nr B48.
    Type of Medium: Online Resource
    ISSN: 1055-9965 , 1538-7755
    URL: Article
    DOI: 10.1158/1538-7755.DISP16-B48
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2017
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    detail.hit.zdb_id: 1153420-5
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  • 5
    Online Resource
    Online Resource
    Table_1.pdf
    Frontiers Media SA ; 2022
    In:  Frontiers in Immunology Vol. 13 ( 2022-9-29)
    Details
    In: Frontiers in Immunology, Frontiers Media SA, Vol. 13 ( 2022-9-29)
    Abstract: Tumor hypoxia and oxidative stress reprograms cancer stem cells (CSCs) to a highly aggressive and inflammatory phenotypic state of tumor stemness. Previously, we characterized tumor stemness phenotype in the ATP Binding Cassette Subfamily G Member 2 (ABCG2)–positive migratory side population (SPm) fraction of CSCs exposed to extreme hypoxia followed by reoxygenation. Here, we report that post-hypoxia/reoxygenation SPm+/ABCG2+ CSCs exerts defense against pathogen invasion that involves bystander apoptosis of non-infected CSCs. In an in vitro assay of cancer cell infection by Bacillus Calmette Guerin (BCG) or mutant Mycobacterium tuberculosis (Mtb) strain 18b (Mtb-m18b) , the pathogens preferentially replicated intracellular to SPm+/ABCG2+ CSCs of seven cell lines of diverse cancer types including SCC-25 oral squamous cancer cell line. The conditioned media (CM) of infected CSCs exhibited direct anti-microbial activity against Mtb and BCG, suggesting niche defense against pathogen. Importantly, the CM of infected CSCs exhibited marked in vitro bystander apoptosis toward non-infected CSCs. Moreover, the CM-treated xenograft bearing mice showed 10- to 15-fold reduction (p & lt; 0.001; n = 7) in the number of CSCs residing in the hypoxic niches. Our in vitro studies indicated that BCG-infected SPm+/ABCG2+ equivalent EPCAM+/ABCG2+ CSCs of SCC-25 cells underwent pyroptosis and released a high mobility group box protein 1 (HMGB1)/p53 death signal into the tumor microenvironment (TME). The death signal can induce a Toll-like receptor 2/4–mediated bystander apoptosis in non-infected CSCs by activating p53/MDM2 oscillation and subsequent activation of capase-3–dependent intrinsic apoptosis. Notably, SPm+/ABCG2+ but not SP cells undergoing bystander apoptosis amplified the death signal by further release of HMGB1/p53 complex into the TME. These results suggest that post-hypoxia SPm+/ABCG2+ CSCs serve a functional role as a tumor stemness defense (TSD) phenotype to protect TME against bacterial invasion. Importantly, the CM of TSD phenotype undergoing bystander apoptosis may have therapeutic uses against CSCs residing in the hypoxic niche.
    Type of Medium: Online Resource
    ISSN: 1664-3224
    URL: Article
    URL: Article
    DOI: 10.3389/fimmu.2022.933329
    DOI: 10.3389/fimmu.2022.933329.s001
    Language: Unknown
    Publisher: Frontiers Media SA
    Publication Date: 2022
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  • 6
    Online Resource
    Online Resource
    3D Multicellular Stem-Like Human Breast Tumor Spheroids Enhance Tumorigenicity of Orthotopic Xenografts in Athymic Nude Rat Model
    MDPI AG ; 2021
    In:  Cancers Vol. 13, No. 11 ( 2021-06-03), p. 2784-
    Details
    In: Cancers, MDPI AG, Vol. 13, No. 11 ( 2021-06-03), p. 2784-
    Abstract: Therapeutic targeting of stem cells needs to be strategically developed to control tumor growth and prevent metastatic burden successfully. Breast cancer presents a unique clinical problem because of the variety of cellular subtypes present, including cancer stem cells (CSCs). The development of 3D stem-like properties of human breast tumor spheroids in stem cell factor conditioned media was investigated in orthotopic xenografts for enhanced tumorgenicity in the athymic nude rat model. MCF-7, ZR-75-1, and MDA-MB-231 breast cancer cell lines were cultured in serum-free, stem cell factor-supplemented medium under non-adherent conditions and passaged to generate 3rd generation spheroids. The spheroids were co-cultured with fetal lung fibroblast (FLF) cells before orthotopic heterotransplantation into the mammary fat pads of athymic nude rats. Excised xenografts were assessed histologically by H & E staining and immunohistochemistry for breast cancer marker (ERB1), proliferation marker (Ki67), mitotic marker (pHH3), hypoxia marker (HIF-2α), CSC markers (CD47, CD44, CD24, and CD133), and vascularization markers (CD31, CD34). Breast cancer cells cultured in stem cell factor supplemented medium generated 3D spheroids exhibited increased stem-like characteristics. The 3D stem-like spheroids co-cultured with FLF as supporting stroma reproducibly and efficiently established orthotopic breast cancer xenografts in the athymic nude rat.
    Type of Medium: Online Resource
    ISSN: 2072-6694
    URL: Article
    DOI: 10.3390/cancers13112784
    Language: English
    Publisher: MDPI AG
    Publication Date: 2021
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  • 7
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    Online Resource
    Hypoxia-Targeting Drug Evofosfamide (TH-302) Enhances Sunitinib Activity in Neuroblastoma Xenograft Models
    Elsevier BV ; 2018
    In:  Translational Oncology Vol. 11, No. 4 ( 2018-08), p. 911-919
    Details
    In: Translational Oncology, Elsevier BV, Vol. 11, No. 4 ( 2018-08), p. 911-919
    Type of Medium: Online Resource
    ISSN: 1936-5233
    URL: Article
    DOI: 10.1016/j.tranon.2018.05.004
    Language: English
    Publisher: Elsevier BV
    Publication Date: 2018
    detail.hit.zdb_id: 2443840-6
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  • 8
    Online Resource
    Online Resource
    Carbonic Anhydrase II Mediates Malignant Behavior of Pulmonary Neuroendocrine Tumors
    American Thoracic Society ; 2015
    In:  American Journal of Respiratory Cell and Molecular Biology Vol. 52, No. 2 ( 2015-02), p. 183-192
    Details
    In: American Journal of Respiratory Cell and Molecular Biology, American Thoracic Society, Vol. 52, No. 2 ( 2015-02), p. 183-192
    Type of Medium: Online Resource
    ISSN: 1044-1549 , 1535-4989
    URL: Article
    DOI: 10.1165/rcmb.2014-0054OC
    RVK:
    XA 20260
    Language: English
    Publisher: American Thoracic Society
    Publication Date: 2015
    detail.hit.zdb_id: 1473629-9
    SSG: 12
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  • 9
    Online Resource
    Online Resource
    Circulating endothelial cells and circulating endothelial precursor cells in patients with osteosarcoma
    Wiley ; 2012
    In:  Pediatric Blood & Cancer Vol. 58, No. 2 ( 2012-02), p. 181-184
    Details
    In: Pediatric Blood & Cancer, Wiley, Vol. 58, No. 2 ( 2012-02), p. 181-184
    Abstract: Circulating endothelial cells (CECs) have been detected at increased numbers in patients with solid cancers. CECs have not been systematically evaluated in patients with osteosarcoma. Procedure Patients 12 months to 30 years of age with newly diagnosed high‐grade osteosarcoma were eligible for this prospective cohort study. Patients provided a single blood sample at study entry for CEC quantification by flow cytometry at a single reference laboratory. CECs were defined as CD146+, CD31+, CD45−, and CD133−. CEC progenitor cells (CEPs) were defined as CD146+, CD31+, CD45−, and CD133+. Results Eighteen patients enrolled (11 males; median age 16 years; range 5–21 years). CEC counts did not differ between patients with osteosarcoma compared to seven pediatric healthy controls (median 645 cells/ml, range 60–5,320 cells/ml vs. 1,670 cells/ml, range 330–4,700 cells/ml, respectively; P  = 0.12). CEP counts did not differ between patients compared to controls (median 126 cells/ml, range 0–5,320 cells/ml vs. median 260 cells/ml, range 0–10,670 cells/ml, respectively; P  = 0.69). CEC and CEP counts did not correlate with metastatic status, tumor size, or histologic response to neoadjuvant chemotherapy. Conclusions CEC and CEP levels are not increased in patients with osteosarcoma compared to healthy controls. CECs and CEPs do not correlate with clinical features of osteosarcoma. Alternative novel markers of disease burden and response are needed in this disease. Pediatr Blood Cancer 2012; 58: 181–184. © 2011 Wiley Periodicals, Inc.
    Type of Medium: Online Resource
    ISSN: 1545-5009 , 1545-5017
    URL: Issue
    URL: Article
    DOI: 10.1002/pbc.v58.2
    DOI: 10.1002/pbc.23046
    Language: English
    Publisher: Wiley
    Publication Date: 2012
    detail.hit.zdb_id: 2130978-4
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  • 10
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    Online Resource
    Combination of carbonic anhydrase inhibitor, acetazolamide, and sulforaphane, reduces the viability and growth of bronchial carcinoid cell lines
    Springer Science and Business Media LLC ; 2013
    In:  BMC Cancer Vol. 13, No. 1 ( 2013-12)
    Details
    In: BMC Cancer, Springer Science and Business Media LLC, Vol. 13, No. 1 ( 2013-12)
    Abstract: Bronchial carcinoids are pulmonary neuroendocrine cell-derived tumors comprising typical (TC) and atypical (AC) malignant phenotypes. The 5-year survival rate in metastatic carcinoid, despite multiple current therapies, is 14-25%. Hence, we are testing novel therapies that can affect the proliferation and survival of bronchial carcinoids. Methods In vitro studies were used for the dose–response (AlamarBlue) effects of acetazolamide (AZ) and sulforaphane (SFN) on clonogenicity, serotonin-induced growth effect and serotonin content (LC-MS) on H-727 (TC) and H-720 (AC) bronchial carcinoid cell lines and their derived NOD/SCID mice subcutaneous xenografts. Tumor ultra structure was studied by electron microscopy. Invasive fraction of the tumors was determined by matrigel invasion assay. Immunohistochemistry was conducted to study the effect of treatment(s) on proliferation (Ki67, phospho histone-H3) and neuroendocrine phenotype (chromogranin-A, tryptophan hydroxylase). Results Both compounds significantly reduced cell viability and colony formation in a dose-dependent manner (0–80 μM, 48 hours and 7 days) in H-727 and H-720 cell lines. Treatment of H-727 and H-720 subcutaneous xenografts in NOD/SCID mice with the combination of AZ + SFN for two weeks demonstrated highly significant growth inhibition and reduction of 5-HT content and reduced the invasive capacity of H-727 tumor cells. In terms of the tumor ultra structure, a marked reduction in secretory vesicles correlated with the decrease in 5-HT content. Conclusions The combination of AZ and SFN was more effective than either single agent. Since the effective doses are well within clinical range and bioavailability, our results suggest a potential new therapeutic strategy for the treatment of bronchial carcinoids.
    Type of Medium: Online Resource
    ISSN: 1471-2407
    URL: Article
    DOI: 10.1186/1471-2407-13-378
    Language: English
    Publisher: Springer Science and Business Media LLC
    Publication Date: 2013
    detail.hit.zdb_id: 2041352-X
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