Artigos de revistas: "Balb-neuT"

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Cabrera, Rosalyn, Pilar Nava-Parada e Larry R. Pease. "IL-10 secretion from BALB-neuT mice cells after stimulation with murine breast tumor cell lines (88.28)". Journal of Immunology 178, n.º 1_Supplement (1 de abril de 2007): S144. http://dx.doi.org/10.4049/jimmunol.178.supp.88.28.

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Abstract Failures in tolerance mechanisms cause autoimmunity. Self reactive cells in the periphery are kept in check by peripheral tolerance. Mice expressing a neoself antigen, called BALB-neuT, were used as a model for delineating mechanisms of peripheral tolerance. Two questions were addressed: Are BALB-neuT tolerant to neoself antigen? Can BALB-neuT tolerance be broken? We first established that BALB-neuT are tolerant to Her2/neu peptide while parental BALB/c mounted a significant response after immunization with Her2/neu peptide in CFA and repeated CpG stimulations. Next we depleted CD25+ cells and used the immunomodulating antibody B7-DC XAb to study the mechanism involved. CD8+ T cells from treated BALB-neuT generated a potent response when compared to untreated BALB-neuT or BALB/c, as measured by IFNγ secretion. Interestingly, IL-10 secretion from BALB-neuT T cells was high after incubation with murine breast cell lines, irrespective of expression of BALB-neuT antigen. After depletion of CD4+CD25+ T cells, secretion of IL-10 was diminished, suggesting that the IL-10 is being secreted by T regulatory cells. In conclusion, BALB-neuT are tolerant to neoself antigen. Tolerance can be broken by depleting Tregs or using B7-DC Xab to modulate immunity. Future studies are aimed at identifying mechanisms regulating IL-10 secretion to unravel pathways important in regulation of autoimmunity.

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Chiodoni, Claudia, Manuela Iezzi, Cristiana Guiducci, Sabina Sangaletti, Isabella Alessandrini, Chiara Ratti, Francesca Tiboni, Piero Musiani, D. Neil Granger e Mario P. Colombo. "Triggering CD40 on endothelial cells contributes to tumor growth". Journal of Experimental Medicine 203, n.º 11 (16 de outubro de 2006): 2441–50. http://dx.doi.org/10.1084/jem.20060844.

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Inflammatory cells can either promote or inhibit tumor growth. Here we studied whether CD40, a key molecule for adaptive immune response, has any role in mammary carcinogenesis of BALB/NeuT transgenic tumor-prone mice. We transferred the HER2/neu oncogene into CD40-null background to obtain the CD40-KO/NeuT strain. CD40-KO/NeuT mice showed delayed tumor onset and reduced tumor multiplicity. BM (BM) transplantation experiments excluded a role of BM-derived cells in the reduced tumorigenicity associated with CD40 deficiency. Rather, CD40 expressed by endothelial cells (ECs) takes part to the angiogenic process. Accordingly, large vessels, well organized around the tumor lobular structures, characterize BALB/NeuT tumors, whereas tiny numerous vessels with scarce extracellular matrix are dispersed in the parenchyma of poorly organized CD40-KO/NeuT tumors. Activated platelets, which may interact with and activate ECs, are a possible source of CD40L. Their localization within tumor vessels prompted the idea of treating BALB/NeuT and CD40-KO/NeuT mice chronically with the anti-platelet drug clopidogrel, known to inhibit platelet CD40L expression. Treatment of BALB/NeuT mice reduced tumor growth to a level similar to CD40-deficient mice, whereas CD40-KO/NeuT mice treated or not showed the same attenuated tumor outgrowth, indicating that activated platelets are the likely source of CD40L in this model. Collectively, these data point to a participation of CD40/CD40L in the angiogenic processes associated with mammary carcinogenesis of BALB/NeuT mice.

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Castro, Sarah A., Alvaro Pena, Khashayarsha Khazaie e Larry R. Pease. "MHC genotype, immune repertoire, and tumor immunity all influence spontaneous cancer development and metastasis in spontaneous breast cancer models". Journal of Immunology 204, n.º 1_Supplement (1 de maio de 2020): 90.16. http://dx.doi.org/10.4049/jimmunol.204.supp.90.16.

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Abstract 20 to 30% of breast cancers overexpress ERRB2, encoding the human epidermal growth factor-2 receptor (HER2). Overexpression of HER2 is associated with poorer prognosis, particularly in metastatic disease. Although HER2 therapeutics exists many patients eventually develop uncontrolled tumor growth. The BALB/c-neuT mouse has been a popular model for investigating HER2-positive breast cancer. We have found that immune responsiveness and MHC genotype are important factors in spontaneous tumor development and tumor rejection in the neuT model. To assess the influence of immune response potential on tumor biology we introduced the skg ZAP-70 mutation or the H-2b MHC haplotype into the neuT model. Spontaneous tumors appeared with decreased frequency and metastasis or increased frequency and metastasis, respectively, in comparison to the BALB/c model. H-2b tumors were readily transplantable into the breast fat pads of syngeneic BALB.B-neuT hosts which developed systemic immune abnormalities very similar to those observed in BALB/c - neuT or BALB/c WT mice bearing neuT tumors. However, BALB.B WT hosts initially accepted the grafts, but subsequently rejected them after they were established. Adoptive transfer of splenocytes from BALB.B WT mice which had rejected tumor conferred resistance to the tumor grafts, as well as to spontaneous tumors developing in BALB.B neuT littermates. The strong H-2b-mediated antitumor response in WT mice indicates efficient antigen presentation, and presumably leads to strong tolerance in neuT+ animals. The importance of an intact T cell signaling and MHC genotype indicate a critical role for T cell-mediated immunity and tolerance in the biology of the spontaneously developing tumor and metastasis.

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Focaccetti, Chiara, Monica Benvenuto, Sara Ciuffa, Sara Fazi, Manuel Scimeca, Alessandra Nardi, Martino Tony Miele et al. "Curcumin Enhances the Antitumoral Effect Induced by the Recombinant Vaccinia Neu Vaccine (rV-neuT) in Mice with Transplanted Salivary Gland Carcinoma Cells". Nutrients 12, n.º 5 (14 de maio de 2020): 1417. http://dx.doi.org/10.3390/nu12051417.

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The survival rate for head and neck cancer patients has not substantially changed in the last two decades. We previously showed that two rV-neuT intratumoral injections induced an efficient antitumor response and rejection of transplanted Neu (rat ErbB2/neu oncogene-encoded protein)-overexpressing salivary gland tumor cells in BALB-neuT mice (BALB/c mice transgenic for the rat ErbB2/neu oncogene). However, reiterated poxviral vaccinations increase neutralizing antibodies to viral proteins in humans that prevent immune response against the recombinant antigen expressed by the virus. Curcumin (CUR) is a polyphenol with antineoplastic and immunomodulatory properties. The aim of this study was to employ CUR administration to boost the anti-Neu immune response and anticancer activity induced by one rV-neuT intratumoral vaccination in BALB-neuT mice. Here, we demonstrated that the combined rV-neuT+CUR treatment was more effective at reducing tumor growth and increasing mouse survival, anti-Neu humoral response, and IFN-γ/IL-2 T-cell release in vitro than the individual treatment. rV-neuT+CUR-treated mice showed an increased infiltration of CD4+/CD8+ T lymphocytes within the tumor as compared to those that received the individual treatment. Overall, CUR enhanced the antitumoral effect and immune response to Neu induced by the rV-neuT vaccine in mice. Thus, the combined treatment might represent a successful strategy to target ErbB2/Neu-overexpressing tumors.

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Melani, Cecilia, Claudia Chiodoni, Guido Forni e Mario P. Colombo. "Myeloid cell expansion elicited by the progression of spontaneous mammary carcinomas in c-erbB-2 transgenic BALB/c mice suppresses immune reactivity". Blood 102, n.º 6 (15 de setembro de 2003): 2138–45. http://dx.doi.org/10.1182/blood-2003-01-0190.

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Abstract Transgenic female mice expressing the transforming rat oncogene c-erbB-2 (HER-2/neu) under the mouse mammary tumor virus (MMTV) promoter (BALB-neuT) spontaneously develop mammary carcinomas with a progression resembling that of human breast cancer. In these mice, activating antitumor immunotherapy fails to induce T cell–mediated cytotoxicity, suggesting a suppression of the immune response. We found a direct correlation between tumor multiplicity and an increased proportion of Gr-1+ (Ly6G)/Mac-1+(CD11b)/ER-MP12+(CD31) immature myeloid cells in the peripheral blood (PB) and spleen, suggesting that tumor load profoundly affects overall BALB-neuT hematopoiesis. In fact, myeloid colony formation was increased in bone marrow (BM) and spleen. The immature myeloid cells displayed suppressive activity on host T lymphocytes, which progressively failed to respond to alloantigens and CD3 triggering, while maintaining the ability to proliferate in response to nonspecific mitogens. Transplantation of normal BM into BALB-neuT mice readily resulted in hypertrophic hematopoiesis with myeloid cell expansion. This persistent influence of the tumor was mediated through the release of vascular endothelial growth factor (VEGF) but not granulocyte-macrophage colony-stimulating factor (GM-CSF), and was down-modulated when tumor load was reduced but not when BM was transplanted. Together, the data obtained in the BALB-neuT model of naturally occurring carcinogenesis show that tumor-associated immune suppression is secondary to a more general alteration of host hematopoiesis, conditioned by tumor-secreted soluble factors.

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Spadaro, Michela, Gabriele Casule, Monica Montone, Irene Merighi, Federica Pericle e Federica Cavallo. "Human recombinant lactoferrin as a new adjuvant in specific DNA vaccination against ErbB2 (75.2)". Journal of Immunology 188, n.º 1_Supplement (1 de maio de 2012): 75.2. http://dx.doi.org/10.4049/jimmunol.188.supp.75.2.

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Abstract Lactoferrin triggers several innate immunity mechanisms. Repeated oral administrations of a recombinant human lactoferrin (Talactoferrin, TLF, Agennix, Houston, TX) hamper the growth of both transplantable tumors and autochthonous mammary carcinomas arising in BALB/c mice transgenic for the rat ErbB2 oncogene (BALB-neuT mice). To evaluate the mechanisms that delay the tumor growth and enhance the immune response elicited by a DNA vaccine against rat ErbB2 oncogene, BALB-neuT mice received by gavage PBS or TLF (1 g/kg) once daily, 5 days per week, 3 weeks on and 1 week rest for seven cycles. Following oral TLF we observed: decrease of serum IL4 and IL5; increase of serum IL12 and IFNγ; decrease of immature myeloid cells in tumor draining lymph nodes. When BALB-neuT mice receiving oral TLF were vaccinated with 50 µg of DNA plasmid coding for the extracellular and transmembrane domain of rat ErbB2 we found: extended tumor-free survivals; increased overall survivals; decrease in the number of tumors/mouse; higher titers of vaccine-induced anti-ErbB2 antibodies; similar cytotoxicity activities against ErbB2+ tumors. These findings suggest that TLF is an interesting new adjuvant in DNA vaccination against ErbB2.

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Lamolinara, Alessia, Lorenzo Stramucci, Albana Hysi, Manuela Iezzi, Cristina Marchini, Marianna Mariotti, Augusto Amici e Claudia Curcio. "Intradermal DNA Electroporation Induces Cellular and Humoral Immune Response and Confers Protection against HER2/neu Tumor". Journal of Immunology Research 2015 (2015): 1–10. http://dx.doi.org/10.1155/2015/159145.

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Skin represents an attractive target for DNA vaccine delivery because of its natural richness in APCs, whose targeting may potentiate the effect of vaccination. Nevertheless, intramuscular electroporation is the most common delivery method for ECTM vaccination. In this study we assessed whether intradermal administration could deliver the vaccine into different cell types and we analyzed the evolution of tissue infiltrate elicited by the vaccination protocol. Intradermal electroporation (EP) vaccination resulted in transfection of different skin layers, as well as mononuclear cells. Additionally, we observed a marked recruitment of reactive infiltrates mainly 6–24 hours after treatment and inflammatory cells included CD11c+. Moreover, we tested the efficacy of intradermal vaccination against Her2/neu antigen in cellular and humoral response induction and consequent protection from a Her2/neu tumor challenge in Her2/neu nontolerant and tolerant mice. A significant delay in transplantable tumor onset was observed in both BALB/c (p≤0,0003) and BALB-neuT mice (p=0,003). Moreover, BALB-neuT mice displayed slow tumor growth as compared to control group (p<0,0016). In addition, while in vivo cytotoxic response was observed only in BALB/c mice, a significant antibody response was achieved in both mouse models. Our results identify intradermal EP vaccination as a promising method for delivering Her2/neu DNA vaccine.

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Conti, Laura, Roberto Ruiu, Giuseppina Barutello, Marco Macagno, Silvio Bandini, Federica Cavallo e Stefania Lanzardo. "Microenvironment, Oncoantigens, and Antitumor Vaccination: Lessons Learned from BALB-neuT Mice". BioMed Research International 2014 (2014): 1–16. http://dx.doi.org/10.1155/2014/534969.

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The tyrosine kinase human epidermal growth factor receptor 2 (HER2) gene is amplified in approximately 20% of human breast cancers and is associated with an aggressive clinical course and the early development of metastasis. Its crucial role in tumor growth and progression makes HER2 a prototypic oncoantigen, the targeting of which may be critical for the development of effective anticancer therapies. The setup of anti-HER2 targeting strategies has revolutionized the clinical outcome of HER2+breast cancer. However, their initial success has been overshadowed by the onset of pharmacological resistance that renders them ineffective. Since the tumor microenvironment (TME) plays a crucial role in drug resistance, the design of more effective anticancer therapies should depend on the targeting of both cancer cells and their TME as a whole. In this review, starting from the successful know-how obtained with a HER2+mouse model of mammary carcinogenesis, the BALB-neuT mice, we discuss the role of TME in mammary tumor development. Indeed, a deeper knowledge of antigens critical for cancer outbreak and progression and of the mechanisms that regulate the interplay between cancer and stromal cell populations could advise promising ways for the development of the best anticancer strategy.

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Konishi, Eiji, Masaoki Yamaoka, Khin-Sane-Win, Ichiro Kurane e Peter W. Mason. "Induction of Protective Immunity against Japanese Encephalitis in Mice by Immunization with a Plasmid Encoding Japanese Encephalitis Virus Premembrane and Envelope Genes". Journal of Virology 72, n.º 6 (1 de junho de 1998): 4925–30. http://dx.doi.org/10.1128/jvi.72.6.4925-4930.1998.

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ABSTRACT A DNA vaccine plasmid containing the Japanese encephalitis (JE) virus premembrane (prM) and envelope (E) genes (designated pcDNA3JEME) was evaluated for immunogenicity and protective efficacy in mice. Two immunizations of 4-week-old female ICR mice with pcDNA3JEME by intramuscular or intradermal injections at a dose of 10 or 100 μg per mouse elicited neutralizing (NEUT) antibodies at titers of 1:10 to 1:20 (90% plaque reduction), and all immunized mice survived a challenge with 10,000 50% lethal doses of the P3 strain of JE virus. A single immunization with 100 μg of pcDNA3JEME did not elicit detectable NEUT antibodies but induced protective immunity. Spleen cells obtained from BALB/c mice immunized once with 10 or 100 μg of pcDNA3JEME contained JE virus-specific memory cytotoxic T lymphocytes (CTLs). BALB/c mice maintained detectable levels of memory B cells and CTLs for at least 6 months after one immunization with pcDNA3JEME at a dose of 100 μg. The CTLs induced in BALB/c mice immunized twice with 100 μg of pcDNA3JEME were CD8 positive and recognized mainly the envelope protein. These results indicate that pcDNA3JEME has the ability to induce a protective immune response which includes JE virus-specific antibodies and CTLs.

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Argenziano, Monica, Casimiro Luca Gigliotti, Nausicaa Clemente, Elena Boggio, Benedetta Ferrara, Francesco Trotta, Stefania Pizzimenti et al. "Improvement in the Anti-Tumor Efficacy of Doxorubicin Nanosponges in In Vitro and in Mice Bearing Breast Tumor Models". Cancers 12, n.º 1 (9 de janeiro de 2020): 162. http://dx.doi.org/10.3390/cancers12010162.

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Doxorubicin (DOX) is an anthracycline widely used in cancer therapy and in particular in breast cancer treatment. The treatment with DOX appears successful, but it is limited by a severe cardiotoxicity. This work evaluated the in vitro and in vivo anticancer effect of a new formulation of β-cyclodextrin nanosponges containing DOX (BNS-DOX). The BNS-DOX effectiveness was evaluated in human and mouse breast cancer cell lines in vitro in terms of effect on cell growth, cell cycle distribution, and apoptosis induction; and in vivo in BALB-neuT mice developing spontaneous breast cancer in terms of biodistribution, cancer growth inhibition, and heart toxicity. BNS-DOX significantly inhibited cancer cell proliferation, through the induction of apoptosis, with higher efficiency than free DOX. The breast cancer growth in BALB-neuT mice was inhibited by 60% by a BNS-DOX dose five times lower than the DOX therapeutic dose, with substantial reduction of tumor neoangiogenesis and lymphangiogenesis. Biodistribution after BNS-DOX treatment revealed a high accumulation of DOX in the tumor site and a low accumulation in the hearts of mice. Results indicated that use of BNS may be an efficient strategy to deliver DOX in the treatment of breast cancer, since it improves the anti-cancer effectiveness and reduces cardiotoxicity.

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Macagno, Marco, Silvio Bandini, Elisabetta Bolli, Amanda Bello, Federica Riccardo, Giuseppina Barutello, Irene Fiore Merighi et al. "Role of ADCC, CDC, and CDCC in Vaccine-Mediated Protection against Her2 Mammary Carcinogenesis". Biomedicines 10, n.º 2 (21 de janeiro de 2022): 230. http://dx.doi.org/10.3390/biomedicines10020230.

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Amplification or mutation of the Her2 oncoantigen in human mammary glands leads to the development of an aggressive breast carcinoma. Several features of this breast carcinoma are reproduced in mammary carcinomas that spontaneously arise in female transgenic mice bearing the activated rat Her2 oncogene under transcriptional control of the mouse mammary tumor virus promoter-BALB-neuT (neuT) mice. We previously demonstrated that carcinoma progression in neuT mice can be prevented by DNA vaccination with RHuT, a plasmid coding for a chimeric rat/human Her2 protein. RHuT vaccination exerts an antitumor effect, mostly mediated by the induction of a strong anti-rat Her2 antibody response. IgG induced by RHuT vaccine mainly acts by blocking Her2 signaling, thus impairing cell cycle progression and inducing apoptosis of cancer cells, but other indirect effector mechanisms could be involved in the antibody-mediated protection. The recruitment of cells with perforin-dependent cytotoxic activity, able to perform antibody-dependent cellular cytotoxicity, has already been investigated. Less is known about the role of the complement system in sustaining antitumor response through complement-dependent cytotoxicity and cellular cytotoxicity in vaccinated mice. This work highlights that the weight of such mechanisms in RHuT-induced cancer protection is different in transplantable versus autochthonous Her2+ tumor models. These results may shed new light on the effector mechanisms involved in antibody-dependent anti-cancer responses, which might be exploited to ameliorate the therapy of Her2+ breast cancer.

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Grange, Cristina, Stefania Lanzardo, Federica Cavallo, Giovanni Camussi e Benedetta Bussolati. "SCA-1 Identifies the Tumor-Initiating Cells in Mammary Tumors of BALB-neuT Transgenic Mice". Neoplasia 10, n.º 12 (dezembro de 2008): 1433–43. http://dx.doi.org/10.1593/neo.08902.

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Cornelissen, B., S. Able, C. Kartsonaki, V. Kersemans, P. D. Allen, F. Cavallo, J. B. Cazier et al. "Imaging DNA Damage Allows Detection of Preneoplasia in the BALB-neuT Model of Breast Cancer". Journal of Nuclear Medicine 55, n.º 12 (13 de novembro de 2014): 2026–31. http://dx.doi.org/10.2967/jnumed.114.142083.

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Gallo, Pasquale, Sridhar Dharmapuri, Maurizio Nuzzo, Daniele Maldini, Barbara Cipriani, Guido Forni e Paolo Monaci. "Adenovirus vaccination againstneu oncogene exerts long-term protection from tumorigenesis in BALB/neuT transgenic mice". International Journal of Cancer 120, n.º 3 (2006): 574–84. http://dx.doi.org/10.1002/ijc.22274.

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Jacob, Jennifer B., Yi-chi M. Kong, Ilke Nalbantoglu, Daniel P. Snower e Wei-Zen Wei. "Th1 and Th17 in tumor Immunity versus autoimmunity (128.15)". Journal of Immunology 178, n.º 1_Supplement (1 de abril de 2007): S213. http://dx.doi.org/10.4049/jimmunol.178.supp.128.15.

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Abstract To determine the role of Th1 and Th17 T cells in the reactivity to self antigens in tumor vs autoimmunity, IFN-γ and IL17 secreting T cells to rat neu and mouse thyroglobulin (mTg) were measured in neu transgenic BALB/c (NeuT) and NeuTxDR3 mice, which expressed neu and HLA-DR3. HLA-DR3 is associated with susceptibility to some autoimmune diseases in humans and experimental autoimmune thyroiditis (EAT) in mice. BALB/c and BALBxDR3 served as controls. α-neu response was induced by vaccination with pneuTM encoding neu ECD and TM & pGM-CSF, or by TC-1/neu, heterologous tumor cells transfected with neu, and LPS. α-mTg response was induced by mTg & LPS, i.v. Regulatory T cells (Treg) were depleted by CD25 mAb 9 d before mTg. In BALBxDR3 & NeuTxDR3 mice, pneuTM & pGM-CSF vaccination induced 59 & 1 ug/ml Ab and 592 & 217 IFN-γ secreting cells. Vaccination with TC-1/neu & LPS induced 18 & 41 ug/ml neu Ab and 241 & 187 IFN-γ cells. Neu+ tumors can be regressed, yet no IL-17 was detected in any group. In BALBxDR3 mice depleted of Treg and immunized with mTg/LPS, 51400 U/ml mTg Ab, 119 IFN-γ secreting cells, and 64 IL-17 secreting cells were present, with 40–60% thyroid destruction. Hence, Th1 but not Th17 were activated by neu vaccination in normal or NeuT mice. Both Th1 and Th17 were activated in mTg-induced EAT. Since Neu vaccination & LPS did not induce IL-17 secretion, Th17 activation is unrelated to LPS. Elucidating the precise roles for Th1 and Th17 in tumor immunity and thyroiditis is critical when both are present in an individual. (CA 125680, CA76340, DK45960, St. John Hosp)

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Msaki, Aichi, Anna Pastò, Matteo Curtarello, Maddalena Arigoni, Giuseppina Barutello, Raffaele Adolfo Calogero, Marco Macagno, Federica Cavallo, Alberto Amadori e Stefano Indraccolo. "A hypoxic signature marks tumors formed by disseminated tumor cells in the BALB-neuT mammary cancer model". Oncotarget 7, n.º 22 (20 de abril de 2016): 33081–95. http://dx.doi.org/10.18632/oncotarget.8859.

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Cipriani, Barbara, Arthur Fridman, Claus Bendtsen, Shridar Dharmapuri, Carmela Mennuni, Irene Pak, Giuseppe Mesiti et al. "Therapeutic Vaccination Halts Disease Progression in BALB-neuT Mice: The Amplitude of Elicited Immune Response Is Predictive of Vaccine Efficacy". Human Gene Therapy 19, n.º 7 (julho de 2008): 670–80. http://dx.doi.org/10.1089/hum.2007.127.

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Lo Iacono, M., F. Cavallo, E. Quaglino, S. Rolla, M. Iezzi, S. M. Pupa, C. De Giovanni et al. "A Limited Autoimmunity to p185neu Elicited by DNA and Allogeneic Cell Vaccine Hampers the Progression of Preneoplastic Lesions in HER-2/NEU Transgenic Mice". International Journal of Immunopathology and Pharmacology 18, n.º 2 (abril de 2005): 351–63. http://dx.doi.org/10.1177/039463200501800217.

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Prevention of the progression of precancerous lesions by vaccines is a virtually uncharted territory. Their potential, however, is being assessed in transgenic mice which develop autochthonous tumors with defined stages of progression. In this paper we show that the DNA micro-array technology significantly helps assessment of the preventive efficacy of a combined DNA and cell vaccine. All female rat Her-2/neu transgenic BALB/c (BALB-neuT) mice develop an invasive carcinoma in each of their mammary glands within 25 weeks of age. This is elicited by the activated transforming rat Her-2/neu oncogene embedded in their genome. We have previously shown that vaccination of mice bearing multiple in situ carcinomas with DNA plasmids which code for the extracellular and transmembrane domain of rat p185neu, the product of the rat Her-2/neu oncogene, followed by a boost with rat p185neu+ allogeneic cells engineered to secrete interferon-γ, keeps 48% of mice tumor free until week 32. We have now extended our follow-up until mice reach one year of age and show that protection vanishes as time progresses. This observation suggests that the accuracy of the results studying immunotherapy against life-threatening tumors is a function of the length of the follow-up. The application of microarrays, and the concordance of morphologic and gene expression data led us to identify antibody as the main mechanism induced by vaccination. Protection is associated with a break of tolerance and a limited autoimmunity against the

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Frajese, Giovanni Vanni, Monica Benvenuto, Rosanna Mattera, Saverio Giampaoli, Elena Ambrosin, Roberta Bernardini, Maria Gabriella Giganti et al. "Electrochemically Reduced Water Delays Mammary Tumors Growth in Mice and Inhibits Breast Cancer Cells SurvivalIn Vitro". Evidence-Based Complementary and Alternative Medicine 2018 (26 de setembro de 2018): 1–14. http://dx.doi.org/10.1155/2018/4753507.

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Electrochemical reduced water (ERW) has been proposed to have beneficial effects on human health due to its rich content of H2and the presence of platinum nanoparticles with antioxidant effects. Many studies have demonstrated that ERW scavenging properties are able to reduce the damage caused by oxidative stress in different experimental models. Although fewin vivostudies have been reported, it has been demonstrated that ERW may display anticancer effects by induction of tumor cells apoptosis and reduction of both angiogenesis and inflammation. In this study, we show that ERW treatment of MCF-7, MDA-MB-453, and mouse (TUBO) breast cancer cells inhibited cell survival in a time-dependent fashion. ERW decreased ErbB2/neuexpression and impaired pERK1/ERK2 and AKT phosphorylation in breast cancer cells. In addition, ERW treatment induced apoptosis of breast cancer cell lines independently of the status of p53 and ER and PR receptors. Ourin vivoresults showed that ERW treatment of transgenic BALB-neuT mice delayed the development of mammary tumors compared to the control. In addition, ERW induced a significant prolongation of tumor-free survival and a reduction in tumor multiplicity. Overall, these results suggest a potential beneficial role of ERW in inhibiting cancer cells growth.

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Grabinski, Nicole, Katharina Möllmann, Karin Milde-Langosch, Volkmar Müller, Udo Schumacher, Burkhard Brandt, Klaus Pantel e Manfred Jücker. "AKT3 regulates ErbB2, ErbB3 and estrogen receptor α expression and contributes to endocrine therapy resistance of ErbB2+ breast tumor cells from Balb-neuT mice". Cellular Signalling 26, n.º 5 (maio de 2014): 1021–29. http://dx.doi.org/10.1016/j.cellsig.2014.01.018.

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Anemone, Annasofia, Lorena Consolino, Laura Conti, Pietro Irrera, Myriam Y. Hsu, Daisy Villano, Walter Dastrù, Paolo E. Porporato, Federica Cavallo e Dario Livio Longo. "Tumour acidosis evaluated in vivo by MRI-CEST pH imaging reveals breast cancer metastatic potential". British Journal of Cancer 124, n.º 1 (1 de dezembro de 2020): 207–16. http://dx.doi.org/10.1038/s41416-020-01173-0.

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Abstract Background Tumour acidosis is considered to play a central role in promoting cancer invasion and migration, but few studies have investigated in vivo how tumour pH correlates with cancer invasion. This study aims to determine in vivo whether tumour acidity is associated with cancer metastatic potential. Methods Breast cancer cell lines with different metastatic potentials have been characterised for several markers of aggressiveness and invasiveness. Murine tumour models have been developed and assessed for lung metastases and tumour acidosis has been assessed in vivo by a magnetic resonance imaging-based chemical exchange saturation transfer (CEST) pH imaging approach. Results The higher metastatic potential of 4T1 and TS/A primary tumours, in comparison to the less aggressive TUBO and BALB-neuT ones, was confirmed by the highest expression of cancer cell stem markers (CD44+CD24−), highlighting their propensity to migrate and invade, coinciding with the measurement obtained by in vitro assays. MRI-CEST pH imaging successfully discriminated the more aggressive 4T1 and TS/A tumours that displayed a more acidic pH. Moreover, the observed higher tumour acidity was significantly correlated with an increased number of lung metastases. Conclusions The findings of this study indicate that the extracellular acidification is associated with the metastatic potential.

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Hoelzinger, Dominique, Ana Dominguez e Joseph Lustgarten. "Critical function of CCL1 in the maintenance of T regulatory cell’s suppressive role. (66.14)". Journal of Immunology 186, n.º 1_Supplement (1 de abril de 2011): 66.14. http://dx.doi.org/10.4049/jimmunol.186.supp.66.14.

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Abstract T-regulatory cells (Tregs) create an immunosuppressive environment that reduces the efficacy of anti-tumor immunotherapy. Depletion of Tregs enhances anti-tumor immune responses, but also affects T-effector cells. Previously we showed that blockade of chemokine ligand 1 (CCL1) inhibits Treg conversion, their suppressive function, and in combination with intra-tumoral CpG-ODN results in complete rejection of tumors in BALB-NeuT tolerant mice. Most importantly, this therapeutic combination does not affect T-effector function and increases tumor-lytic CD8+NKG2D+ cells within the tumor. Here we expand on the role of blocking CCL1 in enhancing anti-tumor immunotherapy. Using CCL1 knockout (CCL1ko) mice, we found no impairment in TGFβ dependent de novo Treg conversion, however CCL1ko Tregs are less suppressive in vitro, than their wild type counterparts. CCL1ko mice treated with intratumoral CpG showed a marked reduction in tumor growth and a significant increase in tumor rejection as compared to similarly treated C57b control mice. Examination of lymphocyte populations within B16 and MucI tumors showed elevated levels of CD8+ cells. Finally the evaluation of levels of intra-tumoral cytokines and chemokines revealed elevated levels of IFNγ, CXCL9, CCL3 and CXCL10 in tumors grown in CCL1ko mice, suggesting a pro-inflammatory environment. Taken together these data support the role of CCL1as a critical factor for the maintenance of the suppressive function of Tregs.

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Riemer, A. B., K. H. Brämswig, H. Pehamberger, O. Scheiner, C. C. Zielinski e E. Jensen-Jarolim. "Trastuzumab mimotope vaccination of HER-2/neu transgenic mice results in prolonged tumor-free survival and reduced tumor load". Journal of Clinical Oncology 24, n.º 18_suppl (20 de junho de 2006): 12510. http://dx.doi.org/10.1200/jco.2006.24.18_suppl.12510.

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12510 Background: Passive immunotherapy with the humanized monoclonal antibody trastuzumab (Herceptin) to date is the most effective treatment for patients with HER-2/neu overexpressing breast cancer. In previous studies we could show that active immunization with peptide mimotopes, i.e. structural mimics of the epitope recognized by trastuzumab, leads to formation of antibodies again recognizing HER-2/neu in mice. Functional in vitro analyses of the induced antibodies demonstrated “trastuzumab-like” properties, such as receptor internalization, inhibition of signaling, and antibody-mediated cytotoxicity against HER-2/neu overexpressing breast cancer cells. The aim of the present study was to test the effects of trastuzumab mimotope vaccination in vivo, namely in a HER-2/neu transgenic mouse model. Methods: We used BALB-neuT mice, which carry the activated neu oncogene on the BALB/c background. These mice constitute the most aggressive animal model for HER-2/neu driven carcinogenesis, as all females uniformly develop mammary carcinomas at the age of 12 weeks. One group of mice was immunized with the previously described trastuzumab mimotope - KLH conjugate, a control group with the carrier protein KLH alone, and a further control group was left naïve. Mice were palpated weekly to monitor tumor development and size, and blood samples were taken at regular intervals to follow up the induced immune responses. Results: Trastuzumab mimotope immunizations lead to delayed tumor development and thus to an increase in tumor-free survival. When tumors occurred, they were smaller and grew more slowly than in the control mice. In contrast, control KLH immunizations did not affect tumor growth kinetics as compared to the naïve mice. Serum analysis demonstrated that all immunized animals had mounted an anti-KLH immune response, so we accredit the observed tumor-inhibitory effects in the mimotope group to the biologic properties of induced anti-HER-2/neu antibodies. Conclusion: These results indicate that epitope-specific vaccination with mimotopes elicits trastuzumab-like antibodies that are effective in vivo against HER-2/neu overexpressing tumor cells also in HER-2/neu expressing organisms. [Table: see text]

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Seifaddinipour, Maryam, Reyhaneh Farghadani, Farideh Namvar, Jamaludin Bin Mohamad e Nur Airina Muhamad. "In Vitro and In Vivo Anticancer Activity of the Most Cytotoxic Fraction of Pistachio Hull Extract in Breast Cancer". Molecules 25, n.º 8 (13 de abril de 2020): 1776. http://dx.doi.org/10.3390/molecules25081776.

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Pistacia (Pistacia vera) hulls (PV) is a health product that has been determined to contain bioactive phytochemicals which have fundamental importance for biomedical use. In this study, PV ethyl acetate extraction (PV-EA) fractions were evaluated with the use of an MTT assay to find the most cytotoxic fraction, which was found to be F13b1/PV-EA. After that, HPTLC was used for identify the most active compounds. The antioxidant activity was analyzed with DPPH and ABTS tests. Apoptosis induction in MCF-7 cells by F13b1/PV-EA was validated via flow cytometry analysis and a distinctive nuclear staining method. The representation of genes like Caspase 3, Caspase 8, Bax, Bcl-2, CAT and SOD was assessed via a reverse transcription (RT_PCR) method. Inhabitation of Tubo breast cancer cell development was examined in the BALB-neuT mouse with histopathology observations. The most abundant active components available in our extract were gallic acid and the flavonoid quercetin. The F13b1/PV-EA has antiradical activity evidence by its inhibition of ABTS and DPPH free radicals. F13b1/PV-EA displayed against MCF-7 a suppressive effect with an IC50 value of 15.2 ± 1.35 µg/mL. Also, the expression of CAT, SOD, Caspase 3, Caspase 8 and Bax increased and the expression of Bcl-2 decreased. F13b1/PV-EA dose-dependently inhibited tumor development in cancer-induced mice. Thus, this finding introduces F13b1/PV-EA as an effectual apoptosis and antitumor active agent against breast cancer.

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Sharma, Sanjay, Ana Lucia Dominguez, Soraya Zorro Manrique, Federica Cavallo, Shimon Sakaguchi e Joseph Lustgarten. "Systemic Targeting of CpG-ODN to the Tumor Microenvironment with Anti–neu-CpG Hybrid Molecule and T Regulatory Cell Depletion Induces Memory Responses in BALB-neuT Tolerant Mice". Cancer Research 68, n.º 18 (14 de setembro de 2008): 7530–40. http://dx.doi.org/10.1158/0008-5472.can-08-1635.

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Hoelzinger, Dominique, Ana Dominguez, Kevin Pollock, Joseph Lustgarten, Peter Cohen e Sandra Gendler. "IL-9 strategy to perturb Treg function and enhance anti-tumor immunity (P4273)". Journal of Immunology 190, n.º 1_Supplement (1 de maio de 2013): 140.9. http://dx.doi.org/10.4049/jimmunol.190.supp.140.9.

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Abstract IL-9 is a cytokine that is primarily associated with mast cells and airway inflammation, however it also plays a role in T regulatory cell (Treg) survival and recruitment to tumors. We previously reported that 4-1BB treatment of Tregs inhibits both Treg function and IL-9 secretion. Neutralization of IL-9 with an anti-IL-9 antibody inhibits the suppressive function of Tregs without affecting the function of CD4+ and CD8+ T effector cells. Furthermore, the combination of intra-tumoral CpG and anti-IL-9 induced tumor rejection in BALB-neuT and MUC1 tolerant transgenic mice. Here we show that the lack of IL-9 inhibits Treg suppression of T cell proliferation, using IL-9 knockout (IL-9ko) mice. Phenotypic analysis of Treg markers showed that tumor draining lymph nodes of 4T1 bearing mice contain fewer CTLA-4+ and CD103+ Tregs, and that these also have reduced of CTLA-4 and CD103 expression. We also observed that IL-9ko mice spontaneously reject TUBO and 4T1 mammary carcinoma cells and that rejection is abrogated by CD8+ T cell depletion. Finally, preliminary studies of human CD4+ T cell proliferation revealed that IL-9 neutralization led to greater proliferation than isotype control treated cells. Taken together our results suggest that IL-9 can have an immunosuppressive function that comes into play in the tumor microenvironment, and that the blockade of IL-9 could serve as a novel strategy to perturb the function of Tregs to enhance the antitumor effect of tumor vaccines.

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Cho, Helen Kim, Paul Cockle, Cindy Wei Li, Steve Burgess, Terrence Coleman, Terri Harder, Dan Xu et al. "Reduction of immune inhibitory myeloid derived suppressor cells by low dose sunitinib combined with a cancer vaccine to provide therapeutic benefit to tumor-bearing mice." Journal of Clinical Oncology 35, n.º 15_suppl (20 de maio de 2017): e23084-e23084. http://dx.doi.org/10.1200/jco.2017.35.15_suppl.e23084.

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e23084 Background: Sunitinib is a receptor tyrosine kinase inhibitor (RTK) approved as a monotherapy for the treatment of advanced RCC, gastrointestinal stromal tumors and advanced pancreatic neuroendocrine tumors. At the approved doses, it inhibits angiogenesis in tumors and targets RTKs (PDGF receptor, VEGF receptor, KIT, FLT-3, and RET) involved in tumor cell growth. Sunitinib also has been shown in murine studies and patients, to exhibit immunomodulatory properties that reduce a heterogeneous population of cells termed myeloid derived suppressor cells (MDSCs) and restore the immune stimulatory Th1 cytokine profile of T cells. The approved anti-angiogenic sunitinib dosing regimens in RCC have a safety profile that is overall manageable with the most commonly reported sunitinib-related grade 3 adverse events including hypertension, fatigue, diarrhea and hand-foot syndrome. Although the tolerability of sunitinib as monotherapy was acceptable in advanced stage diseases, the drug’s side effect profile could potentially pose challenges for use in combination with other oncology therapies. Thus, if the dose of sunitinib could be lowered to improve the side effect profile without impacting its immune modulatory properties, it could be combined with cancer vaccine regimens, offering a better tolerated and highly potent immunotherapy for patients with cancer of all stages. Methods: To evaluate the relationship of dose of sunitinib on its immunomodulatory properties, the pharmacokinetic profile, the frequency of MDSCs, cytokine profile, vaccine induced immune responses and anti-tumor efficacy were monitored in a subcutaneous tumor bearing BALB-neuT mice in the presence or absence of a cancer vaccine. Results: The data suggested that sunitinib doses below the approved daily dose of 50 mg may maintain the drug’s immune modulatory properties and improve overall survival when given concurrently with a cancer vaccine. Conclusions: The data suggested that low dose sunitinib can be administered as an immunomodulator to reduce MDSCs safely in combination with potent, multi-component cancer vaccine regimens.

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Benvenuto, Monica, Sara Ciuffa, Chiara Focaccetti, Diego Sbardella, Sara Fazi, Manuel Scimeca, Grazia Raffaella Tundo et al. "Proteasome inhibition by bortezomib parallels a reduction in head and neck cancer cells growth, and an increase in tumor-infiltrating immune cells". Scientific Reports 11, n.º 1 (24 de setembro de 2021). http://dx.doi.org/10.1038/s41598-021-98450-6.

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AbstractHead and neck cancer (HNC) has frequently an aggressive course for the development of resistance to standard chemotherapy. Thus, the use of innovative therapeutic drugs is being assessed. Bortezomib is a proteasome inhibitor with anticancer effects. In vitro antitumoral activity of Bortezomib was investigated employing human tongue (SCC-15, CAL-27), pharynx (FaDu), salivary gland (A-253) cancer cell lines and a murine cell line (SALTO-5) originated from a salivary gland adenocarcinoma arising in BALB-neuT male mice transgenic for the oncogene neu. Bortezomib inhibited cell proliferation, triggered apoptosis, modulated the expression and activation of pro-survival signaling transduction pathways proteins activated by ErbB receptors and inhibited proteasome activity in vitro. Intraperitoneal administration of Bortezomib delayed tumor growth of SALTO-5 cells transplanted in BALB-neuT mice, protracted mice survival and adjusted tumor microenvironment by increasing tumor-infiltrating immune cells (CD4+ and CD8+ T cells, B lymphocytes, macrophages, and Natural Killer cells) and by decreasing vessels density. In addition, Bortezomib modified the expression of proteasome structural subunits in transplanted SALTO-5 cells. Our findings further support the use of Bortezomib for the treatment of HNC and reveal its ineffectiveness in counteracting the activation of deregulated specific signaling pathways in HNC cell lines when resistance to proteasome inhibition is developed.

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