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  • American Association for Cancer Research (AACR)  (8)
  • 1
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    Online Resource
    Dormant SOX9-Positive Cells Facilitate MYC-Driven Recurrence of Medulloblastoma
    American Association for Cancer Research (AACR) ; 2022
    In:  Cancer Research Vol. 82, No. 24 ( 2022-12-16), p. 4586-4603
    Details
    In: Cancer Research, American Association for Cancer Research (AACR), Vol. 82, No. 24 ( 2022-12-16), p. 4586-4603
    Abstract: Relapse is the leading cause of death in patients with medulloblastoma, the most common malignant pediatric brain tumor. A better understanding of the mechanisms underlying recurrence could lead to more effective therapies for targeting tumor relapses. Here, we observed that SOX9, a transcription factor and stem cell/glial fate marker, is limited to rare, quiescent cells in high-risk medulloblastoma with MYC amplification. In paired primary-recurrent patient samples, SOX9-positive cells accumulated in medulloblastoma relapses. SOX9 expression anti-correlated with MYC expression in murine and human medulloblastoma cells. However, SOX9-positive cells were plastic and could give rise to a MYC high state. To follow relapse at the single-cell level, an inducible dual Tet model of medulloblastoma was developed, in which MYC expression was redirected in vivo from treatment-sensitive bulk cells to dormant SOX9-positive cells using doxycycline treatment. SOX9 was essential for relapse initiation and depended on suppression of MYC activity to promote therapy resistance, epithelial–mesenchymal transition, and immune escape. p53 and DNA repair pathways were downregulated in recurrent tumors, whereas MGMT was upregulated. Recurrent tumor cells were found to be sensitive to treatment with an MGMT inhibitor and doxorubicin. These findings suggest that recurrence-specific targeting coupled with DNA repair inhibition comprises a potential therapeutic strategy in patients affected by medulloblastoma relapse. Significance: SOX9 facilitates therapy escape and recurrence in medulloblastoma via temporal inhibition of MYC/MYCN genes, revealing a strategy to specifically target SOX9-positive cells to prevent tumor relapse.
    Type of Medium: Online Resource
    ISSN: 0008-5472 , 1538-7445
    URL: Article
    DOI: 10.1158/0008-5472.CAN-22-2108
    RVK:
    XA 36000
    RVK:
    XA 10000
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2022
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  • 2
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    Abstract 2311: Adenovirus-transduced allogeneic dendritic cells for cancer immunotherapy
    American Association for Cancer Research (AACR) ; 2016
    In:  Cancer Research Vol. 76, No. 14_Supplement ( 2016-07-15), p. 2311-2311
    Details
    In: Cancer Research, American Association for Cancer Research (AACR), Vol. 76, No. 14_Supplement ( 2016-07-15), p. 2311-2311
    Abstract: Immunotherapy is currently being established as standard treatment for cancer. Immune checkpoint blockade antibodies can cure a large proportion of patients with refractory melanoma and lung cancer, and adoptive transfer of patient-derived CD19 chimeric antigen receptor (CAR) T cells results in complete remission in a majority of patient with refractory leukemia. Cancer vaccines based on patient-derived dendritic cells (DC) modified ex vivo to present tumor antigens are promising for cancer treatment especially when combined with immune checkpoint blockade antibodies. Ex vivo-modified DCs are however poor in migrating to secondary lymphoid organs after re-administration. In reality, it is more likely endogenous DC that endocytos the injected DC, mature and then migrate to lymph nodes where they present peptide fragments of tumor antigen to T cells together with required co-stimulation. Herein, we present a new strategy utilizing adenovirus (Ad)-transduced allogeneic DCs (alloDCs) as immunostimulatory adjuvant to induce both innate and adaptive immune response. Ad/alloDC can be prepared, tested and made ready for release in advance and quickly be prepared for injection in cancer patients upon request, thereby minimizing GMP-processing and handling of cells. Besides encoding tumor antigens, adenovirus also provides stimulatory danger signals for DC activation. We show that Ad/alloDCs secret a panel of proinflammatory cytokines and chemokines including IL-12 and CXCL10 at high levels in a sustainable fashion. We also show that Ad/alloDC recruit and activate neutrophils and NKs to the site of injection. Ad/alloDC can also recruit and interact with allo-reactive T cells to create a proinflammatory milieu, which further recruit and activate endogenous DCs. We verified that endogenous DCs activated in situ by an Ad/alloDC injection migrate to draining lymph node, where they present the engulfed tumor antigen to T cells. We show that these migratory endogenous DCs facilitate T cell activation and proliferation. Moreover, when injected intratumorally, Ad/alloDCs modulate the immunosuppressive environment by reducing the ratio of monocytic to granulocytic myeloid-derived suppressor cells (MDSC). To evaluate the therapeutic efficacy, we use B16 melanoma tumor-bearing C57Bl/6 mice injected with adenovirus-transduced DCs from Balb/c origin to obtain an allogeneic reaction. We show that Ad/alloDC treatment could significantly delay tumor growth and prolong survival of tumor-bearing mice. Citation Format: Magnus Essand, Grammatiki Fotaki, Chuan Jin, Mohanraj Ramachandran, Jing Ma, Alex Karlsson-Parra, Di Yu. Adenovirus-transduced allogeneic dendritic cells for cancer immunotherapy. [abstract]. In: Proceedings of the 107th Annual Meeting of the American Association for Cancer Research; 2016 Apr 16-20; New Orleans, LA. Philadelphia (PA): AACR; Cancer Res 2016;76(14 Suppl):Abstract nr 2311.
    Type of Medium: Online Resource
    ISSN: 0008-5472 , 1538-7445
    URL: Article
    DOI: 10.1158/1538-7445.AM2016-2311
    RVK:
    XA 36000
    RVK:
    XA 10000
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2016
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    detail.hit.zdb_id: 1432-1
    detail.hit.zdb_id: 410466-3
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  • 3
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    Abstract A171: Long-term episomal gene transfer for safe engineering of T cells for adoptive cell therapy of cancer
    American Association for Cancer Research (AACR) ; 2016
    In:  Cancer Immunology Research Vol. 4, No. 1_Supplement ( 2016-01-01), p. A171-A171
    Details
    In: Cancer Immunology Research, American Association for Cancer Research (AACR), Vol. 4, No. 1_Supplement ( 2016-01-01), p. A171-A171
    Abstract: Success in T-cell therapy of cancer is currently relying on long-term gene expression owing to retrovirus/lentivirus (RV/LV) integration. However, uncontrolled RV/LV integration in host cell genomes has the potential risk of causing insertional mutagenesis. Herein, we describe a novel episomal and long-term cell engineering method using non-integrating lentiviral (NILV) vector containing a scaffold matrix attachment region (S/MAR) element for either over-expression or down-regulation of genes. T-cells engineered with a NILV-S/MAR(CD19CAR) vector have similar levels of CAR expression as T-cells engineered with an integrating LV vector, even after numerous rounds of cell division. NILV-S/MAR-engineered CD19CAR-T-cells exhibited similar cytotoxic capacity upon CD19+ target cells recognition as LV-engineered T-cells. We propose that NILV-S/MAR vectors are superior to current options for enabling long-term gene expression without the risk of insertional mutagenesis. Citation Format: Chuan Jin, Mohanraj Ramachandran, Grammatiki Fotaki, Berith Nilsson, Magnus Essand, Di Yu. Long-term episomal gene transfer for safe engineering of T cells for adoptive cell therapy of cancer. [abstract]. In: Proceedings of the CRI-CIMT-EATI-AACR Inaugural International Cancer Immunotherapy Conference: Translating Science into Survival; September 16-19, 2015; New York, NY. Philadelphia (PA): AACR; Cancer Immunol Res 2016;4(1 Suppl):Abstract nr A171.
    Type of Medium: Online Resource
    ISSN: 2326-6066 , 2326-6074
    URL: Article
    DOI: 10.1158/2326-6074.CRICIMTEATIAACR15-A171
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2016
    detail.hit.zdb_id: 2732517-9
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  • 4
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    Online Resource
    Abstract A128: Tumor endothelial cells say IDO to CD40-stimulating immunotherapy
    American Association for Cancer Research (AACR) ; 2019
    In:  Cancer Immunology Research Vol. 7, No. 2_Supplement ( 2019-02-01), p. A128-A128
    Details
    In: Cancer Immunology Research, American Association for Cancer Research (AACR), Vol. 7, No. 2_Supplement ( 2019-02-01), p. A128-A128
    Abstract: CD40, a tumor necrosis factor receptor superfamily member, is a promising immune-boosting target in cancer immunotherapy due to its role in promoting antitumor responses of immune cells. CD40 is also expressed on endothelial cells but the response of the tumor-associated vasculature to CD40-stimulating immunotherapy has not been studied. Herein, we have performed RNA-sequencing analysis of murine tumor endothelial cells (TECs) isolated from B16.F10 melanoma and MB49 bladder cancer treated with agonistic CD40 monoclonal antibody (mAb) or isotype control. Gene set and gene ontology enrichment analyses of the differentially expressed genes revealed that CD40 mAb treatment induces interferon-γ (IFNγ) signaling in the tumor microenvironment associated with up-regulation of immunosuppressive genes in TECs, including the enzyme indoleamine 2, 3-dioxygenase 1 (IDO1). Importantly, IDO1 was preferentially expressed in endothelial cells in the tumor and was positively correlated to infiltration of T-cells in the tumor microenvironment. In vitro, endothelial cells up-regulated IDO1 in response to T-cell-derived IFNγ, but not in response to CD40-stimulation. Collectively, our data suggest that IDO1 up-regulation in TECs occurs as a response to T-cell activation. Combining CD40 mAb therapy with the IDO1 inhibitor epacadostat delayed tumor growth and increased survival of B16.F10 tumor-bearing mice, which was associated with increased activation of cytotoxic T-cells. Hereby, we have uncovered a novel immunosuppressive feedback mechanism, in which the tumor vasculature limits the response to cancer immunotherapy by up-regulating IDO1. Citation Format: Anna Dimberg, Alexandros Karampatzakis, Sander Tuit, Mohanraj Ramachandran, Grammatiki Fotaki, Luuk van Hooren, Hua Huang, Roberta Lugano, Kaunisto Aura, Peter Ellmark, Sara M Mangsbo, Joachim L. Schultze, Magnus Essand, Maria Georganaki. Tumor endothelial cells say IDO to CD40-stimulating immunotherapy [abstract]. In: Proceedings of the Fourth CRI-CIMT-EATI-AACR International Cancer Immunotherapy Conference: Translating Science into Survival; Sept 30-Oct 3, 2018; New York, NY. Philadelphia (PA): AACR; Cancer Immunol Res 2019;7(2 Suppl):Abstract nr A128.
    Type of Medium: Online Resource
    ISSN: 2326-6066 , 2326-6074
    URL: Article
    DOI: 10.1158/2326-6074.CRICIMTEATIAACR18-A128
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2019
    detail.hit.zdb_id: 2732517-9
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  • 5
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    Abstract A172: Allogeneic dendritic cells (AlloDCs) transduced with an infection-enhanced adenovirus as adjuvant for cancer immunotherapy
    American Association for Cancer Research (AACR) ; 2016
    In:  Cancer Immunology Research Vol. 4, No. 1_Supplement ( 2016-01-01), p. A172-A172
    Details
    In: Cancer Immunology Research, American Association for Cancer Research (AACR), Vol. 4, No. 1_Supplement ( 2016-01-01), p. A172-A172
    Abstract: AlloDC cancer immunotherapy utilizes the allogeneic reaction as an immunostimulatory adjuvant. Intratumoral alloDC vaccination reverses the immune suppressed tumor micro-environment and activates anti-tumor immune responses. Herein, we aim to examine the use of Ad5f35PTD, an infection-enhanced serotype 5 adenovirus containing fibers from serotype 35 and cell-penetrating peptides on the hexons, as a vector to deliver tumor-associated antigens to monocyte-derived immature DCs in combination with an established DC maturation cocktail. Ad5f35PTD-transduced, cocktail-matured DCs expressed co-stimulatory and activation molecules and secreted the Th-1 type cytokine IL-12, in vitro. Natural killer (NK) cells migrated better towards medium from Ad5f35PTD-transduced, cocktail-matured DCs than medium from only cocktail-matured DCs, which was in accordance with a higher CXCL-10 chemokine level. The alloDC effect was examined in vivo using mature murine DCs of BALB/c origin (D2SC/I), transduced with Ad5f35PTD encoding the melanoma-associated antigen gp100, injected subcutaneously into C57BL/6 mice. They induced a higher migration of host DCs in the draining lymph node, in comparison to the D2SC/I cells alone. The migrated host DCs efficiently presented the captured gp100 and activated gp100-specific CD8+ T-cells. Moreover, alloDCs transduced with the gp100-encoding Ad5f35PTD reduced the immunosuppressive environment when injected intratumoraly by reducing the ratio of monocytic to granulocytic myeloid-derived suppressor cell compartment and delay tumor growth in a B16 melanoma model, in comparison with the D2SC/I cells alone. Concluding, the Ad5f35PTD transduced alloDCs expressing gp100 showed potency in eliciting tumor-specific immune responses in comparison to the alloDCs alone. Citation Format: Grammatiki Fotaki, Chuan Jin, Alex Karlsson-Parra, Di Yu, Magnus Essand. Allogeneic dendritic cells (AlloDCs) transduced with an infection-enhanced adenovirus as adjuvant for cancer immunotherapy. [abstract]. In: Proceedings of the CRI-CIMT-EATI-AACR Inaugural International Cancer Immunotherapy Conference: Translating Science into Survival; September 16-19, 2015; New York, NY. Philadelphia (PA): AACR; Cancer Immunol Res 2016;4(1 Suppl):Abstract nr A172.
    Type of Medium: Online Resource
    ISSN: 2326-6066 , 2326-6074
    URL: Article
    DOI: 10.1158/2326-6074.CRICIMTEATIAACR15-A172
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2016
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  • 6
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    Abstract B110: Proinflammatory allogeneic dendritic cells promote activation of bystander immune cells and indirectly license antigen-specific T-cells
    American Association for Cancer Research (AACR) ; 2019
    In:  Cancer Immunology Research Vol. 7, No. 2_Supplement ( 2019-02-01), p. B110-B110
    Details
    In: Cancer Immunology Research, American Association for Cancer Research (AACR), Vol. 7, No. 2_Supplement ( 2019-02-01), p. B110-B110
    Abstract: Autologous patient-derived dendritic cells (DCs) modified ex vivo to present tumor-associated antigens have frequently been utilized as cancer vaccines. However, apart from the stringent logistics in producing DCs on a patient basis, accumulating evidences indicate that such DCs are poor in migration and in fact do not directly interact with naïve T-cells in vivo. Instead, it is the bystander host-DCs taking up material from apoptotic vaccine DCs and subsequently initiate antitumor T-cell responses. We examine the possibility of harnessing allogeneic pro-inflammatory DCs (alloDCs) as immune enhancers which may affect the activation of bystander immune cells and promote antigen-specific T-cell responses. We have verified the inflammatory state of DCs matured with a maturation cocktail in combination with an infection-enhanced adenovirus. Such proinflammatory alloDCs expressed co-stimulatory and activation molecules and secreted Th-1 type cytokines in vitro. T and NK cells up-regulated activation markers after co-culture with such alloDCs and created an immunostimulatory environment which was found to promote maturation of antigen-loaded DCs and the subsequent activation of antigen-specific T-cells by cross-presentation. Our findings were evaluated as a therapeutic strategy in murine models with success. We are proposing that vaccination with proinflammatory alloDCs in combination with the use of Ad5M as possible antigen delivery vehicle can be a cost-effective strategy to induce antitumor immune responses. Citation Format: Grammatiki Fotaki, Chuan Jin, Iliana Kyriaki Kerzeli, Mohanraj Ramachandran, Alex Karlsson-Parra, Di Yu, Magnus Essand. Proinflammatory allogeneic dendritic cells promote activation of bystander immune cells and indirectly license antigen-specific T-cells [abstract]. In: Proceedings of the Fourth CRI-CIMT-EATI-AACR International Cancer Immunotherapy Conference: Translating Science into Survival; Sept 30-Oct 3, 2018; New York, NY. Philadelphia (PA): AACR; Cancer Immunol Res 2019;7(2 Suppl):Abstract nr B110.
    Type of Medium: Online Resource
    ISSN: 2326-6066 , 2326-6074
    URL: Article
    DOI: 10.1158/2326-6074.CRICIMTEATIAACR18-B110
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2019
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  • 7
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    Abstract B175: Semliki Forest virus-mediated oncolytic immunotherapy in mouse GL261 glioblastoma model
    American Association for Cancer Research (AACR) ; 2019
    In:  Cancer Immunology Research Vol. 7, No. 2_Supplement ( 2019-02-01), p. B175-B175
    Details
    In: Cancer Immunology Research, American Association for Cancer Research (AACR), Vol. 7, No. 2_Supplement ( 2019-02-01), p. B175-B175
    Abstract: Glioblastoma (GBM) is a devastating cancer of the central nervous system with no cure currently available. Oncolytic virotherapy with viruses that infect and destroy cancer cells provides a novel promising candidate therapy. We have previously shown that Semliki Forest virus (SFV) has therapeutic potency against orthotopic xenograft and syngeneic glioma models in mice. Here we show that SFV-infected cancer cells undergo immunogenic apoptosis, which triggers phagocytosis and maturation in co-cultured dendritic cells. SFV-killed GL261 mouse GBM cell lysate was also able to induce protective antitumor immune response in syngeneic mouse model, indicating that SFV oncolysis is immunogenic in vivo. By introducing mutations into the viral genome we have been able to produce a novel SFV clone which shows notably enhanced oncolytic potency in GL261 cells. As compared to the wild-type virus, the mutated SFV replicates faster and induces significantly stronger cytopathic effect. Robust viral replication and cytopathic effect were detected despite of activated type-I interferon signaling in the infected cells. This suggests that the enhanced SFV has increased resistance to antiviral response in mouse GBM cells. Viral proteins were detected by immunohistochemistry in orthotopic GL261 tumors after intratumoral injection of the mutated SFV virus. This provides evidence that the enhanced SFV is able to replicate in GL261 tumors in the face of antiviral in vivo microenvironment. Unwanted SFV replication in healthy brain cells can be inhibited by microRNA-mediated de-targeting. Taken together, the results indicate that oncolytic virotherapy with SFV can trigger antitumor immune responses, and support that SFV is a potent new candidate for oncolytic immunotherapy of GBM. These findings pave way for future clinical trials with oncolytic SFV. Citation Format: Miika Martikainen, Di Yu, Mohanraj Ramachandran, Grammatiki Fotaki, Minttu-Maria Martikainen, Andres Merits, Magnus Essand. Semliki Forest virus-mediated oncolytic immunotherapy in mouse GL261 glioblastoma model [abstract]. In: Proceedings of the Fourth CRI-CIMT-EATI-AACR International Cancer Immunotherapy Conference: Translating Science into Survival; Sept 30-Oct 3, 2018; New York, NY. Philadelphia (PA): AACR; Cancer Immunol Res 2019;7(2 Suppl):Abstract nr B175.
    Type of Medium: Online Resource
    ISSN: 2326-6066 , 2326-6074
    URL: Article
    DOI: 10.1158/2326-6074.CRICIMTEATIAACR18-B175
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2019
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  • 8
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    Abstract 996: Metastasis and tumor recurrence from rare SOX9-positive cells in Group 4 medulloblastoma
    American Association for Cancer Research (AACR) ; 2014
    In:  Cancer Research Vol. 74, No. 19_Supplement ( 2014-10-01), p. 996-996
    Details
    In: Cancer Research, American Association for Cancer Research (AACR), Vol. 74, No. 19_Supplement ( 2014-10-01), p. 996-996
    Abstract: Tumor recurrence is the main cause of death in children with medulloblastoma (MB). MYCN is a marker for poor prognosis which is amplified in SHH and Group 4 but rarely in WNT and Group 3 subgroups of MB. The exact mechanisms for MB relapse are not known but recent findings (Ramaswamy et al. Lancet Oncol., 2013) suggest temporal differences within the four MB subgroups. For instance, SHH tumors recur locally while SHH-independent Group 4 tumors develop distant metastases. In order to study these processes further, we used a previously described transgenic mouse model of MYCN-driven SHH-independent MB (GTML mouse) to recreate the metastatic recurrence of such brain tumors in vivo. We previously showed that the expression of SOX9 transcription factor correlates well with SHH tumors and that only a few scattered SOX9-positive cells are found in SHH-independent GTML tumors similarly to Group 4 human MB. By using a combination of Tet-ON and Tet-OFF inducible systems we managed to target this rare population of SOX9-positive GTML tumor cells in vivo. These cells were able to form a distant recurrence after the tumor bulk in the mice was removed by using dox-inducible oncogene depletion. These relapses showed similar morphology and immunoreactivity of defined MB markers but presented generally higher levels of SOX9 compared to the primary GTML tumors. Additionally, we overexpressed SOX9 in cerebellar stem cells transfected with a mutationally stabilized MYCNT58A and injected them back into the cerebellum of adult mice. Surprisingly, the MB-like tumors that formed migrated and developed in the forebrain in contrast to the cerebellar tumors induced by the same cells transfected with MYCNT58A only. These findings suggest that increased levels of SOX9 drives migration of MYCN-driven MB cells. A similar correlation was found in Group 4 MB patients where isolated metastases had consistently higher SOX9 levels as compared to the corresponding primary tumor. Significance: We have developed a new mouse model for MB recurrence. We show how a rare population of SOX9-positive cells in SHH-independent MB is capable of initiating recurrence after primary tumor removal. The relapsed MB has similar characteristics to the initial tumor but develops at a distant site in the brain, in line with recent data from human tumors. Further characterization of cells with such properties will help to improve our understanding of the mechanisms behind metastatic MB recurrence and to develop treatments against those migrating cell populations. Citation Format: Vasil Savov, Grammatiki Fotaki, Marc Remke, Adrian M. Dubuc, Vijay Ramaswamy, Matko Cancer, Holger Weishaupt, Michael D. Taylor, Fredrik J. Swartling. Metastasis and tumor recurrence from rare SOX9-positive cells in Group 4 medulloblastoma. [abstract]. In: Proceedings of the 105th Annual Meeting of the American Association for Cancer Research; 2014 Apr 5-9; San Diego, CA. Philadelphia (PA): AACR; Cancer Res 2014;74(19 Suppl):Abstract nr 996. doi:10.1158/1538-7445.AM2014-996
    Type of Medium: Online Resource
    ISSN: 0008-5472 , 1538-7445
    URL: Article
    DOI: 10.1158/1538-7445.AM2014-996
    RVK:
    XA 36000
    RVK:
    XA 10000
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2014
    detail.hit.zdb_id: 2036785-5
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    detail.hit.zdb_id: 410466-3
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