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  • 1
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    The Autophagy Gene ULK1 Plays a Role In AML Differentiation and Is Negatively Regulated by the Oncogenic MicroRNA 106a
    American Society of Hematology ; 2010
    In:  Blood Vol. 116, No. 21 ( 2010-11-19), p. 503-503
    Details
    In: Blood, American Society of Hematology, Vol. 116, No. 21 ( 2010-11-19), p. 503-503
    Abstract: Abstract 503 Autophagy is a degradative mechanism mainly involved in the recycling and turnover of cytoplasmic constituents allowing for example survival upon a variety of stress stimuli. Although often referred to as type II programmed cell death, autophagy is primarily a pro-survival mechanism rather than an important cell death effector. During autophagy, part of the cytoplasm or entire organelles are sequestered into double-membraned vesicles, called autophagosomes, that ultimately fuse with lysosomes and degrade their contents. Regarding hematopoiesis there is accumulating evidence that autophagic mechanisms are operative in the development of different hematopoietic lineages. To identify ATG genes with a function in neutrophil differentiation, we employed an shRNA library targeting autophagy regulators in acute myeloid leukemia (AML) cells as a model for neutrophil differentiation. Among others, we found that inhibiting the key autophagy kinase ULK1 (also known as ATG1) using RNAi significantly attenuated all-trans retinoic acid (ATRA)-induced neutrophil differentiation of NB4 and HL60 AML cells. In agreement, we observed significantly elevated ULK1 mRNA and protein levels during neutrophil differentiation of these cells. Moreover, ULK1 expression was significantly reduced in primary AML patient samples as compared to mature myeloid cells from healthy donors. Given the aberrant microRNAs (miRNAs) expression in myeloid malignancies, we wondered if altered miRNA expression in AML might contribute to the low ULK1 levels seen. MiRNAs are 19–25 nucleotide, non-protein coding RNAs that regulate gene expression by directly binding to partially complementary sequences in the 3′-untranslated regions (3′-UTR) of their target mRNAs. Several target prediction software's identified a putative miR-106a binding site in the ULK1 3′-UTR. Interestingly, miR-106a is part of a highly oncogenic miRNA family. We then confirmed direct inhibition of ULK1 by miR-106a using wild-type and miR-106a mutated 3′-UTR ULK1 reporters. Moreover, a decrease of miR-106a expression was seen during ATRA-induced differentiation of AML cells paralleled by increased ULK1 mRNA levels. Lastly, stable overexpression of miR-106a in NB4 cells resulted in decreased ULK1 levels and markedly impaired neutrophil differentiation upon ATRA treatment. In summary, we show for the first time a significant involvement of the autophagy gene ULK1 in neutrophil differentiation and an association of low ULK1 levels with primary AML. Our studies indicate that ULK1 is a putative tumor suppressor in AML that is targeted by the oncogenic miR-106a. Disclosures: No relevant conflicts of interest to declare.
    Type of Medium: Online Resource
    ISSN: 0006-4971 , 1528-0020
    URL: Article
    DOI: 10.1182/blood.V116.21.503.503
    RVK:
    XA 33000
    RVK:
    XA 10000
    Language: English
    Publisher: American Society of Hematology
    Publication Date: 2010
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  • 2
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    Mir-29c and Mir-424 Are Novel Myeloid Differentiation-Associated MicroRNAs in Acute Promyelocytic Leukemia.
    American Society of Hematology ; 2008
    In:  Blood Vol. 112, No. 11 ( 2008-11-16), p. 3346-3346
    Details
    In: Blood, American Society of Hematology, Vol. 112, No. 11 ( 2008-11-16), p. 3346-3346
    Abstract: MicroRNAs (miRNAs) are a class of small non-coding RNAs that regulate gene expression at the post-transcriptional level. Recent studies showed that they are critically involved in hematopoietic differentiation and function by a coordinating multi-target repression of hematopoiesis-related genes. To identify miRNAs involved in the pathogenesis of acute promyelocytic leukemia (APL), characterized by the t(15;17) translocation, we performed TaqMan Low Density Array-based miRNA expression profiling on blast cells from an APL patient under all-trans retinoic acid (ATRA) treatment. Although recent reports investigated miRNA expression patterns in APL blast cells and cell lines subjected to ATRA in vitro, to our knowledge this is the first study that relies on cells from an APL patient treated with ATRA in vivo. Since the downregulation of the PML-RARA transcript cannot be assessed within a time period of a few days, we monitored effective ATRA treatment by measuring mRNA downregulation of the panleukemic marker Wilms’ tumor (WT)-1. WT1 mRNA levels decreased 64% and 92% at day 3 and 6 upon ATRAtherapy, respectively. Total RNA obtained at diagnosis and at days 3/6 following ATRA therapy were screened for expression patterns of 384 human miRNAs including two endogenous controls, RNU44 and RNU48, for normalization of miRNA expression. Since these controls were regulated upon ATRA treatment, we normalized miRNA expression to miR-93, which showed stable expression in our samples. Consistent with previous in vitro APL miRNA profiling data, the granulocyte-specific miR-223 was induced 6.6-fold at day 6 upon ATRA treatment. For further analysis, we focused on two hematopoietic lineage-specific miRNAs, miR-29c and miR-424 that have not yet been associated with neutrophil development. miR-29c and miR-424 were upregulated 6.5- and 6.0-fold at day 6 in response to ATRA, respectively. Induction of these miRNAs was confirmed by individual real-time RT-PCR assays. Moreover, expression of miR-29c and miR-424 was further investigated in NB4 and HT93 APL cell lines. In both cell lines, miR-424 was upregulated in response to ATRA similar to the patient samples, suggesting a role for miR-424 in granulocytic differentiation in addition to that described in macrophage development. miR-29c, however, showed an upregulation in HT93 but not in NB4 cells implying cell type specific regulation. Additionally, we tested the involvement of miR- 29c in macrophage differentiation of HL60 leukemic cells using phorbol 12-myristate 13-acetate (PMA) as a differentiating agent. Interestingly, miR-29c showed an 8.0- fold upregulation similar to an 8.7-fold induction of miR-424, a known target of the transcription factor PU.1 upon PMA treatment. Based on the similar regulation of miR-29c and miR-424 and the presence of several putative PU.1 binding elements in the miR-29c promoter, we are currently investigating whether miR-29c is a novel transcriptional target of PU.1. A confirmed target of miR-29c is the protein DNA methyltransferase (DNMT 3A and 3B), which is overexpressed in myeloid leukemias. Therefore, induction of miR-29c during myelopoiesis might be needed to target DNMT. In conclusion, we propose a novel association of miR-29c and miR-424 with ATRA-induced neutrophil differentiation.
    Type of Medium: Online Resource
    ISSN: 0006-4971 , 1528-0020
    URL: Article
    DOI: 10.1182/blood.V112.11.3346.3346
    RVK:
    XA 33000
    RVK:
    XA 10000
    Language: English
    Publisher: American Society of Hematology
    Publication Date: 2008
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  • 3
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    Abstract B30: Src tyrosine kinase inhibitors activate protective, ULK1-dependent autophagy by downregulating oncomir-106-393-cluster expression in non-small cell lung cancer cells
    American Association for Cancer Research (AACR) ; 2012
    In:  Clinical Cancer Research Vol. 18, No. 3_Supplement ( 2012-02-01), p. B30-B30
    Details
    In: Clinical Cancer Research, American Association for Cancer Research (AACR), Vol. 18, No. 3_Supplement ( 2012-02-01), p. B30-B30
    Abstract: Autophagy has been proposed to play a role as cytoprotective mechanism for tumor cell survival under unfavorable conditions and upon anticancer treatment. In lung cancer autophagy is mostly studied as possible resistance mechanism to therapy. There is increasing evidence that protective autophagy occurs upon various types of anti-cancer treatments, including chemo- and radiation therapy. Src tyrosine kinase inhibitors (TKIs) have been shown to inhibit cell migration and invasion in non-small cell lung cancer (NSCLC) cell lines. In clinical trials, however, they show modest activity in combination with chemotherapeutic agents. In the current study we show a marked induction of autophagic activity upon incubation of NSCLC cell lines with Src TKIs as measured by an increased LC3-I to -II conversion, a significant increase in GFP-LC3 dot formation, and a decrease in p62/SQSTM1 protein expression. Increased autophagic activity was found in three NSCLC cell lines (A549, H460, H1299) with two different Src TKIs (saracatinib, dasatinib). Interestingly, the addition of pharmacological autophagy inhibitors such as chloroquine or bafilomycin resulted in cell death in combination with Src TKI treatment. Moreover, we found that Src TKI-induced autophagy is associated with ULK1 expression in all three cell lines investigated. This effect was Src-specific since knocking down endogenous Src using RNAi resulted in a similar induction of ULK1. Using shRNA targeting ULK1 we showed that Src inhibitor induced autophagy is ULK1-dependent. Furthermore, ULK1 is a novel target of microRNA (miR)-106a as shown by ULK1 3′-UTR luciferase experiments and ectopic expression of miR-106a and antimiR-106a in NSCLC cell lines resulting in decreased and increased ULK1 expression upon Src inhibition, respectively. Lastly, in human lung adenocarcinoma compared to matched normal lung tissue (n = 23) miR-106a levels were significantly increased (p & lt;0.0001) whereas ULK1 mRNA expression levels were significantly lower (p & lt;0.0002) in tumor tissue. In conclusion, Src inhibitor-induced protective autophagy might explain their low success in clinical trials. Autophagy induced by Src TKIs depends on ULK1 and combining Src with autophagy inhibitors results in massive cell death as compared to single treatments. Furthermore, downregulation of the ULK1 targeting miR-106a upon Src inhibition allows for the induction of protective autophagy. Combining Src and autophagy inhibitors or Src inhibitors and miR-106a expression may represent attractive treatment options for NSCLC.
    Type of Medium: Online Resource
    ISSN: 1078-0432 , 1557-3265
    URL: Article
    DOI: 10.1158/1078-0432.12AACRIASLC-B30
    RVK:
    XA 36791
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2012
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  • 4
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    Abstract 2263: Autophagy protects against Src tyrosine kinase inhibitor treatment in non-small cell lung cancer cells via a novel miR-106a/ULK1 pathway
    American Association for Cancer Research (AACR) ; 2012
    In:  Cancer Research Vol. 72, No. 8_Supplement ( 2012-04-15), p. 2263-2263
    Details
    In: Cancer Research, American Association for Cancer Research (AACR), Vol. 72, No. 8_Supplement ( 2012-04-15), p. 2263-2263
    Abstract: Autophagy is a bulk degradation mechanism mainly involved in cell survival responses to a variety of stress stimuli. Its role in tumorigenesis is still ambiguous. Low levels of basal autophagy are crucial in order to sustain cellular homeostasis thereby also contributing to tumor prevention, whereas autophagy induction upon a variety of anti-cancer treatments is often involved in resistance mechanism to therapy. Src tyrosine kinase inhibitors (TKIs) inhibit cell migration and invasion in non-small cell lung cancer (NSCLC) cells. In clinical trials, however, they show modest activity in combination with chemotherapeutic agents. We hypothesized that cytoprotective autophagy plays a role in resistance mechanisms against Src TKIs. We found a marked induction of autophagic activity in NSCLC cell lines (A549, H460, H1299) treated with two different Src TKIs (saracatinib, dasatinib) as measured by increased LC3-I to -II conversion, increased GFP-LC3 dot formation, and decreased p62/SQSTM1 protein expression. Most importantly, the addition of pharmacological autophagy inhibitors (chloroquine, bafilomycin) in combination with Src TKI inhibitors resulted in cell death as compared to only decreased migration by Src TKI treatment alone. Next, we identified ULK1 as a key player in Src TKI-induced autophagy using a set of lentiviral vectors expressing shRNAs targeting ATG genes. Src TKIs significantly induced ULK1 mRNA and protein expression and knocking down ULK1 significantly attenuated Src TKI-induced autophagy. Furthermore, to exclude Src inhibition-independent effects of saracatinib and dasatinib on ULK1 expression, we targeted Src by RNAi and found similar induction of ULK1 as seen with the Src TKI treatment. We further investigated if micro(mi)RNAs are involved in ULK1 regulation during Src inhibitor treatment. Using miRNA target identification software and 3′-UTR luciferase reporter assays we identified miR-106a as ULK1-targeting miRNA. Incubating NSCLC cells with Src inhibitors resulted in a dose-dependent decrease of miR-106a paralleled by an increase in ULK1 expression. Moreover, ectopic expression of miR-106a and anti-miR-106a in NSCLC cell lines caused decreased and increased ULK1 expression upon Src inhibition, respectively. Importantly, similar to the pharmacological autophagy inhibition and or knocking down ULK1, expression of miR-106a enhanced the cytotoxicity of Src TKIs. Lastly, we found significantly higher miR-106a levels in human lung adenocarcinoma compared to matched normal lung tissue (n=23), whereas ULK1 mRNA expression levels were significantly lower (p & lt;0.0002) in tumor tissue than in normal lung tissue. In conclusion, Src inhibitors induce protective autophagy in NSCLC cells that is mediated via miR-106 and its target ULK1. Combining Src and autophagy inhibitors may represent attractive treatment option for certain NSCLC. 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 2263. doi:1538-7445.AM2012-2263
    Type of Medium: Online Resource
    ISSN: 0008-5472 , 1538-7445
    URL: Article
    DOI: 10.1158/1538-7445.AM2012-2263
    RVK:
    XA 36000
    RVK:
    XA 10000
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2012
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  • 5
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    Low Autophagy (ATG) Gene Expression Is Associated with an Immature AML Blast Cell Phenotype and Can Be Restored during AML Differentiation Therapy
    Hindawi Limited ; 2018
    In:  Oxidative Medicine and Cellular Longevity Vol. 2018 ( 2018), p. 1-16
    Details
    In: Oxidative Medicine and Cellular Longevity, Hindawi Limited, Vol. 2018 ( 2018), p. 1-16
    Abstract: Autophagy is an intracellular degradation system that ensures a dynamic recycling of a variety of building blocks required for self-renewal, homeostasis, and cell survival under stress. We used primary acute myeloid leukemia (AML) samples and human AML cell lines to investigate the regulatory mechanisms of autophagy and its role in AML differentiation. We found a significantly lower expression of key autophagy- (ATG-) related genes in primary AML as compared to healthy granulocytes, an increased autophagic activity during all- trans retinoic acid- (ATRA-) induced neutrophil differentiation, and an impaired AML differentiation upon inhibition of ATG3, ATG4D, and ATG5. Supporting the notion of noncanonical autophagy, we found that ATRA-induced autophagy was Beclin1-independent compared to starvation- or arsenic trioxide- (ATO-) induced autophagy. Furthermore, we identified PU.1 as positive transcriptional regulator of ATG3, ATG4D, and ATG5. Low PU.1 expression in AML may account for low ATG gene expression in this disease. Low expression of the autophagy initiator ULK1 in AML can partially be attributed to high expression of the ULK1-targeting microRNA-106a. Our data clearly suggest that granulocytic AML differentiation relies on noncanonical autophagy pathways and that restoring autophagic activity might be beneficial in differentiation therapies.
    Type of Medium: Online Resource
    ISSN: 1942-0900 , 1942-0994
    URL: Article
    DOI: 10.1155/2018/1482795
    Language: English
    Publisher: Hindawi Limited
    Publication Date: 2018
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  • 6
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    MicroRNA-106a targets autophagy and enhances sensitivity of lung cancer cells to Src inhibitors
    Elsevier BV ; 2017
    In:  Lung Cancer Vol. 107 ( 2017-05), p. 73-83
    Details
    In: Lung Cancer, Elsevier BV, Vol. 107 ( 2017-05), p. 73-83
    Type of Medium: Online Resource
    ISSN: 0169-5002
    URL: Article
    DOI: 10.1016/j.lungcan.2016.06.004
    Language: English
    Publisher: Elsevier BV
    Publication Date: 2017
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  • 7
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    Inhibition of the miR-143/145 cluster attenuated neutrophil differentiation of APL cells
    Elsevier BV ; 2012
    In:  Leukemia Research Vol. 36, No. 2 ( 2012-02), p. 237-240
    Details
    In: Leukemia Research, Elsevier BV, Vol. 36, No. 2 ( 2012-02), p. 237-240
    Type of Medium: Online Resource
    ISSN: 0145-2126
    URL: Article
    DOI: 10.1016/j.leukres.2011.10.006
    Language: English
    Publisher: Elsevier BV
    Publication Date: 2012
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  • 8
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    Abstract 4186: miR-218 suppresses invasion and migration via inhibition of ZEB2 and N-Cadherin in colon cancer.
    American Association for Cancer Research (AACR) ; 2013
    In:  Cancer Research Vol. 73, No. 8_Supplement ( 2013-04-15), p. 4186-4186
    Details
    In: Cancer Research, American Association for Cancer Research (AACR), Vol. 73, No. 8_Supplement ( 2013-04-15), p. 4186-4186
    Abstract: The great majority of cancer deaths are due to metastasis. A hallmark of cancer metastasis is the process of epithelial to mesenchymal transition (EMT), in which cells alter their gene expression program resulting in loss of their epithelial characteristics and gain of typical mesenchymal properties. Recently, microRNAs have been shown to play key roles in the dynamic process of EMT, orchestrating a coordinated multi-target repression of genes and, together with master transcription factors, act in regulatory networks to alter cell function. We used a miRNA-microarray platform to identify differentially expressed microRNA genes in primary tumor, distant metastatic and corresponding normal samples in a cohort of resected patient tissues. From our list of differentially regulated microRNAs we focused on miR-218 as so far very little information has been accumulated regarding its function in cancer. In our microarray analysis, miR-218 was significantly downregulated in tumor/metastatic tissue compared to normal colon tissue. We validated miR-218 expression in an additional series of 42 colorectal cancer patient tissues, where we found a significant downregulation of miR-218 in tumor as compared to the corresponding normal tissues in over 80% of cases. Furthermore, ectopic expression of miR-218 significantly reduced in vitro invasion and migration of invasive colorectal cancer cell lines and upregulated the key epithelial marker E-cadherin, while silencing of miR-218 lead to enhanced migration and invasion. In addition, we identified two novel miR-218 target genes that are associated with EMT including ZEB2, a zinc-finger transcription factor, and N-Cadherin, using reporter gene, RT-PCR and Western blot analysis. In our present study, we show that miR-218 is a direct suppressor of EMT by its ability to downregulate ZEB2 and N-Cadherin expression and represents an additional molecule contributing to the complexity of the EMT regulatory network. Citation Format: Jasmin Batliner, Mohammed Abba, Christine Hauser, Heike Allgayer. miR-218 suppresses invasion and migration via inhibition of ZEB2 and N-Cadherin in colon cancer. [abstract]. In: Proceedings of the 104th Annual Meeting of the American Association for Cancer Research; 2013 Apr 6-10; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2013;73(8 Suppl):Abstract nr 4186. doi:10.1158/1538-7445.AM2013-4186
    Type of Medium: Online Resource
    ISSN: 0008-5472 , 1538-7445
    URL: Article
    DOI: 10.1158/1538-7445.AM2013-4186
    RVK:
    XA 36000
    RVK:
    XA 10000
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2013
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  • 9
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    A Systematic Approach to Defining the microRNA Landscape in Metastasis
    American Association for Cancer Research (AACR) ; 2015
    In:  Cancer Research Vol. 75, No. 15 ( 2015-08-01), p. 3010-3019
    Details
    In: Cancer Research, American Association for Cancer Research (AACR), Vol. 75, No. 15 ( 2015-08-01), p. 3010-3019
    Abstract: The microRNA (miRNA) landscape changes during the progression of cancer. We defined a metastasis-associated miRNA landscape using a systematic approach. We profiled and validated miRNA and mRNA expression in a unique series of human colorectal metastasis tissues together with their matched primary tumors and corresponding normal tissues. We identified an exclusive miRNA signature that is differentially expressed in metastases. Three of these miRNAs were identified as key drivers of an EMT-regulating network acting though a number of novel targets. These targets include SIAH1, SETD2, ZEB2, and especially FOXN3, which we demonstrated for the first time as a direct transcriptional suppressor of N-cadherin. The modulation of N-cadherin expression had significant impact on migration, invasion, and metastasis in two different in vivo models. The significant deregulation of the miRNAs defining the network was confirmed in an independent patient set as well as in a database of diverse malignancies derived from more than 6,000 patients. Our data define a novel metastasis-orchestrating network based on systematic hypothesis generation from metastasis tissues. Cancer Res; 75(15); 3010–9. ©2015 AACR.
    Type of Medium: Online Resource
    ISSN: 0008-5472 , 1538-7445
    URL: Article
    DOI: 10.1158/0008-5472.CAN-15-0997
    RVK:
    XA 36000
    RVK:
    XA 10000
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2015
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  • 10
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    Abstract 1443: A systematic approach to the metastatically relevant microRNA landscape
    American Association for Cancer Research (AACR) ; 2014
    In:  Cancer Research Vol. 74, No. 19_Supplement ( 2014-10-01), p. 1443-1443
    Details
    In: Cancer Research, American Association for Cancer Research (AACR), Vol. 74, No. 19_Supplement ( 2014-10-01), p. 1443-1443
    Abstract: Distant metastasis is the major determinant of patient outcome in colorectal cancer. By systematically analysing the miR expression profiles of resected metastasis-, corresponding primary tumor and normal tissues of colorectal cancer patients, we were able to delineate a miR-signature indicative of the metastatically critical microRNA landscape. This “hot list” of miRNAs, including established metastasis-related miRs like the miR-34- and let -7 families, as well as rather novel miR-candidates like miR-552, -218, -135, -210 and -654, together with their putative common targets were bioinformatically predicted to regulate the most significant metastasis-associated signaling pathways currently known. We were able to show for the first time that miR-135b, miR-210 and the loss of miR-218 constitute a novel network that regulates both E- and N-cadherin expression, which is achieved, in part, via several novel common targets such as the recently described tumor suppressors SIAH1 and SETD2, and, most importantly, FOXN3 transcription factor. This is paralleled by a significant impact on migration, invasion, in vivo intravasation and metastasis in chicken embryo and mouse models. We conclude that miR-218 as a novel metastasis suppressor, and pro-metastatic miR-135b and miR-210, constitute one important novel network critical for metastasis, resulting from the first study to systematically suggest the microRNA-driven master pathways of metatasis from solid cancer tissues. Citation Format: Giridhar Mudduluru, Mohammed Abba, Jasmin Batliner, Nitin Patil, Taral R. Lunavat, Maike Scharp, Jörg Leupold, Olga Oleksiuk, Ivo Buchhalter, Wilko Thiele, Melanie Rothley, Axel Benner, Jonathan Sleeman, Heike Allgayer. A systematic approach to the metastatically relevant microRNA landscape. [abstract]. In: Proceedings of the 105th Annual Meeting of the American Association for Can cer Research; 2014 Apr 5-9; San Diego, CA. Philadelphia (PA): AACR; Cancer Res 2014;74(19 Suppl):Abstract nr 1443. doi:10.1158/1538-7445.AM2014-1443
    Type of Medium: Online Resource
    ISSN: 0008-5472 , 1538-7445
    URL: Article
    DOI: 10.1158/1538-7445.AM2014-1443
    RVK:
    XA 36000
    RVK:
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    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2014
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