Relevant bibliographies by topics / Inv 16

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  1. Journal articles
  2. Dissertations / Theses
  3. Books
  4. Book chapters
  5. Conference papers
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Academic literature on the topic 'Inv 16'

Author: Grafiati
Published: 4 June 2021
Last updated: 5 February 2022

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Journal articles on the topic "Inv 16"

1

Lazarchick, J. "AML with inv(16)." ASH Image Bank 2004, no. 0214 (February 14, 2004): 101005. http://dx.doi.org/10.1182/ashimagebank-2004-101005.

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2

Eskelin, Sebastian, and Tero Kivel?? "INV 16 Metastatic uveal melanoma." Melanoma Research 17, no. 1 (February 2007): A7—A8. http://dx.doi.org/10.1097/00008390-200702000-00026.

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3

Bennett, John M. "Inv(16) and eosinophilia in CMMoL." Cancer Genetics and Cytogenetics 101, no. 1 (February 1998): 81. http://dx.doi.org/10.1016/s0165-4608(97)00252-5.

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4

Maslak, P. "Acute Myeloid Leukemia with inv 16." ASH Image Bank 2002, no. 1029 (October 29, 2002): 100528. http://dx.doi.org/10.1182/ashimagebank-2002-100528.

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5

Surapally, Sridevi, Daniel G. Tenen, and John A. Pulikkan. "Emerging therapies for inv(16) AML." Blood 137, no. 19 (May 13, 2021): 2579–84. http://dx.doi.org/10.1182/blood.2020009933.

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Abstract The core binding factor composed of CBFβ and RUNX subunits plays a critical role in most hematopoietic lineages and is deregulated in acute myeloid leukemia (AML). The fusion oncogene CBFβ-SMMHC expressed in AML with the chromosome inversion inv(16)(p13q22) acts as a driver oncogene in hematopoietic stem cells and induces AML. This review focuses on novel insights regarding the molecular mechanisms involved in CBFβ-SMMHC–driven leukemogenesis and recent advances in therapeutic approaches to target CBFβ-SMMHC in inv(16) AML.
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6

Helbling, Daniel, Beatrice U. Mueller, Nikolai A. Timchenko, David R. Betts, Martine Jotterand, Sandrine Meyer-Monard, Martin F. Fey, and Thomas Pabst. "Inv (16) Suppresses CEBPA in Acute Myeloid Leukemia by Activation of Calreticulin." Blood 104, no. 11 (November 16, 2004): 3388. http://dx.doi.org/10.1182/blood.v104.11.3388.3388.

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Abstract Inversion of chromosome 16 (inv(16)) results in the reciprocal chromosomal rearrangement of the CBFB and MYH11 genes and it is the hallmark of malignant cells observed in patients with acute myeloid leukemia (AML) subtype M4Eo. Alterations of structure or expression of CEBPA - a key myeloid transcription factor - have been implicated in particular subtypes of AML. To investigate the effects of inv(16) on CEBPA we conditionally expressed inv(16) in U937 cells and found that CEBPA mRNA levels remained unchanged. However, CEBPA protein and binding activity were suppressed by 100% and 71%, respectively. In parallel, analysis of patients with inv(16) (n=12) as compared to normal karyotype AML M4 patients (n=6) showed that CEBPA protein and binding activity were significantly reduced (100% and 71.6%, respectively) whereas CEBPA mRNA levels remained similar. Calreticulin, an inhibitor of CEBPA translation, was induced on mRNA and on protein level in inv(16) AML patients as well as after conditional expression of inv(16) in a U937 cell system. Furthermore, inhibition of Calreticulin by siRNA powerfully restored CEBPA levels. Our results identify CEBPA as a key target gene of the leukemic fusion protein inv(16) and suggest that suppression of CEBPA by Calreticulin contributes to the differentiation block in AML with inv(16).
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7

Pelzer, Benedikt W., Anita Hollenbeck, Stefanie Weber, Bertram Opalka, Lucio H. Castilla, Ulrich Dührsen, and Joachim R. Göthert. "HIF-1α Promotes Cbfbeta-SMMHC-Induced Acute Myeloid Leukemia Development." Blood 128, no. 22 (December 2, 2016): 1559. http://dx.doi.org/10.1182/blood.v128.22.1559.1559.

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Abstract Acute myeloid leukemia (AML) develops by the acquisition of genomic alterations which initiate different pathways leading to full-blown malignancy. The type of genomic driver alteration governs AML biology and clinical disease course. Translocations involving the core-binding factor (CBF) complex such as t(8:21) and inv(16) represent distinct subgroups of AML genomic drivers. However, additional factors promoting CBF AML leukemogenesis remain largely unknown. Due to the hypoxic nature of the bone marrow the activation of the ubiquitous hypoxia-sensing pathway via HIF-1a might promote CBF leukemogenesis. Nevertheless, in different AML models HIF proteins were recently considered as oncogenic drivers and also as tumor suppressors. Therefore, we here aimed to clarify the role of HIF-1a in CBF AML. Initially, we investigated the impact of hypoxia-sensing pathway activation on the growth of the CBF AML cell lines Kasumi-1 [t(8:21)] and ME-1 [inv(16)]. Kasumi-1 cells showed increased growth after 24 as well as 48 hours at 3% compared to 21% oxygen conditions. In contrast, ME-1 cellular growth was not altered by hypoxic culture conditions. Next, we genetically modified the HIF-1a pathway in the CBF AML leukemogenesis context with a previously established conditional inv(16) mouse model (Cbfb+/56M). These mice express the Cbfbeta-SMMHC oncoprotein upon Cre-mediated recombination. In preliminary studies we could show neither vav-iCre mediated Hif-1a gain- nor loss-of-function altered steady-state hematopoiesis, which was recently confirmed by others (Milica Vukovic et al., Blood 2016). We proceeded by crossing conditional inv(16) with conditional mice overexpressing a HIF-1a variant (LSL-HIF1dPA) being insensitive to oxygen-dependent degradation. The conditional inv(16) and HIF1dPA alleles were simultaneously activated using the ubiquitous hematopoietic vav-iCre transgene. Strikingly, we observed accelerated leukemia development in inv16;HIF1dPA mice compared to inv(16) mice without genetic HIF-1a pathway alterations (median survival 68 vs. 116 days; Figure 1). In a complementary approach we crossed the vavi-Cre conditional inv(16) system into a conditional Hif-1a knock-out (KO) background [inv(16);Hif-1aKO mice]. Here we observed significantly delayed leukemia onset in inv(16);Hif-1aKO mice compared to inv(16) control mice (median survival 223 vs. 116 days; Figure 1). The gross leukemic phenotype with high peripheral leukocyte count, splenomegaly and liver infiltration did not differ between the groups. Finally, we analyzed deletion of the conditional Hif-1aKO allele of leukemic inv(16);Hif-1aKO mice and observed complete recombination resulting in a Hif-1a null constellation. Thus, AML in inv(16);Hif-1aKO mice did not develop from clones which evaded vav-iCre mediated Hif-1a deletion. In conclusion, HIF-1a represents a critical factor promoting murine inv(16) leukemogenesis and it will be worthwhile studying the impact of genetic or pharmacologic HIF-1a alteration in established inv(16) leukemia. Figure 1 Kaplan-Meier curves of leukemia-free survival in control [Cre-negative littermates; n=55], inv(16) [n=31], inv(16);HIF1dPA [n=17] and inv(16);Hif-1aKO [n=18] mice. Figure 1. Kaplan-Meier curves of leukemia-free survival in control [Cre-negative littermates; n=55], inv(16) [n=31], inv(16);HIF1dPA [n=17] and inv(16);Hif-1aKO [n=18] mice. Disclosures Dührsen: Roche: Honoraria, Research Funding; Alexion Pharmaceuticals: Honoraria, Research Funding; Amgen: Honoraria, Research Funding. Göthert:Proteros: Consultancy; Ariad Pharmaceuticals: Consultancy; Bristol-Myers Squibb: Honoraria; Novartis: Honoraria.
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8

Li, Jianyong, Huifen Zhou, Lijuan Chen, Jinlan Pan, Hairong Qiu, Wei Xu, Yongquan Xue, and Hua Lu. "Trisomy 22 as the Sole Abnormality Is an Important Marker for Inversion 16 in Acute Myeloid Leukemia." Blood 108, no. 11 (November 16, 2006): 4445. http://dx.doi.org/10.1182/blood.v108.11.4445.4445.

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Abstract Inv(16) has been reported in 10%~12% of acute myeloid leukemia (AML), mostly being associated with the M4Eo subtype, and is associated with a relatively favorable outcome. However, it is a cryptic rearrangement and often difficult to recognize in conventional cytogenetics (CC). Trisomy 22 is an uncommon karyotypic aberration in AML and is often associated with inv(16)(p13q22). In order to explore the value of trisomy 22 in the diagnosis of AML with inv(16), dual-color interphase fluorescence in situ hybridization (FISH) was performed in 19 AML cases with trisomy 22 abnormality. The probe was two-color break apart probe for CBFb with SpectrumRed on the centromeric side and SpectrumGreen on the telomeric side. And the results were compared with that of R-banding CC. CC did not reveal inv(16) in any of the 19 AML with trisomy 22, but FISH analysis showed inv(16) in 11 cases and del(16)(q22) in one case. Among 11 cases with inv(16), 9 were trisomy 22 as the sole abnormality, one was complicated with trisomy 8, and one was del(16)(q22). Four AML patients with trisomy 22 and inv(16) were analyzed by multiplex FISH (M-FISH) which revealed trisomy 22 only. This study further confirmed that trisomy 22 as the sole abnormality can be regarded as an important marker for the inv(16) in AML.
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9

Bank, Ingrid E. M., Válerie de Haas, H. Berna Beverloo, Christian M. Zwaan, and Gertjan J. Kaspers. "Clinical and Prognostic Significance of Eosinophilia and Inv(16)/t(16;16) In Pediatric Acute Myelomonocytic Leukemia (AML-M4)." Blood 116, no. 21 (November 19, 2010): 1664. http://dx.doi.org/10.1182/blood.v116.21.1664.1664.

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Abstract Abstract 1664 The prognosis of pediatric AML has improved considerably in the past decades, with overall long-term survival rates around 60%. This has been achieved by the more effective use of anti-leukemic drugs, improved supportive care and the use of risk-group stratification. A well-known prognostic factor is cytogenetics, and inv(16)(p13.1q22) or t(16;16)(p13.1q22) leading to the CBFβ-MYHII fusion gene and usually detected in AML FAB type M4, is associated with excellent outcome. However, information on cytogenetics is not always available due to lack of material, assay failures or limited resources. With that background, we retrospectively studied the association between morphology and cytogenetics in Dutch patients with newly diagnosed AML-M4, aged 0 to 18 years and treated uniformly with Dutch protocols, starting with SNWLK-ANLL-1982. Main study questions were the association between eosinophilia and inv(16)/t(16;16), and the correlation between these characteristics with other clinical and biological features on one hand, and with clinical outcome on the other hand. A total of 129 patients with AML-M4 were identified, and in 126 out of 129 cases morphologic analysis on eosinophilia could be performed on the diagnostic bone marrow smear. Eosinophilia was observed in 33 patients (26.2%), and was classified as AML M4eo+. In 100 out of 126 patients the presence or absence of inv(16)/t(16;16) could be determined. This was initially done by karyotyping, and if this did not show inv(16)/t(16;16), additional FISH or PCR was performed. In 27 out of 100 patients (27%), inv(16) (n=25) or t(16;16) (n=2) was observed. Combining the morphologic and cytogenetic data, 59% had AML M4eo- without inv(16)/t(16;16), 14% had AML M4eo+ without inv(16)/t(16;16), 12% had AML M4eo- with inv(16)/t(16;16) and 15% had both AML M4eo+ and inv(16)/t(16;16). The presence of eosinophilia was associated with inv(16)/t(16;16) (p< 0.001), extramedullary disease at diagnosis (p=0.010) and less frequent WBC count >100×109/L (p=0.037), but not with other clinical or biological features. The presence of inv(16)/t(16;16) was associated with the presence of eosinophilia (p<0.001) and extramedullary disease at diagnosis (p=0.009), but not with other features. Concerning a relation with clinical outcome, the probability of overall survival (pOS) and event-free survival (pEFS) were significantly higher both in AML patients presenting with M4eo+ as compared to M4eo- (pOS at 3 years 63% vs. 46%, p=0.047 and pEFS at 3 years 59% vs. 39%, p=0.04, respectively) and in patients with inv(16)/t(16;16) as compared to patients without (3-yr pOS 78% vs. 46%, p=0.005 and 3-yr pEFS 70 vs. 40%, p=0.006, respectively). Among the four subgroups as defined by the presence or absence of both eosinophilia and inv(16)/t(16;16), EFS and OS differed significantly. The 3-yr pEFS and pOS were lowest in the 59 patients with M4eo- without inv(16)/t(16;16), 36% and 40% respectively, and were highest in the 12 patients with M4eo- but with inv(16)/t(16;16), at 71% and 92%, respectively. At multivariate Cox regression analysis, the presence of inv(16)/t(16;16) had an independent statistically significant and favourable impact on both EFS and OS, while this was not the case for the presence of eosinophilia. In addition, higher WBC and extramedullary disease each had an independent statistically significant and negative impact on OS and EFS. In conclusion, within pediatric AML-M4, there is a clear association between the presence of eosinophilia and inv(16)/t(16;16). While the incidence of eosinophilia is 26% and of inv(16)/t(16;16) is 27% in this series of AML, more than half of patients with inv(16)/t(16;16) has M4eo+ and more than half of patients with M4eo+ has inv(16)/t(16;16). Both eosinophilia and the presence of inv(16);t(16;16) are each associated with extramedullary disease. Finally, eosinophilia irrespective of the presence of inv(16)/t(16;16) is associated with a significantly better outcome. Thus, in case of lacking cytogenetic data, it seems reasonable to consider these patients as good-risk. However, at multivariate analysis, the presence of eosinophilia loses its prognostic significance, in contrast to high WBC, extramedullary disease and inv(16)/t(16;16). It is therefore clinically relevant to obtain information on the presence of inv(16)/t(16;16). Disclosures: No relevant conflicts of interest to declare.
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10

Pulsoni, Alessandro, Simona Iacobelli, Paola Fazi, Paolo Falcucci, Marco Vignetti, Maria Elena Tosti, Giovanna Caterina Valentini, et al. "AML-M4: Role of Eosinophilia and Cytogenetics on Treatment Response and Survival. The GIMEMA Experience." Blood 106, no. 11 (November 16, 2005): 4501. http://dx.doi.org/10.1182/blood.v106.11.4501.4501.

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Abstract Background: The acute myeloid leukemia (AML)-M4 subtype is frequently associated to eosinophilia and/or to the cytogenetic alteration inv(16)/t(16;16). The presence of these features is generally associated with good prognosis, but the studies concerning their exact role are hampered by the low number of cases. We retrospectively analyzed patients with AML-M4 enrolled in two consecutive GIMEMA studies to assess the influence of eosinophilia and of the inv(16) cytogenetic abnormality on the prognosis of acute myelomonocytic leukemia (M4) and acute myelomonocytic leukemia with abnormal eosinophils (M4eos). Setting: A retrospective study, conducted over 9 years in patients affected by AML, admitted to 35 Italian hematological divisions. Patients and methods: Between December 1993 and December 2002, 1686 patients aged over 15 years with a diagnosis of AML were admitted to the EORTC-GIMEMA AML10 and AML 99p trials; of these, 400 patients (355 M4 and 45 M4Eo) were studied. The diagnosis of M4 and M4eos was first established at each institution and subsequently centrally reviewed at the time of study entry. The following parameters were evaluated: morphology, immunophenotype, cytogenetics performed at the onset of the disease, complete remission achievement and duration, overall survival (OS) and event-free survival (EFS) from AML diagnosis. Patients with M4eo were younger and more frequently associated with inv(16) compared to M4. Cytogenetic analisis failed or was not carried out in 40% of cases, while it was successfully analyzed in 240 cases; inv(16) was found in 17% of them. Results: Concerning the probability of obtaining a CR after standard treatment, at univariate analysis M4Eo had a non significant advantage compared to M4, while presence of inv(16) was significantly correlated to a higher CR probability; multivariate analysis showed a significant advantage only of M4Eo+ inv(16) compared to M4-without eosinophilia and without inv(16). DFS was not different in univariate analysis between patients carrying or not inv(16), while a borderline advantage of M4Eo was observed with respect of M4, not confirmed at multivariate analysis. OS curves showed at univariate analysis a significant advantage both of the presence of eosinophilia (P=0.004) and of inv(16) (P=0.01); at multivariate analysis, patients with M4Eo+ inv(16) had a highly significant advantage compared to M4 without eosinophilia and without inv(16) (P=0.004), but also compared to M4+ inv(16) (P=0.045), and M4Eo-without inv(16) (P=0.076). Conclusions: AML-M4 with or without eosinophilia represent 23.7% of AML. The presence of eosinophilia and of inv(16)/t(16;16) can be both considered favorable prognostic factors; however, only the association of both features allows a highly significant advantage in terms of CR and OS.
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Dissertations / Theses on the topic "Inv 16"

1

Xue, Liting. "Oncogene Function in Pre-Leukemia Stage of INV(16) Acute Myeloid Leukemia: A Dissertation." eScholarship@UMMS, 2010. http://escholarship.umassmed.edu/gsbs_diss/740.

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The CBFbeta-SMMHC fusion protein is expressed in acute myeloid leukemia (AML) samples with the chromosome inversion inv(16)(p13;q22). This fusion protein binds the transcription factor RUNX with higher affinity than its physiological partner CBFbeta and disrupts the core binding factor (CBF) activity in hematopoietic stem and progenitor cells. Studies in the Castilla laboratory have shown that CBFbeta-SMMHC expression blocks differentiation of hematopoietic progenitors, creating a pre-leukemic progenitor that progresses to AML in cooperation with other mutations. However, the combined function of cumulative cooperating mutations in the pre-leukemic progenitor cells that enhance their expansion to induce leukemia is not known. The standard treatment for inv(16) AML is based on the use of non-selective cytotoxic chemotherapy, resulting in a good initial response, but with limited long-term survival. Therefore, there is a need for developing targeted therapies with improved efficacy in leukemic cells and minimal toxicity for normal cells. Here, we used conditional Nras+/LSL-G12D; Cbfb+/56M; Mx1Cre knock-in mice to show that allelic expression of oncogenic N-RasG12D expanded the multi-potential progenitor (MPP) compartment by 8 fold. Allelic expression of Cbfbeta-SMMHC increased the MPPs and short-term hematopoietic stem cells (ST-HSCs) by 2 to 4 fold both alone and in combination with N-RasG12D expression. In addition, allelic expression of oncogenic N-RasG12D and Cbfbeta-SMMHC increases survival of pre-leukemic stem and progenitor cells. Differential analysis of bone marrow cells determined that Cbfb+/MYH11 and Nras+/G12D; vii Cbfb+/MYH11 cells included increased number of blasts, myeloblasts and promyelocytes and a reduction in immature granulocytes, suggesting that expression of N-RasG12D cannot bypass Cbfbeta-SMMHC driven differentiation block. N-RasG12D and Cbfbeta-SMMHC synergized in leukemia, in which Nras+/G12D; Cbfb+/MYH11 mice have a shorter median latency than Cbfb+/MYH11 mice. In addition, the synergy in leukemogenesis was cell autonomous. Notably, leukemic cells expressing N-RasG12D and Cbfbeta-SMMHC showed higher (over 100 fold) leukemia-initiating cell activity in vivo than leukemic cells expressing Cbfbeta-SMMHC (L-IC activity of 1/4,000 and 1/528,334, respectively). Short term culture and biochemical assays revealed that pre-leukemic and leukemic cells expressing N-RasG12D and Cbfbeta-SMMHC have reduced levels of pro-apoptotic protein Bim compared to control. The Nras+/G12D; CbfbMYH11 pre-leukemic and leukemic cells were sensitive to pharmacologic inhibition of MEK/ERK signaling pathway with increasing apoptosis and Bim protein levels but not sensitive to PI3K inhibitors. In addition, knock-down of Bcl2l11 (Bim) expression in Cbfbeta-SMMHC pre-leukemic progenitors decreased their apoptosis levels. In collaboration with Dr. John Bushweller’s and other research laboratories, we recently developed a CBFbeta-SMMHC inhibitor named AI-10-49, which specifically binds to CBFbeta-SMMHC, prevents its binding to RUNX proteins and restores CBF function. Biochemical analysis in human leukemic cells showed that AI-10-49 has significant specificity in reducing the viability of leukemic cells expressing CBFbeta-SMMHC (IC50= 0.83μM), and negligible toxicity in normal cells. Likewise, mouse Nras+/G12D; viii Cbfb+/MYH11 leukemic cells were sensitive to AI-10-49 (IC50= 0.93μM). By using the NrasLSL-G12D; Cbfb56M mouse model, we also show that AI-10-49 significantly prolongs the survival of mice bearing the leukemic cells. Preliminary mechanistic analysis of AI-10-49 activity has shown that AI-10-49 increased BCL2L11 transcript levels in a dose and time dependent manner in murine and human leukemic cells, suggesting that the viability through BIM-mediated apoptosis may be targeted by both oncogenic signals. My thesis study demonstrates that Cbfbeta-SMMHC and N-RasG12D promote the survival of pre-leukemic myeloid progenitors primed for leukemia by activation of the MEK/ERK/Bim axis, and define NrasLSL-G12D; Cbfb56M mice as a valuable genetic model for the study of inv(16) AML targeted therapies. For instance, the novel CBFbeta-SMMHC inhibitor AI-10-49 shows a significant efficacy in this mouse model. This small molecule will serve as a promising first generation drug for targeted therapy of inv(16) leukemia and also a very useful tool to understand mechanisms of leukemogenesis driving by CBFbeta-SMMHC.
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2

Xue, Liting. "Oncogene Function in Pre-Leukemia Stage of INV(16) Acute Myeloid Leukemia: A Dissertation." eScholarship@UMMS, 2014. https://escholarship.umassmed.edu/gsbs_diss/740.

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The CBFbeta-SMMHC fusion protein is expressed in acute myeloid leukemia (AML) samples with the chromosome inversion inv(16)(p13;q22). This fusion protein binds the transcription factor RUNX with higher affinity than its physiological partner CBFbeta and disrupts the core binding factor (CBF) activity in hematopoietic stem and progenitor cells. Studies in the Castilla laboratory have shown that CBFbeta-SMMHC expression blocks differentiation of hematopoietic progenitors, creating a pre-leukemic progenitor that progresses to AML in cooperation with other mutations. However, the combined function of cumulative cooperating mutations in the pre-leukemic progenitor cells that enhance their expansion to induce leukemia is not known. The standard treatment for inv(16) AML is based on the use of non-selective cytotoxic chemotherapy, resulting in a good initial response, but with limited long-term survival. Therefore, there is a need for developing targeted therapies with improved efficacy in leukemic cells and minimal toxicity for normal cells. Here, we used conditional Nras+/LSL-G12D; Cbfb+/56M; Mx1Cre knock-in mice to show that allelic expression of oncogenic N-RasG12D expanded the multi-potential progenitor (MPP) compartment by 8 fold. Allelic expression of Cbfbeta-SMMHC increased the MPPs and short-term hematopoietic stem cells (ST-HSCs) by 2 to 4 fold both alone and in combination with N-RasG12D expression. In addition, allelic expression of oncogenic N-RasG12D and Cbfbeta-SMMHC increases survival of pre-leukemic stem and progenitor cells. Differential analysis of bone marrow cells determined that Cbfb+/MYH11 and Nras+/G12D; vii Cbfb+/MYH11 cells included increased number of blasts, myeloblasts and promyelocytes and a reduction in immature granulocytes, suggesting that expression of N-RasG12D cannot bypass Cbfbeta-SMMHC driven differentiation block. N-RasG12D and Cbfbeta-SMMHC synergized in leukemia, in which Nras+/G12D; Cbfb+/MYH11 mice have a shorter median latency than Cbfb+/MYH11 mice. In addition, the synergy in leukemogenesis was cell autonomous. Notably, leukemic cells expressing N-RasG12D and Cbfbeta-SMMHC showed higher (over 100 fold) leukemia-initiating cell activity in vivo than leukemic cells expressing Cbfbeta-SMMHC (L-IC activity of 1/4,000 and 1/528,334, respectively). Short term culture and biochemical assays revealed that pre-leukemic and leukemic cells expressing N-RasG12D and Cbfbeta-SMMHC have reduced levels of pro-apoptotic protein Bim compared to control. The Nras+/G12D; CbfbMYH11 pre-leukemic and leukemic cells were sensitive to pharmacologic inhibition of MEK/ERK signaling pathway with increasing apoptosis and Bim protein levels but not sensitive to PI3K inhibitors. In addition, knock-down of Bcl2l11 (Bim) expression in Cbfbeta-SMMHC pre-leukemic progenitors decreased their apoptosis levels. In collaboration with Dr. John Bushweller’s and other research laboratories, we recently developed a CBFbeta-SMMHC inhibitor named AI-10-49, which specifically binds to CBFbeta-SMMHC, prevents its binding to RUNX proteins and restores CBF function. Biochemical analysis in human leukemic cells showed that AI-10-49 has significant specificity in reducing the viability of leukemic cells expressing CBFbeta-SMMHC (IC50= 0.83μM), and negligible toxicity in normal cells. Likewise, mouse Nras+/G12D; viii Cbfb+/MYH11 leukemic cells were sensitive to AI-10-49 (IC50= 0.93μM). By using the NrasLSL-G12D; Cbfb56M mouse model, we also show that AI-10-49 significantly prolongs the survival of mice bearing the leukemic cells. Preliminary mechanistic analysis of AI-10-49 activity has shown that AI-10-49 increased BCL2L11 transcript levels in a dose and time dependent manner in murine and human leukemic cells, suggesting that the viability through BIM-mediated apoptosis may be targeted by both oncogenic signals. My thesis study demonstrates that Cbfbeta-SMMHC and N-RasG12D promote the survival of pre-leukemic myeloid progenitors primed for leukemia by activation of the MEK/ERK/Bim axis, and define NrasLSL-G12D; Cbfb56M mice as a valuable genetic model for the study of inv(16) AML targeted therapies. For instance, the novel CBFbeta-SMMHC inhibitor AI-10-49 shows a significant efficacy in this mouse model. This small molecule will serve as a promising first generation drug for targeted therapy of inv(16) leukemia and also a very useful tool to understand mechanisms of leukemogenesis driving by CBFbeta-SMMHC.
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3

Kuss, Bryone Jean. "Molecular and gene expression studies of the genes involved in the breakpoints of the inv(16) leukaemias." Title page, abstract and contents only, 1996. http://web4.library.adelaide.edu.au/theses/09PH/09phk972.pdf.

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4

Quesnel, Bruno. "Les leucemies aigues induites a caryotype t (8;21) inv (16,) t (8;16) : une nouvelle forme de leucemie aigue induite ?" Lille 2, 1994. http://www.theses.fr/1994LIL2M180.

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5

Du, Juan. "RAS, KIT, FLT3 and JAK2 gene mutations in Acute Myeloid Leukemia (AML) with inv(16) and t(8;21): Incidence and relevance on clinical outcome." [S.l. : s.n.], 2007. http://nbn-resolving.de/urn:nbn:de:bsz:289-vts-60221.

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6

Kurz, Stephan. "cDNA-Microarray basierte Identifizierung von molekularen und prognostischen Subgruppen bei der akuten myeloischen Leukämie mit einer Inversion inv(16)/ Translokation t(16;16) und einer Translokation t(8;21)." [S.l. : s.n.], 2008. http://nbn-resolving.de/urn:nbn:de:bsz:289-vts-64925.

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7

Mariani, Giacomo <1979&gt. "Theoretical and Experimental Study of the Magnetic Separation of Pollutants from Wastewater." Doctoral thesis, Alma Mater Studiorum - Università di Bologna, 2010. http://amsdottorato.unibo.it/2305/.

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This Thesys reports the study of a HGMS (High GradientMagnetic Separation) process for the treatment of industrialwastewaters that considers an assisted chemical-physical pre-treatment for the removal of heavy metals through the bound by adsorption with added iron-oxide particulate matter (hematite). The considered filter, constituted by ferromagnetic stainless steel wool and permanent magnets, is studied with a new approach based on a statistical analysis that requires the study of the trajectories of the particles. Experimental activity on a laboratory device has been carried out in order to test the model.
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8

Salsi, Emilio <1983&gt. "Caratterizzazione e simulazione di processi di colata in sabbia di ghise sferoidali." Doctoral thesis, Alma Mater Studiorum - Università di Bologna, 2014. http://amsdottorato.unibo.it/6970/.

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L’oggetto principale delle attività di tesi è la caratterizzazione numerico-sperimentale di processi di colata in sabbia di ghisa sferoidale. Inizialmente è stata effettuata un’approfondita indagine bibliografica per comprendere appieno le problematiche relative all’influenza dei parametri del processo fusorio (composizione chimica, trattamento del bagno, velocità di raffreddamento) sulle proprietà microstrutturali e meccaniche di getti ottenuti e per valutare lo stato dell’arte degli strumenti numerici di simulazione delle dinamiche di solidificazione e di previsione delle microstrutture. Sono state definite, realizzate ed impiegate attrezzature sperimentali di colata per la caratterizzazione di leghe rivolte alla misura ed alla differenziazione delle condizioni di processo, in particolare le velocità di raffreddamento, ed atte a validare strumenti di simulazione numerica e modelli previsionali. Inoltre sono stati progettati ed impiegati diversi sistemi per l’acquisizione ed analisi delle temperature all’interno di getti anche di grandi dimensioni. Lo studio, mediante analisi metallografica, di campioni di materiale ottenuto in condizioni differenziate ha confermato l’effetto dei parametri di processo considerati sulle proprietà microstrutturali quali dimensioni dei noduli di grafite e contenuto di ferrite e perlite. In getti di grandi dimensioni si è riscontrata anche una forte influenza dei fenomeni di macrosegregazione e convezione della lega su microstrutture e difettologie dei getti. Le attività si sono concentrate principalmente nella simulazione numerica FEM dei processi fusori studiati e nell’impiego di modelli empirico-analitici per la previsione delle microstrutture. I dati misurati di temperature di processo e di microstrutture sono stati impiegati per la validazione ed ottimizzazione degli strumenti numerici previsionali impiegati su un ampio intervallo di condizioni di processo. L’impiego di strumenti affidabili di simulazione del processo fusorio, attraverso l’implementazione di correlazioni sperimentali microstrutture-proprietà meccaniche, permette la valutazione di proprietà e difettologie dei getti, fornendo un valido aiuto nell’ottimizzazione del prodotto finito e del relativo processo produttivo.
This work focuses on a numerical-experimental characterization of casting processes of sand ductile iron. Initially, a deep phase of literary review has been carried out in order to completely understand the effects of the process parameters (alloy chemical composition, melt treatment and cooling rates) on defects, microstructures and mechanical properties of castings and to evaluate the state of the art of the numerical instruments of simulation of solidification dynamics and microstructure prediction. Experimental casting equipments have been designed and developed in order to measure and control the cooling rates and to validate instrument of numerical simulation and microstructure prediction. Moreover, specific methods and instruments have been designed, tested and used in order to measure and analyze temperatures inside the central parts of castings, also in case of heavy sections. Metallographic samples of material, obtained with different conditions, have been studied by means of optical analysis in order to evaluate microstructural features gradient, verifying the effect of the considered process parameters on microstructures parameters such as dimension and distribution of graphite nodules and content of ferrite and pearlite. In heavy section castings, a strong influence of macrosegregation and convective phenomena on microstructures and defects was found. The main part of the activities focused on numerical simulation FEM of the performed casting processes. The measured data of temperatures and microstructures have been used for the validation and optimization of the numerical simulations and of the analytical-empirical models for microstructure prediction in a wide range of process condition. The use of reliable instruments for simulation of casting process, with the adding of the implementation of experimental correlation microstructures-mechanical properties, allows for the evaluation of final properties and defects of castings, giving an important help in the optimization of the final product and its relative production process.
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Ascari, Alessandro <1974&gt. "Giunzione mediante laser di materiali difficili, ibridi ed a struttura cellulare." Doctoral thesis, Alma Mater Studiorum - Università di Bologna, 2014. http://amsdottorato.unibo.it/6358/.

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Lo studio presentato in questa sede concerne applicazioni di saldatura LASER caratterizzate da aspetti di non-convenzionalità ed è costituito da tre filoni principali. Nel primo ambito di intervento è stata valutata la possibilità di effettuare saldature per fusione, con LASER ad emissione continua, su pannelli Aluminum Foam Sandwich e su tubi riempiti in schiuma di alluminio. Lo studio ha messo in evidenza numerose linee operative riguardanti le problematiche relative alla saldatura delle pelli esterne dei componenti ed ha dimostrato la fattibilità relativa ad un approccio di giunzione LASER integrato (saldatura seguita da un post trattamento termico) per la realizzazione della giunzione completa di particolari tubolari riempiti in schiuma con ripristino della struttura cellulare all’interfaccia di giunzione. Il secondo ambito di intervento è caratterizzato dall’applicazione di una sorgente LASER di bassissima potenza, operante in regime ad impulsi corti, nella saldatura di acciaio ad elevato contenuto di carbonio. Lo studio ha messo in evidenza come questo tipo di sorgente, solitamente applicata per lavorazioni di ablazione e marcatura, possa essere applicata anche alla saldatura di spessori sub-millimetrici. In questa fase è stato messo in evidenza il ruolo dei parametri di lavoro sulla conformazione del giunto ed è stata definita l’area di fattibilità del processo. Lo studio è stato completato investigando la possibilità di applicare un trattamento LASER dopo saldatura per addolcire le eventuali zone indurite. In merito all’ultimo ambito di intervento l’attività di studio si è focalizzata sull’utilizzo di sorgenti ad elevata densità di potenza (60 MW/cm^2) nella saldatura a profonda penetrazione di acciai da costruzione. L’attività sperimentale e di analisi dei risultati è stata condotta mediante tecniche di Design of Experiment per la valutazione del ruolo preciso di tutti i parametri di processo e numerose considerazioni relative alla formazione di cricche a caldo sono state suggerite.
This dissertation concerns LASER-based joining and welding applications characterized by non-conventional prerogatives. The work is divided into three main topics: LASER joining of hybrid cellular-structured materials, with particular attention to aluminum foam sandwiches and foam-cored tubes, short-pulse LASER micro welding of high carbon steels and high power density continuous wave LASER welding of structural steels. The first topic investigates the role of LASER in joining hybrid components characterized by an external dense skin and an internal foam core. In particular the possibility of achieving both the fusion welding of the skin and the restoration of the cellular structure at the welding interface is assessed and the main guidelines concerning an integrated LASER welding - LASER heat treatment processing cycle are suggested. The second topic deals with the application of a low-power nanosecond pulsed LASER source in welding high carbon steels. The study points out that an accurate selection of pulse-related parameters allows to achieve sound micro-joints characterized by a penetration between 20 and 200 microns. These results point out the possibility to consider the construction of integrated LASER manufacturing cells in which, with the same low-cost source and on the same workpiece positioning, welding, cutting, marking and texturing processes can be performed. The study is completed by the investigation of the possibility to carry out a LASER post welding heat treatment for annealing the eventual hardened zones occurring in the welded material. The last topic deals with high power density LASER welding of carbon steels: by exploiting a high brilliance fiber source, capable of achieving 60 MW/cm^2, high penetration weld beads were obtained. By means of Design of Experiment techniques the role of radiation power, welding speed and beam focal position is assessed and several considerations were made concerning the influence of this kind of process on hot cracks formation.
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Ferretti, Stefano <1976&gt. "Innovative technologies for Space habitats." Doctoral thesis, Alma Mater Studiorum - Università di Bologna, 2008. http://amsdottorato.unibo.it/958/.

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Books on the topic "Inv 16"

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Giger, Felix. Sun e senn: ina tschientina d'insatgs per il tschientenari dal DRG. Edited by Felix Giger. Chur, CH: Societad Retorumantscha, 2004.

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Probate Law Seminar (1986 Bangor, Me.). Probate Law Seminar: Presented May 16, 1986, Ramada Inn, Bangor. [Augusta, Me.]: The Association, 1986.

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Sulzgruber, Werner. Zeiterfahrung und Zeitordnung vom frühen Mittelalter bis ins 16. Jahrhundert. Hamburg: Kovač, 1995.

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David, Hockney. Egyptian Journeys: Palace of Arts, Cairo, 16 January to 16 February 2002. [Cairo]: American University in Cairo Press, 2002.

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Gheldman, Georges. 16 juillet 1942. Paris: Berg international, 2005.

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Gheldman, Georges. 16 juillet 1942. Paris: Berg, 2005.

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Mütterchen Wolga: Ein Fluss als Erinnerungsort vom 16. bis ins frühe 20. Jahrhundert. Frankfurt am Main: Campus, 2009.

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Landshut ins Bild gesetzt: Karten und Ansichten vom 16. bis zum 20. Jahrhundert. Landshut: Museen der Stadt, 2001.

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Clogston, John S. Disability coverage in 16 newspapers. Louisville, KY: Avocado Press, 1990.

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Hakubutsukan, Tsuchiura Shiritsu. Inu monogatari: Hito to inu no bunkashi : dai 13-kai tokubetsuten : 1994-nen 10-gatsu 16-nichi--11gatsu 27-nichi. Ibaraki-ken Tsuchiura-shi: Tsuchiura Shiritsu Hakubutsukan, 1994.

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Book chapters on the topic "Inv 16"

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Hajra, A., P. P. Liu, and F. S. Collins. "Transforming Properties of the Leukemic Inv(16) Fusion Gene CBFB-MYH11." In Molecular Aspects of Myeloid Stem Cell Development, 289–98. Berlin, Heidelberg: Springer Berlin Heidelberg, 1996. http://dx.doi.org/10.1007/978-3-642-85232-9_29.

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Plantier-Colcher, I., J. L. Lai, C. Preudhomme, N. Cambier-Lot, L. Detourmignies, F. Bauters, and P. Fenaux. "Presence of inv (16) May Be One of the Only “Favorable” Prognostic Factors in AML: A Report on 16 Cases." In Haematology and Blood Transfusion / Hämatologie und Bluttransfusion, 602–5. Berlin, Heidelberg: Springer Berlin Heidelberg, 1994. http://dx.doi.org/10.1007/978-3-642-78350-0_108.

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Schoch, C., T. Büchner, M. Freund, H. Link, H. Bartels, T. Haferlach, H. Löffler, C. Sauerland, and C. Fonatsch. "Fifty-nine Cases of Acute Myeloid Leukemia with Inversion inv(16) (p13q22): Do Additional Chromosomal Aberrations Influence Prognosis?" In Acute Leukemias VI, 11–16. Berlin, Heidelberg: Springer Berlin Heidelberg, 1997. http://dx.doi.org/10.1007/978-3-642-60377-8_2.

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Krauter, J., F. Herrmann, D. Hoelzer, R. Mertelsmann, G. Schlimok, U. Pascheberg, G. Schwab, A. Ganser, and G. Heil. "RT-PCR for the Diagnosis of Acute Myeloblastic Leukemia with Inv(16) and Detection of Minimal Residual Disease." In Haematology and Blood Transfusion / Hämatologie und Bluttransfusion, 1026–30. Berlin, Heidelberg: Springer Berlin Heidelberg, 1998. http://dx.doi.org/10.1007/978-3-642-71960-8_143.

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Hiebert, S. W., B. Lutterbach, J. Amann, K. Durst, and B. Linggi. "The t(8;21), t(12;21), and inv(16) fusion Proteins Contact Co-Repressors and Histone Deacetylase to Repress Transcription." In Haematology and Blood Transfusion Hämatologie und Bluttransfusion, 21–24. Berlin, Heidelberg: Springer Berlin Heidelberg, 2003. http://dx.doi.org/10.1007/978-3-642-59358-1_6.

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Negra, Diane, and Anthony P. McIntyre. "Ireland Inc." In Routledge International Handbook of Irish Studies, 158–71. Abingdon, Oxon ; New York: Routeldge, 2021.: Routledge, 2020. http://dx.doi.org/10.4324/9780367259228-16.

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Suters, Everett T. "Samstag, 16. März, Colonial Inn." In Auf Kurs Gebracht, 157–73. Wiesbaden: Gabler Verlag, 1991. http://dx.doi.org/10.1007/978-3-322-82657-2_21.

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Vogel, Irene. "Introduction." In Romance Languages and Linguistic Theory 16, 2–6. Amsterdam: John Benjamins Publishing Company, 2020. http://dx.doi.org/10.1075/rllt.16.int.

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Allwood, Jens, Olga Pombo, and Giovanni Scarafile. "Introduction. Crossing borderlines." In Controversies, 1–4. Amsterdam: John Benjamins Publishing Company, 2020. http://dx.doi.org/10.1075/cvs.16.int.

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Bekker, Sheree, and Katlego K. Kolanyane-Kesupile. "Fighting a System Built to Exclude Queer(ing) Bodies." In Developing and Supporting Athlete Wellbeing, 225–38. London: Routledge, 2021. http://dx.doi.org/10.4324/9780429287923-16.

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Conference papers on the topic "Inv 16"

1

Richter, Lisa, Yiqian Wang, Michelle Becker, Jake Williams, and R. Katherine Hyde. "Abstract 5419: HDAC1 regulates RUNX1 activity in inv(16) acute myeloid leukemia." In Proceedings: AACR Annual Meeting 2018; April 14-18, 2018; Chicago, IL. American Association for Cancer Research, 2018. http://dx.doi.org/10.1158/1538-7445.am2018-5419.

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Agarwal, S., JG Jones, M. Oktay, M. Balsamo, J. Condeelis, F. Gertler, and DL Rimm. "Abstract P3-10-16: Quantitative Subtractive Immunofluorescence To Develop a Surrogate for Mena Inv(asive) Isoform Is Associated with Poor Outcome in Breast Cancer." In Abstracts: Thirty-Third Annual CTRC‐AACR San Antonio Breast Cancer Symposium‐‐ Dec 8‐12, 2010; San Antonio, TX. American Association for Cancer Research, 2010. http://dx.doi.org/10.1158/0008-5472.sabcs10-p3-10-16.

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Gruber, Tanja A., Amanda L. Gedman, Huy Ta, Jinghui Zhang, Cary Koss, Suresh Marada, Shann-Ching Chen, et al. "Abstract 4867: Identification of an inv(16)-encodedCBFA2T3-GLIS2fusion protein in 34% of non-infant acute megkaryoblastic leukemias: A report from the Pediatric Cancer Genome Project." In Proceedings: AACR 103rd Annual Meeting 2012‐‐ Mar 31‐Apr 4, 2012; Chicago, IL. American Association for Cancer Research, 2012. http://dx.doi.org/10.1158/1538-7445.am2012-4867.

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Tan, Bin, John J. Dellomo, Robert E. Wolfe, and Alan D. Reth. "GOES-16 and GOES-17 ABI INR assessment." In Earth Observing Systems XXIV, edited by James J. Butler, Xiaoxiong (Jack) Xiong, and Xingfa Gu. SPIE, 2019. http://dx.doi.org/10.1117/12.2529336.

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Li, Haozhe. "Ink fall." In SA '16: SIGGRAPH Asia 2016. New York, NY, USA: ACM, 2016. http://dx.doi.org/10.1145/3004257.3004484.

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Doerr, C. R., L. Zhang, P. J. Winzer, and A. H. Gnauck. "28-Gbaud InP Square or Hexagonal 16-QAM Modulator." In Optical Fiber Communication Conference. Washington, D.C.: OSA, 2011. http://dx.doi.org/10.1364/ofc.2011.omu2.

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Soares, F. M., N. K. Fontaine, J. Wei, S. W. Seo, J. H. Baek, R. G. Broeke, J. Cao, et al. "Compact InP-Based 16-Channel O-CDMA Encoder/Decoder." In LEOS 2007 - IEEE Lasers and Electro-Optics Society Annual Meeting. IEEE, 2007. http://dx.doi.org/10.1109/leos.2007.4382611.

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Xiao, David. "Session details: Session 4: 16:00--16:10." In ITCS'14: Innovations in Theoretical Computer Science. New York, NY, USA: ACM, 2014. http://dx.doi.org/10.1145/3255056.

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Filmus, Yuval. "Session details: Session 8: 16:00--16:10." In ITCS'14: Innovations in Theoretical Computer Science. New York, NY, USA: ACM, 2014. http://dx.doi.org/10.1145/3255060.

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Etessami, Kousha. "Session details: Session 12: 16:00--16:10." In ITCS'14: Innovations in Theoretical Computer Science. New York, NY, USA: ACM, 2014. http://dx.doi.org/10.1145/3255064.

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Reports on the topic "Inv 16"

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Goodwin, R. C., Paul C. Armstrong, Eva J. Harris, and James M. Wojtala. Archeological Testing at Two Sites Near White Castle, Iberville Parish, Louisiana: 16 IV 147 and 16 IV 149. Fort Belvoir, VA: Defense Technical Information Center, July 1988. http://dx.doi.org/10.21236/ada199158.

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Deupree, R. G. GRMPY surface ground motion measurements in Area 16. Office of Scientific and Technical Information (OSTI), September 1995. http://dx.doi.org/10.2172/104510.

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Bair, Andrew. Strategic Forum. Number 16. Which End-Game in Bosnia? Fort Belvoir, VA: Defense Technical Information Center, January 1995. http://dx.doi.org/10.21236/ada290376.

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McInerney, M. J., and R. M. Knapp. Quantitation of microbial products and their effectiveness in enhanced oil recovery. Quarterly technical progress report, October 16, 1992--January 16, 1993. Office of Scientific and Technical Information (OSTI), December 1992. http://dx.doi.org/10.2172/10133675.

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Burger, Johan. Africa Digest: Trends and Issues in Business Vol. 2020-16. Nanyang Business School, February 2020. http://dx.doi.org/10.32655/africadigest.2020.16.

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Liby, Karen, and Nira Ben-Jonathan. 16 K Prolactin as an Angiogenic Inhibitor in Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, June 2000. http://dx.doi.org/10.21236/ada391620.

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Andersson, Gunnar, and Dimiter Philipov. Life-table representations of family dynamics in 16 FFS countries. Rostock: Max Planck Institute for Demographic Research, August 2001. http://dx.doi.org/10.4054/mpidr-wp-2001-024.

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Gray, Thomas H., Bernell J. Edwards, and Dee H. Andrews. A Survey of F-16 Squadron-Level Pilot Training in PACAF. Fort Belvoir, VA: Defense Technical Information Center, April 1993. http://dx.doi.org/10.21236/ada265053.

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Dana, V. Line Intensities and Self-Broadening Coefficients of 12 Carbon 16 Oxygen(2) and 13 Carbon 16 Oxygen(2) Lines in the Laser Band Region. Fort Belvoir, VA: Defense Technical Information Center, March 1992. http://dx.doi.org/10.21236/ada248612.

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R. W. Schaefer. CONFIGURATIONS AND EXPERIMENTS IN THE ZPPR-16 POWER REACTOR SPACE BENCHMARK PROGRAM. Office of Scientific and Technical Information (OSTI), August 2005. http://dx.doi.org/10.2172/911243.

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