DVCS on spinless nuclear targets in impulse approximation

Within the impulse approximation, we derive expressions for the amplitude of deeply virtual Compton scattering on spinless nuclei in terms of the generalized parton distributions of the nucleon. As an application, nuclear effects in the beam-charge and single-spin asymmetries are discussed.Comment: 13 pages, 2 figures, Late

Generalized parton distributions and Deeply Virtual Compton Scattering in Color Glass Condensate model

Within the framework of the Color Glass Condensate model, we evaluate quark and gluon Generalized Parton Distributions (GPDs) and the cross section of Deeply Virtual Compton Scattering (DVCS) in the small-$x_{B}$ region. We demonstrate that the DVCS cross section becomes independent of energy in the limit of very small $x_{B}$, which clearly indicates saturation of the DVCS cross section. Our predictions for the GPDs and the DVCS cross section at high-energies can be tested at the future Electron-Ion Collider and in ultra-peripheral nucleus-nucleus collisions at the LHC.Comment: 20 pages, 8 Figure

QCD Form Factors and Hadron Helicity Non-Conservation

Recent data for the ratio $R(Q)= QF_{2}(Q^{2})/F_{1}(Q^{2})$ shocked the community by disobeying expectations held for 50 years. We examine the status of perturbative QCD predictions for helicity-flip form factors. Contrary to common belief, we find there is no rule of hadron helicity conservation for form factors. Instead the analysis yields an inequality that the leading power of helicity-flip processes may equal or exceed the power of helicity conserving processes. Numerical calculations support the rule, and extend the result to the regime of laboratory momentum transfer $Q^{2}$. Quark orbital angular momentum, an important feature of the helicity flip processes, may play a role in all form factors at large $Q^{2}$, depending on the quark wave functions.Comment: 25 pages, 5 figure

Survey of nucleon electromagnetic form factors

A dressed-quark core contribution to nucleon electromagnetic form factors is calculated. It is defined by the solution of a Poincare' covariant Faddeev equation in which dressed-quarks provide the elementary degree of freedom and correlations between them are expressed via diquarks. The nucleon-photon vertex involves a single parameter; i.e., a diquark charge radius. It is argued to be commensurate with the pion's charge radius. A comprehensive analysis and explanation of the form factors is built upon this foundation. A particular feature of the study is a separation of form factor contributions into those from different diagram types and correlation sectors, and subsequently a flavour separation for each of these. Amongst the extensive body of results that one could highlight are: r_1^{n,u}>r_1^{n,d}, owing to the presence of axial-vector quark-quark correlations; and for both the neutron and proton the ratio of Sachs electric and magnetic form factors possesses a zero.Comment: 43 pages, 17 figures, 12 tables, 5 appendice

Transverse Momentum Dependent Parton Distribution/Fragmentation Functions at an Electron-Ion Collider

We present a summary of a recent workshop held at Duke University on Partonic Transverse Momentum in Hadrons: Quark Spin-Orbit Correlations and Quark-Gluon Interactions. The transverse momentum dependent parton distribution functions (TMDs), parton-to-hadron fragmentation functions, and multi-parton correlation functions, were discussed extensively at the Duke workshop. In this paper, we summarize first the theoretical issues concerning the study of partonic structure of hadrons at a future electron-ion collider (EIC) with emphasis on the TMDs. We then present simulation results on experimental studies of TMDs through measurements of single spin asymmetries (SSA) from semi-inclusive deep-inelastic scattering (SIDIS) processes with an EIC, and discuss the requirement of the detector for SIDIS measurements. The dynamics of parton correlations in the nucleon is further explored via a study of SSA in D (`D) production at large transverse momenta with the aim of accessing the unexplored tri-gluon correlation functions. The workshop participants identified the SSA measurements in SIDIS as a golden program to study TMDs in both the sea and valence quark regions and to study the role of gluons, with the Sivers asymmetry measurements as examples. Such measurements will lead to major advancement in our understanding of TMDs in the valence quark region, and more importantly also allow for the investigation of TMDs in the sea quark region along with a study of their evolution.Comment: 44 pages 23 figures, summary of Duke EIC workshop on TMDs accepted by EPJ

Prospects for e+e- physics at Frascati between the phi and the psi

We present a detailed study, done in the framework of the INFN 2006 Roadmap, of the prospects for e+e- physics at the Frascati National Laboratories. The physics case for an e+e- collider running at high luminosity at the phi resonance energy and also reaching a maximum center of mass energy of 2.5 GeV is discussed, together with the specific aspects of a very high luminosity tau-charm factory. Subjects connected to Kaon decay physics are not discussed here, being part of another INFN Roadmap working group. The significance of the project and the impact on INFN are also discussed. All the documentation related to the activities of the working group can be found in http://www.roma1.infn.it/people/bini/roadmap.html.Comment: INFN Roadmap Report: 86 pages, 25 figures, 9 table

Alterations in WNT Signaling in Leukemias

The WNT/β–catenin signaling pathway plays an important role in the differentiation and proliferation of hematopoietic cells. In recent years, special attention has been paid to the role of impairments in the WNT signaling path–way in pathogenesis of malignant neoplasms of the hematopoietic system. Disorders in the WNT/β–catenin signaling in leukemias identified to date include hypersensitivity to the WNT ligands, epigenetic repression of WNT antagonists, over–expression of WNT ligands, impaired β–catenin degradation in the cytoplasm, and changes in the activity of the TCF/Lef transcription factors. At the molecular level, these impairments involve overexpression of the FZD protein, hypermethylation of the SFRP, DKK, WiF, Sox, and CXXC gene promoters, overexpression of Lef1 and plakoglobin, mutations in GSK3β, and β–catenin phosphorylation by the BCR–ABL kinase. This review is devoted to the systematization of these data. © 2018, Pleiades Publishing, Inc

РОЛЬ НАРУШЕНИЙ СИГНАЛЬНОГО ПУТИ WNT В ПАТОГЕНЕЗЕ ЛЕЙКОЗОВ

The WNT/β-catenin signaling pathway plays an important role in the differentiation and proliferation of hematopoietic cells. In this regard, in recent years, much attention has been paid to studying the role of WNT signal transduction disorders in the pathogenesis of various malignant neoplasms of the hematopoietic system. The main mechanisms of the signaling pathology in leukemias identified to date are: hypersensitivity to the WNT ligand, epigenetic repression of WNT antagonists, overexpression of WNT ligands, degradation of β-catenin in the cytoplasm, and changes in the activity of TCF/Lef transcription factors. The corresponding molecular changes are represented by overexpression of FZD protein, hypermethylation of the SFRP, DKK, WiF, Sox, and CXXC gene promoters, overexpression of Lef1 and plakoglobin, GSK3β mutation, and β-catenin phosphorylation by BCR-ABL kinase. The present review is devoted to the systematization of these data.Сигнальный путь WNT/β-катенин играет важную роль в дифференцировке и пролиферации клеток гемопоэза. В связи с этим в последние годы значительное внимание уделяется изучению роли нарушений передачи WNT-сигнала в патогенезе различных злокачественных новообразований кроветворной системы. Основными механизмами нарушения сигнального пути, выявленными к настоящему времени в лейкозах, являются: повышение чувствительности к WNT-лиганду, эпигенетическая репрессия WNT антагонистов, гиперэкспрессия WNT-лигандов, нарушения деградации β-катенина в цитоплазме и изменение активности TCF/Lef. Соответствующие молекулярные изменения представлены гиперэкспрессией FZD, гиперметилированием промоторов генов SFRP, DKK, WiF, Sox, CXXC, гиперэкспрессией Lef1 и плактоглобина, мутацией GSK3β и фосфорилированием β-катенина киназой BCR-ABL. Систематизации этих данных посвящен представленный обзор

Current Approaches for Personalized Therapy of Soft Tissue Sarcomas

Soft tissue sarcomas (STS) are a highly heterogeneous group of cancers of mesenchymal origin with diverse morphologies and clinical behaviors. While surgical resection is the standard treatment for primary STS, advanced and metastatic STS patients are not eligible for surgery. Systemic treatments, including standard chemotherapy and newer chemical agents, still play the most relevant role in the management of the disease. Discovery of specific genetic alterations in distinct STS subtypes allowed better understanding of mechanisms driving their pathogenesis and treatment optimization. This review focuses on the available targeted drugs or drug combinations based on genetic aberration involved in STS development including chromosomal translocations, oncogenic mutations, gene amplifications, and their perspectives in STS treatment. Furthermore, in this review, we discuss the possible use of chemotherapy sensitivity and resistance assays (CSRA) for the adjustment of treatment for individual patients. In summary, current trends in personalized management of advanced and metastatic STS are based on combination of both genetic testing and CSRA. © 2020 Kirill I. Kirsanov et al

Противоопухолевая активность кураксина CBL0137 на моделях острых лейкозов in vitro

Background. Curaxin CBL0137 is a novel non-genotoxic compound with anti-cancer activity based on CBL0137 ability of non-covalent interaction with DNA causing histone chaperone FACT relocation. Anti-cancer activity of this drug was demonstrated previously on the wide panel of solid cancer models in vitro and in vivo.Objectives. Estimation of anticancer effects of CBL0137 on the acute myeloblastic leukemia cells (THP-1) and acute lymphoblastic leukemia (CCRF-CEM).Materials and methods. CBL0137 cytotoxicity was analyzed using the MTT test, the effects on the cell cycle and the induction of apoptosis was assessed by flow cytometry, the activity of signaling pathways in cells treated with CBL0137 was determined by real-time polymerase chain reaction.Results. Cell treatment with CBL0137 led to cell cycle arrest and apoptosis induction. In the study of CBL0137 effect on target gene clusters of 10 signal transduction pathways involved in the pathogenesis of acute leukemia we have showed that CBL0137 inhibited the expression of down-stream genes of WNT and Hedgehog signaling in both cell lines. In THP-1 cells we also observed the inhibition of the expression of PPARγ target and hypoxia-activated genes. In CCRF-CEM cells CBL0137 also induced the expression of Notch signaling target genes.Conclusion. The antitumor activity of CBL0137 was demonstrated on acute leukemia cell cultures, the drug possesses cytotoxicity, causes cell cycle arrest and activation of apoptosis. Significant changes in the expression of efferent gene clusters of several signaling pathways were observed in the cells treated with CBL0137.Введение. Кураксин CBL0137 - новое негенотоксичное соединение, обладающее противоопухолевой активностью, в основе которой лежит способность препарата нековалентно взаимодействовать с ДНК, вызывая транслокацию гистонового шаперона FACT в хроматиновую фракцию. Ранее противоопухолевая активность этого агента была продемонстрирована относительно широкого спектра солидных опухолей in vitro и in vivo.Цель исследования - изучение противоопухолевой активности CBL0137 в отношении клеток острого миелобластного лейкоза (THP-1) и острого лимфобластного лейкоза (CCRF-CEM) in vitro.Материалы и методы. Для определения цитотоксичности CBL0137 использовали МТТ-тест, влияние на клеточный цикл и индукцию апоптоза оценивали с помощью проточной цитофлуориметрии, активность функционирования сигнальных путей при действии на клетки CBL0137 определяли с помощью полимеразной цепной реакции в реальном времени.Результаты. Обработка клеток CBL0137 приводит к аресту клеточного цикла и активации апоптоза. При исследовании влияния CBL0137 на кластеры таргетных генов 10 сигнальных путей, вовлеченных в онкогенез острых лейкозов, его ингибирующее действие было выявлено для сигнальных путей WNT и Hedgehog в обеих клеточных линиях. В клеточной линии THP-1 также наблюдалось ингибирование эфферентных генов PPARγ и генов, активирующихся при гипоксии. В клетках CCRF-CEM при действии CBL0137, кроме того, наблюдалось усиление экспрессии всех исследованных таргетных генов сигнального пути Notch.Заключение. На культурах клеток острых лейкозов продемонстрирована противоопухолевая активность CBL0137, препарат обладает цитотоксичностью, вызывает арест клеточного цикла и активацию апоптоза. При действии CBL0137 наблюдаются значительные изменения в экспрессии кластеров эфферентных генов сразу нескольких сигнальных путей