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    <title>DSpace Collection:</title>
    <link>http://dspace.hmtu.edu.vn/handle/DHKTYTHD_123/164</link>
    <description />
    <pubDate>Wed, 08 Apr 2026 03:51:44 GMT</pubDate>
    <dc:date>2026-04-08T03:51:44Z</dc:date>
    <item>
      <title>Pathogenesis and clinical implications of HIV-related anemia in 2013</title>
      <link>http://dspace.hmtu.edu.vn/handle/DHKTYTHD_123/421</link>
      <description>Title: Pathogenesis and clinical implications of HIV-related anemia in 2013
Authors: Redig, Amanda J.; Berliner, Nancy
Abstract: Anemia is a common feature of HIV-related disease and has been uniformly demonstrated to be an independent&#xD;
predictor of morbidity and mortality. Although anemia often responds to combination antiretroviral therapy, many&#xD;
patients remain anemic despite therapy and such persistent anemia continues to negatively affect prognosis&#xD;
regardless of drug response. Anemia is also a common feature of normal aging. We postulate that the pathophysiology&#xD;
of anemia in HIV, especially that which persists in the face of combination antiretroviral therapy, is a reflection of&#xD;
underlying proinflammatory pathways that are also thought to contribute to anemia in the elderly, as well as other&#xD;
age-related chronic diseases such as cardiovascular disease and chronic obstructive pulmonary disease. This&#xD;
suggests that HIV induces inflammatory pathways that are associated with a pattern of accelerated aging and that&#xD;
anemia is a biomarker of these processes. A better understanding of the pathophysiology of HIV-related anemia may&#xD;
provide important entry points for improving the chronic manifestations of HIV-related disease.</description>
      <content:encoded>Article</content:encoded>
      <pubDate>Tue, 01 Jan 2013 00:00:00 GMT</pubDate>
      <guid isPermaLink="false">https://ikr.inceif.org/retrieve/56b802c0-8f7d-44fc-9e5f-0303fb979ee6/Hematology-2013-Redig-377-81.pdf.jpg</guid>
      <dc:date>2013-01-01T00:00:00Z</dc:date>
    </item>
    <item>
      <title>Who benefits from allogeneic transplantation for myelodysplastic syndromes?: new insights</title>
      <link>http://dspace.hmtu.edu.vn/handle/DHKTYTHD_123/417</link>
      <description>Title: Who benefits from allogeneic transplantation for myelodysplastic syndromes?: new insights
Authors: Platzbecker, Uwe
Abstract: Recently, a refined cytogenetic and molecular classification fundamentally changed the prognostication of patients&#xD;
with myelodysplastic syndromes (MDS). The increasingly complex heterogeneity of this disease entity is mirrored by&#xD;
life expectancy rates ranging from almost a decade for very low-risk disease down to several months in higher-risk&#xD;
patients, even with conventional treatments. Intensive treatment approaches are hampered by the older age of most of&#xD;
the patients, potentially leading to an unacceptable adverse event rate. This is especially true for allogeneic&#xD;
hematopoietic stem cell transplantation (HCT), which, albeit of curative intent, can lead to considerable morbidity and&#xD;
mortality mostly as a result of organ toxicity, infectious complications, and GVHD. Furthermore, innovative drug&#xD;
developments, including hypomethylating agents, have broadened the therapeutic armamentarium and, although not&#xD;
curative, can lead to durable responses in subgroups of patients with higher-risk MDS. In fact, there is still no&#xD;
prospective randomized trial available that formally demonstrates the benefit of allogeneic HCT compared with&#xD;
standard treatments in MDS patients. In the absence of randomized data, when considering allogeneic HCT, emphasis&#xD;
should be put on patient selection and optimization of the pre- and posttransplantation treatment period. In these&#xD;
patients, a thorough comorbidity evaluation is mandatory and stratification according to age, cytogenetics, cytopenias,&#xD;
disease-related quality of life, and available alternative treatments should be performed in deciding whether, when, and&#xD;
how to perform allogeneic HCT.</description>
      <content:encoded>Article</content:encoded>
      <pubDate>Tue, 01 Jan 2013 00:00:00 GMT</pubDate>
      <guid isPermaLink="false">https://ikr.inceif.org/retrieve/c79489ce-0392-4d0d-b780-e10a29a119d2/Hematology-2013-Platzbecker-522-8.pdf.jpg</guid>
      <dc:date>2013-01-01T00:00:00Z</dc:date>
    </item>
    <item>
      <title>Core-binding factor acute myeloid leukemia: can we improve on HiDAC consolidation?</title>
      <link>http://dspace.hmtu.edu.vn/handle/DHKTYTHD_123/416</link>
      <description>Title: Core-binding factor acute myeloid leukemia: can we improve on HiDAC consolidation?
Authors: Paschka, Peter; Dohner, Konstanze
Abstract: Acute myeloid leukemia (AML) with t(8;21) or inv(16) is commonly referred to as core-binding factor AML&#xD;
(CBF-AML). The incorporation of high-dose cytarabine for postremission therapy has substantially improved the&#xD;
outcome of CBF-AML patients, especially when administered in the setting of repetitive cycles. For many years,&#xD;
high-dose cytarabine was the standard treatment in CBF-AML resulting in favorable long-term outcome in&#xD;
approximately half of the patients. Therefore, CBF-AML patients are generally considered to be a favorable AML&#xD;
group. However, a substantial proportion of patients cannot be cured by the current treatment. Additional genetic&#xD;
alterations discovered in CBF-AML help in our understanding of the process of leukemogenesis and some of them&#xD;
may refine the risk assessment in CBF-AML and, importantly, also serve as targets for novel therapeutic&#xD;
approaches. We discuss the clinical and genetic heterogeneity of CBF-AML, with a particular focus on the role of&#xD;
KIT mutations as a prognosticator, and also discuss recent efforts to target the KIT kinase in the context of existing&#xD;
therapeutic regimens.</description>
      <content:encoded>Article</content:encoded>
      <pubDate>Tue, 01 Jan 2013 00:00:00 GMT</pubDate>
      <guid isPermaLink="false">https://ikr.inceif.org/retrieve/2e6f47d8-184c-4455-83cb-a855d2f5dcab/Hematology-2013-Paschka-209-19.pdf.jpg</guid>
      <dc:date>2013-01-01T00:00:00Z</dc:date>
    </item>
    <item>
      <title>UnderstandingMYC-driven aggressive B-cell lymphomas: pathogenesis and classification</title>
      <link>http://dspace.hmtu.edu.vn/handle/DHKTYTHD_123/415</link>
      <description>Title: UnderstandingMYC-driven aggressive B-cell lymphomas: pathogenesis and classification
Authors: Ott, German; Rosenwald, Andreas; Campo3, Elias
Abstract: MYC is a potent oncogene initially identified as the target of the t(8;14)(q24;q32) chromosome translocation in Burkitt&#xD;
lymphoma. MYC gene alterations have been identified in other mature B-cell neoplasms that are usually associated&#xD;
with an aggressive clinical behavior. Most of these tumors originate in cells that do not normally express MYC protein.&#xD;
The oncogenic events leading to MYC up-regulation seem to overcome the inhibitory effect of physiological repressors&#xD;
such as BCL6 or BLIMP1. Aggressive lymphomas frequently carry additional oncogenic alterations that cooperate with&#xD;
MYC dysregulation, likely counteracting its proapoptotic function. The development of FISH probes and new reliable&#xD;
antibodies have facilitated the study of MYC gene alterations and protein expression in large series of patients,&#xD;
providing new clinical and biological perspectives regarding MYC dysregulation in aggressive lymphomas. MYC gene&#xD;
alterations in large B-cell lymphomas are frequently associated with BCL2 or BCL6 translocations conferring a very&#xD;
aggressive behavior. Conversely, MYC protein up-regulation may occur in tumors without apparent gene alterations,&#xD;
and its association with BCL2 overexpression also confers a poor prognosis. In this review, we integrate all of this new&#xD;
information and discuss perspectives, challenges, and open questions for the diagnosis and management of patients&#xD;
with MYC-driven aggressive B-cell lymphomas.</description>
      <content:encoded>Article</content:encoded>
      <pubDate>Tue, 01 Jan 2013 00:00:00 GMT</pubDate>
      <guid isPermaLink="false">https://ikr.inceif.org/retrieve/2882a9ad-a2b7-4d52-9695-fb01218f2ecd/Hematology-2013-Ott-575-83.pdf.jpg</guid>
      <dc:date>2013-01-01T00:00:00Z</dc:date>
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