Relevant bibliographies by topics / Neoplastic Leukemia

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  1. Journal articles
  2. Dissertations / Theses
  3. Books
  4. Book chapters
  5. Conference papers

Academic literature on the topic 'Neoplastic Leukemia'

Author: Grafiati
Published: 4 June 2021
Last updated: 1 February 2022

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Journal articles on the topic "Neoplastic Leukemia"

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Sandoval, Salemiz, Martina Pigazzi, and Kathleen M. Sakamoto. "CREB: A Key Regulator of Normal and Neoplastic Hematopoiesis." Advances in Hematology 2009 (2009): 1–8. http://dx.doi.org/10.1155/2009/634292.

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The cAMP response element-binding protein (CREB) is a nuclear transcription factor downstream of cell surface receptors and mitogens that is critical for normal and neoplastic hematopoiesis. Previous work from our laboratory demonstrated that a majority of patients with acute myeloid leukemia (AML) and acute lymphoid leukemia (ALL) overexpress CREB in the bone marrow. To understand the role of CREB in leukemogenesis, we examined the biological effect of CREB overexpression on primary leukemia cells, leukemia cell lines, and CREB overexpressing transgenic mice. Our results demonstrated that CREB overexpression leads to an increase in cellular proliferation and survival. Furthermore, CREB transgenic mice develop a myeloproliferative disorder with aberrant myelopoiesis in both the bone marrow and spleen. Additional research from other groups has shown that the expression of the cAMP early inducible repressor (ICER), a CREB repressor, is also deregulated in leukemias. And, miR-34b, a microRNA that negative regulates CREB expression, is expressed at lower levels in myeloid leukemia cell lines compared to that of healthy bone marrow. Taken together, these data suggest that CREB plays a role in cellular transformation. The data also suggest that CREB-specific signaling pathways could possibly serve as potential targets for therapeutic intervention.
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Azizidoost, Shirin, Sadegh Babashah, Fakher Rahim, Mohammad Shahjahani, and Najmaldin Saki. "Bone marrow neoplastic niche in leukemia." Hematology 19, no. 4 (November 25, 2013): 232–38. http://dx.doi.org/10.1179/1607845413y.0000000111.

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Sonneck, Karoline, Richard Fritz, Leonhard Muellauer, Karoline V. Gleixner, Matthias Mayerhofer, Stefan Florian, Marc Kerenyi, et al. "Detection of Activated STAT5 in the Cytoplasm of Neoplastic Cells in Patients with AML, CML, and Systemic Mastocytosis." Blood 108, no. 11 (November 1, 2006): 2305. http://dx.doi.org/10.1182/blood.v108.11.2305.2305.

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Abstract The signal transducer and activator of transcription 5 (STAT5) has recently been implicated as essential pro-oncogenic factor in the pathogenesis of myeloid leukemias in mice (Cancer Cell2005;7:87–99). More recently, STAT5 activation has also been described to occur in human leukemias. However, so far, little is known about the expression of activated/tyrosine phosphorylated STAT5 (pSTAT5) in various myeloid neoplasms and about the distribution of pSTAT5 in the cellular compartments of the normal and leukemic bone marrow (bm). We have examined the expression of pSTAT5 in the bm in patients with acute myeloid leukemia (AML, FAB M0, n=3, M1, n=6, M2, n=4, M3, n=5, M4, n=5, M5, n=4, M6, n=5, M7, n=4), chronic myeloid leukemia (CML, chronic phase, n=4, accelerated phase, n=5, blast phase, n=5), and systemic mastocytosis (SM, n=30), as well as in the normal bm (n=5). Expression of pSTAT5 was determined on paraffin-embedded bm sections by immunohistochemistry using the pSTAT5-specific antibody AX1. In the normal bm, the antibody AX1 was found to react with megakaryocytes and immature myeloid progenitor cells, whereas erythroid cells and mature granulocytic cells did not stain positive for AX1. In patients with AML and CML, the distribution of pSTAT5 showed a similar pattern. In fact, pSTAT5 was found to be expressed in leukemic blast cells without differences among FAB types as well as megakaryocytic cells, but not in erythroid cells. In patients with SM, neoplastic mast cells were found to be immunoreactive for pSTAT5. Interestingly, in all patients and all cells examined, pSTAT5 was found to be localized in the cytoplasm rather than in the nucleus. The cytoplasmic distribution of pSTAT5 in neoplastic cells was confirmed by immunocytochemical staining experiments performed on primary isolated neoplastic cells (AML, CML, mastocytosis) and respective cell lines (U937, KG1, K562, KU812, HMC-1). In each case, the reactivity of neoplastic cells with the AX1 antibody was abrogated by preincubation of the antibody with a pSTAT5-specific blocking peptide. Moreover, the expression of cytoplasmic pSTAT5 in the leukemic cell lines was demonstrable by flow cytometry. To study the molecular mechanisms underlying STAT5-activation in neoplastic cells, Ba/F3 cells with doxycycline-inducible expression of disease-specific oncoproteins, namely BCR/ABL (CML) and KIT-D816V (SM) were employed. Induction of these oncoproteins in Ba/F3 cells resulted in massive activation of pSTAT5 and DNA binding activity as shown by EMSA and supershift assays. In summary, our data show that neoplastic cells in AML, CML, and SM express cytoplasmic pSTAT5, and that disease-related oncoproteins contribute to STAT5-activation. The particular cytoplasmic localization of pSTAT5 in neoplastic cells suggests that apart from its function as a transcription factor, pSTAT5 may have an additional role as a cytoplasmic regulator in these malignancies.
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Freiman, Anatoli, Channy Y. Muhn, Michel Trudel, and Robin C. Billick. "Leukemia Cutis Presenting with Fingertip Hypertrophy." Journal of Cutaneous Medicine and Surgery 7, no. 1 (January 2003): 57–60. http://dx.doi.org/10.1177/120347540300700110.

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Background: Patients with leukemia often manifest cutaneous findings, which include nonspecific lesions and specific leukemic infiltrates termed leukemia cutis. Objective: A case of leukemia cutis involving distal finger pads is reported and literature describing hand involvement of specific leukemic infiltrates is reviewed. Methods and Results: An 80-year-old woman with a 10-year history of chronic lymphocytic leukemia developed painful symmetric tumors of her distal finger pads. Histopathological examination of the biopsy specimen revealed infiltration by neoplastic lymphocytes. Only a few cases of leukemia cutis involving the hands have been reported in the literature, none with this particular presentation. The clinical and histopathologic features of leukemia cutis are reviewed. Conclusion: This case emphasizes the importance of obtaining a biopsy specimen for histopathological examination of any suspicious skin lesion in a patient with leukemia.
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Digel, W., M. Schmid, G. Heil, P. Conrad, S. Gillis, and F. Porzsolt. "Human interleukin-7 induces proliferation of neoplastic cells from chronic lymphocytic leukemia and acute leukemias." Blood 78, no. 3 (August 1, 1991): 753–59. http://dx.doi.org/10.1182/blood.v78.3.753.753.

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Abstract The biologic effects of interleukin-7 (IL-7) and the expression of specific IL-7 membrane receptors on isolated neoplastic cells from previously untreated patients with chronic lymphocytic leukemia as well as acute leukemias were investigated in vitro. Leukemic cells were incubated for up to 6 days with various concentrations of IL-7 (0.01 to 2,000 U/mL). Neoplastic cells of the T- or B-phenotype from chronic as well as from acute leukemias proliferated in a dose-dependent manner. Cells from acute myeloid leukemias also proliferated in response to IL- 7. An optimal proliferative effect was achieved between 96 and 120 hours with 200 U/mL IL-7. Combinations of IL-7 with IL-2 and tumor necrosis factor-alpha showed an additive effect on [3H]TdR incorporation. IL-7 binding assays gave a value of approximately 33 to 180 high-affinity (kd approximately 20 pmol/L) binding sites/cell and approximately 241 to 3,280 low-affinity (kd approximately 600 pmol/L) binding sites/cell. Receptor expression correlated with the proliferation in response to IL-7. These data indicate that IL-7 can induce proliferation of relatively mature tumor cells, and that this effect is not restricted to the lymphoid lineage.
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Digel, W., M. Schmid, G. Heil, P. Conrad, S. Gillis, and F. Porzsolt. "Human interleukin-7 induces proliferation of neoplastic cells from chronic lymphocytic leukemia and acute leukemias." Blood 78, no. 3 (August 1, 1991): 753–59. http://dx.doi.org/10.1182/blood.v78.3.753.bloodjournal783753.

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The biologic effects of interleukin-7 (IL-7) and the expression of specific IL-7 membrane receptors on isolated neoplastic cells from previously untreated patients with chronic lymphocytic leukemia as well as acute leukemias were investigated in vitro. Leukemic cells were incubated for up to 6 days with various concentrations of IL-7 (0.01 to 2,000 U/mL). Neoplastic cells of the T- or B-phenotype from chronic as well as from acute leukemias proliferated in a dose-dependent manner. Cells from acute myeloid leukemias also proliferated in response to IL- 7. An optimal proliferative effect was achieved between 96 and 120 hours with 200 U/mL IL-7. Combinations of IL-7 with IL-2 and tumor necrosis factor-alpha showed an additive effect on [3H]TdR incorporation. IL-7 binding assays gave a value of approximately 33 to 180 high-affinity (kd approximately 20 pmol/L) binding sites/cell and approximately 241 to 3,280 low-affinity (kd approximately 600 pmol/L) binding sites/cell. Receptor expression correlated with the proliferation in response to IL-7. These data indicate that IL-7 can induce proliferation of relatively mature tumor cells, and that this effect is not restricted to the lymphoid lineage.
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Rezanka, Louis J., Jennifer L. Rojko, and James C. Neil. "Feline Leukemia Virus: Pathogenesis of Neoplastic Disease." Cancer Investigation 10, no. 5 (January 1992): 371–89. http://dx.doi.org/10.3109/07357909209024796.

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Gleixner, Karoline V., Mayerhofer Matthias, Anja Vales, Alexander Gruze, Michael Kneidinger, Gregor Hoermann, Maria T. Krauth, et al. "Targeting of Heat Shock Protein 32 (Hsp32) in Neoplastic Cells by Styrene Maleic Acid Zinc Protoporphyrin (SMA-ZnPP) Is Associated with Reduced Growth and Induction of Apoptosis." Blood 108, no. 11 (November 16, 2006): 4323. http://dx.doi.org/10.1182/blood.v108.11.4323.4323.

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Abstract Heat shock protein 32 (Hsp32), also known as heme oxygenase-1 (HO-1), is a stress-related survival factor that has recently been implicated in enhanced survival of neoplastic cells. We here show that Hsp32/HO-1 is expressed abundantly in primary neoplastic cells in various solid tumors and hematopoietic neoplasms such as acute myeloid leukemia (AML) or chronic myeloid leukemia (CML), and in respective cell lines including the AML cell lines HL60, KG1, KG1a, and U937, CML cell lines K562 and KU812, eosinophilic leukemia cell line EOL-1, mast cell leukemia cell line HMC-1, myeloma cell lines RPMI8226 and U266, breast cancer cell line MDA MB 231, lung cancer cell line A549, pancreatic carcinoma cell line BxPC-3, colon carcinoma cell lines COLO201, COLO205, COLO320DM, and DLD-1, and the ovarian carcinoma cell line OVCAR-3. Expression of Hsp32 mRNA was demonstrable by RT-PCR and Northern blotting, and expression of the Hsp32 protein by Western blotting and immunocytochemistry. The CML-specific oncoprotein BCR/ABL and the transforming oncoprotein KIT D816V that is expressed in neoplastic mast cells, were found to promote expression of Hsp32 in Ba/F3 cells. In order to examine the functional role of Hsp32 in neoplastic cells, a specific siRNA was employed. Expression of Hsp32 siRNA resulted in reduced viability and induction of apoptosis in all cell lines tested. To further explore the value of Hsp32 as a target in neoplastic cells, a novel specific Hsp32-targeting compound, styrene maleic acid copolymer zinc protoporphyrin micelles (SMA-ZnPP) was applied. Exposure to SMA-ZnPP resulted in a significant decrease in proliferation determined by 3H-thymidine uptake, in all cell lines as well as in all primary neoplastic cells tested (AML, n=5; CML, n=5; mastocytosis, n=3; breast cancer, n=2; lung cancer, n=1). As assessed by AnnexinV-staining, Tunel assay and electron microscopy, the growth-inhibitory effects of SMA-ZnPP were found to be associated with induction of apoptosis. In each cell type, the effect of SMA-ZnPP on growth was dose-dependent and found to occur at pharmacologic concentrations (IC50 1–30 μM). Moreover, SMA-ZnPP was found to synergize with various anti-neoplastic drugs (tumor cell lines: cisplatin, leukemias: cytarabine, myeloma: bortezomib) in producing growth inhibition. In summary, these data show that Hsp32/HO-1 is an important survival factor and novel interesting target in various hematopoietic and non-hematopoietic neoplasms. Based on these data, it seems desirable to explore the value of the Hsp32-targeting drug SMA-ZnPP in clinical trials in patients with leukemias and solid tumors.
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Ruan, Yongsheng, Hye Na Kim, Heather Ogana, and Yong-Mi Kim. "Wnt Signaling in Leukemia and Its Bone Marrow Microenvironment." International Journal of Molecular Sciences 21, no. 17 (August 28, 2020): 6247. http://dx.doi.org/10.3390/ijms21176247.

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Leukemia is an aggressive hematologic neoplastic disease. Therapy-resistant leukemic stem cells (LSCs) may contribute to the relapse of the disease. LSCs are thought to be protected in the leukemia microenvironment, mainly consisting of mesenchymal stem/stromal cells (MSC), endothelial cells, and osteoblasts. Canonical and noncanonical Wnt pathways play a critical role in the maintenance of normal hematopoietic stem cells (HSC) and LSCs. In this review, we summarize recent findings on the role of Wnt signaling in leukemia and its microenvironment and provide information on the currently available strategies for targeting Wnt signaling.
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Pandey, Sony, Mustafa Moazam, Kurtis Eisermann, Jeffrey Hord, Gail Fraizer, and Steven J. Kuerbitz. "The Importance of WT1 in Leukemia." Blood 118, no. 21 (November 18, 2011): 4645. http://dx.doi.org/10.1182/blood.v118.21.4645.4645.

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Abstract Abstract 4645 Acute leukemias collectively comprise the most common group of malignancies in the pediatric age group. Increasingly, therapeutic approach and prognosis are influenced by leukemia-specific cytogenetic abnormalities and genetic alterations, thus highlighting the importance of identifying novel prognostic markers. The Wilms’ tumor suppressor gene WT1 is expressed in leukemic blasts and is found to be mutated in approximately 10 percent of leukemia cases. Although it is unclear whether WT1 acts as an oncogene or a tumor suppressor gene in leukemia, it is known to regulate genes involved in cancer progression, including the angiogenic and mitogenic factor, VEGF. Previous studies in kidney and prostate cell lines identified potential WT1 binding sites on the VEGF-A gene promoter and demonstrated that WT1 transcriptionally regulated VEGF expression. Thus, we hypothesized that WT1 transcriptionally regulates VEGF expression in leukemia. To examine WT1 and VEGF expression patterns in pediatric Acute Lymphocytic Leukemia (ALL), Acute Myeloid Leukemia (AML) and non-neoplastic bone marrow samples, we performed quantitative real time PCR. It was observed that WT1 and VEGF expression varied depending upon the type and sub-type of leukemia. Furthermore, to understand the significance of WT1 expression, we over-expressed GFP- WT1 in Molt-4 cells (T-ALL), HL-60 (AML) and K562 cells (CML) and then quantified mRNA levels of VEGF and the potential WT1 target genes CCNA1 and JAG. The results showed that WT1 levels induced variable expression of VEGF, CCNA1 and JAG in these different leukemic cell lines. Elevated expression of WT1 genes harboring mutations of the zinc finger (ZF) DNA binding domain has also been described in a subset of leukemias and has been associated with a poor prognosis. We therefore screened pediatric acute leukemia samples for novel ZF mutations that would abrogate its ability to regulate VEGF and other target genes. Conversely, a well described SNP rs16754 (in exon 7 of the WT1 gene) identified as a good prognostic marker in Cytogenetically Normal AML (CN-AML) was observed in our pediatric population as both homozygous and heterozygous variants of the WT1 gene. Our long term goal is to determine the molecular basis of the prognostic impact associated with variant WT1 expression in pediatric and adult leukemias. Disclosures: No relevant conflicts of interest to declare.
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Dissertations / Theses on the topic "Neoplastic Leukemia"

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Scuderi, Richard. "G1-phase cyclin expression in neoplastic B cells /." Stockholm, 2002. http://diss.kib.ki.se/2002/91-7349-292-2/.

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Jackson, Marion Louise. "Molecular detection and analysis of feline leukemia virus (FeLV) long terminal repeat (LTR) sequences in neoplastic and non-neoplastic FeLV-induced diseases of domestic cats." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1996. http://www.collectionscanada.ca/obj/s4/f2/dsk3/ftp04/nq24060.pdf.

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Dimberg, Anna. "The role of Stat 1 in retinoic acid-induced myelomonocytic differentiation of human leukemia cells /." Uppsala : Acta Universitatis Upsaliensis : Univ.-bibl. [distributör], 2002. http://publications.uu.se/theses/91-554-5224-8/.

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Hultdin, Magnus. "Telomere analysis of normal and neoplastic hematopoietic cells : studies focusing on fluorescence in situ hybridization and flow cytometry." Doctoral thesis, Umeå University, Medical Biosciences, 2003. http://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-76.

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The telomeres are specialized structures at the end of the chromosomes composed of the repeated DNA sequence (TTAGGG)n and specific proteins bound to the DNA. The telomeres protect the chromosomes from degradation and end to end fusions. Due to the end-replication problem, the telomeric DNA shortens every cell division, forcing the cells into senescence at a critical telomere length. This process can be counteracted by activating a specialized enzyme, telomerase, which adds telomeric repeats to the chromosome ends leading to an extended or infinite cellular life span. Telomerase activity is absent in most somatic tissues but is found in germ cells, stem cells, activated lymphocytes and the vast majority of tumor cells and permanent cell lines. Hence, telomerase has been suggested as a target for cancer treatment as malignant cells almost exclusively express the enzyme and in that context telomere length measurements will be of great importance.

Telomere length is traditionally measured with a Southern blot based technique. A new method for telomere analysis of cells in suspension, called flow-FISH, was developed based on fluorescence in situ hybridization using a telomeric peptide nucleic acid (PNA) probe,

DNA staining with propidium iodide and quantification by flow cytometry. Flow-FISH had high reproducibility and the telomere length measurements showed good correlation with Southern blotting results. The flow-FISH technique also allows studies of cells in specific phases of the cell cycle and the replication timing of telomeric, centromeric and other repetitive sequences were analyzed in a number of cells. Like previous studies, centromeres were shown to replicate late in S phase while the telomere repeats were found to replicate early in S phase or concomitant with the bulk DNA, which is opposite to the patterns described in yeast.

In benign immunopurified lymphocytes from tonsils, high telomerase activity was found in germinal center (GC) B cells. This population also had high hTERT mRNA levels and displayed a telomere elongation as shown by flow-FISH and Southern blotting. Combined immunophenotyping and flow-FISH on unpurified tonsil cells confirmed the results.

Chronic lymphocytic leukemia (CLL), the most common leukemia in adults, can be divided into pre-GC CLL, characterized by unmutated immunoglobulin VH genes and worse prognosis, and post-GC CLL, with mutated VH genes and better prognosis. In 61 cases of CLL, telomere length was measured with Southern blotting and VH gene mutation status was analyzed. A new association was found between VH mutation status and telomere length, where cases with longer telomeres and mutated VH genes (post-GC CLL) had better prognosis

than CLL with short telomeres and unmutated VH genes (pre-GC CLL). A larger study of 112 CLL cases was performed using flow-FISH. The same correlation between telomere length and VH mutation status was found but gender seemed to be of importance as telomere length was a significant prognostic factor for the male CLL patients but not in the female group. Age of the patients and spread of disease seemed to affect the prognostic value of VH gene mutation status.

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Chen, Yaoyu. "Critical Molecular Pathways in Cancer Stem Cells of Chronic Myeloid Leukemia: A Dissertation." eScholarship@UMMS, 2011. https://escholarship.umassmed.edu/gsbs_diss/536.

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Chronic myeloid leukemia (CML) is a disease characterized by the expansion of granulocytic cells. The BCR-ABL tyrosine kinase inhibitor imatinib, the frontline treatment for Ph+ leukemias, can induce complete hematologic and cytogenetic response in most chronic phase CML patients. Despite the remarkable initial clinic effects, it is now recognized that imatinib will unlikely cure patients because a small cell population containing leukemic stem cells (LSCs) with self-renewal capacity is insensitive to tyrosine kinase inhibitors. In Chapter I, I briefly review the BCR-ABL kinase and its related signaling pathways. BCR-ABL kinase activates several signaling pathways including MAPK, STAT, and JNK/SAPK. BCR-ABL also mediates kinase-independent pathways through SRC family kinases. I will also discuss pathways involving β-catenin, hedgehog, FoxO and Alox5 are critical to the regulation of self-renewal and differentiation in LSC of CML. As detailed in Chapter II, I describe our work evaluating the effects of omacetaxine, a novel CML drug inducing cell apoptosis by inhibition of protein synthesis, on self-renewal and differentiation of LSCs and BCR-ABL-induced CML and acute lymphoblastic leukemia (B-ALL) in mice. We found that treatment with omacetaxine decreased the number of LSCs and prolonged the survival of mice with CML or B-ALL. In chapter III, I describe that Alox5 is an essential gene in the function of LSCs and CML development. We show evidence that Alox5 affects differentiation, cell division, and survival of long-term LSCs. Treatment of CML mice with a 5-LO inhibitor also impaired the function of LSCs similarly and prolonged survival. In chapter IV, I present evidence of our work showing a further dissection the Alox5 pathway by comparing the gene expression profiles of wild type and Alox5-/- LSCs. We show that Msr1 deletion causes acceleration of CML development. We also show that Msr1 affects CML development by regulating the PI3K-AKT pathway and β-catenin. Taken together, these results demonstrate that some pathways including Alox5 and Msr1 play an important role in regulating the self-renewal and differentiation of LSC. More efforts should be put into developing the novel strategies that may effectively target LSCs and thus cure CML.
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Zhang, Haojian. "The Molecular Mechanisms for Maintenance of Cancer Stem Cells in Chronic Myeloid Leukemia: A Dissertation." eScholarship@UMMS, 2012. https://escholarship.umassmed.edu/gsbs_diss/614.

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Chronic myeloid leukemia (CML) is a clonal hematopoietic stem cell disorder associated with the Philadelphia chromosome (Ph) that arises from a reciprocal translocation between chromosomes 9 and 22, thereby resulting in the formation of the chimeric BCR-ABL oncogene encoding a constitutively activated tyrosine kinase. BCR-ABL tyrosine kinase inhibitors (TKIs) induce a complete hematologic and cytogenetic response in the majority of chronic phrase CML patients. However, TKIs cannot efficiently eradicate leukemia stem cells (LSCs) because of the insensitivity of LSCs to TKIs. Therefore, developing new strategies to target LSCs is necessary and critical for curing CML, and success of this approach depends on further understanding the molecular mechanisms by which LSCs survive and are maintained. In Chapter I, I briefly introduce CML disease, BCR-ABL oncoprotein, and TKIs. I also describe the identification and features of LSCs. Several key pathways in LSCs including Wnt/ß-catenin, hedgehog, FoxO, Bcl6 and HIF1, are discussed. I also propose our strategy to identify unique molecular pathways that are important for LSCs but not their normal stem cell counterparts. In Chapter II, I describe our finding about the function of the positive regulator, HIF1α, in CML development and LSC survival. I show that loss of HIF1α impairs the maintenance of CML through impairing cell cycle progression and inducing apoptosis of LSCs, and I also report that p16Ink4a and p19Arf mediate the effect of HIF1α on LSCs, as knockdown of p16Ink4a and p19Arf rescues the defective colony-forming ability of HIF1α-/- LSCs. As detailed in Chapter III and IV, through comparing the global gene expression profiles of LSCs and HSCs, I find two novel regulators, Blk and Scd1, which act as tumor suppressors in CML development. In Chapter III, I show that Blk is markedly down-regulated by BCR-ABL in LSCs, and that c-Myc and Pax5 mediate this down-regulation. Deletion of Blk accelerates CML development; conversely, Blk overexpression significantly delays the development of CML and impairs the function of LSCs. I also demonstrate that p27, as a downstream effector, is involved in the function of Blk in LSCs. Blk also functions as a tumor suppressor in human CML stem cells, and inhibits the colony-forming ability of human CML cells. In Chapter IV, I investigate the function of another negative regulator, Scd1, in CML LSCs, and find that expression of Scd1 is down-regulated in mouse LSCs and human CML cells. We report that Scd1 acts as a tumor suppressor in CML, as loss of Scd1 causes acceleration of CML development and overexpression of Scd1 delays CML development. Using a colony-forming assay, I demonstrate that Scd1 impairs the maintenance of LSCs due to the change of expression of Pten, p53 and Bcl2. Importantly, I find that both Blk and Scd1 do not affect normal hematopoietic stem cells (HSCs) or hematopoiesis. Taken together, our findings demonstrate that HIF1α is required for the maintenance of CML LSCs, and conversely that Blk and Scd1 suppress the function of LSCs, suggesting that combining TKI treatment with specific targeting of LSCs will be necessary for curing CML.
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Hess, Patricia M. "Role of c-Jun NH-terminal Kinase in Bcr/Abl Induced Cell Transformation: a dissertation." eScholarship@UMMS, 2003. https://escholarship.umassmed.edu/gsbs_diss/88.

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The c-Jun NH2-terminal kinase (JNK) group of kinases include ten members that are created by alternative splicing of transcripts derived from Jnk1, Jnk2 and Jnk3 genes. The JNK1 and JNK2 protein kinases are ubiquitously expressed while JNK3 is expressed in a limited number of tissues. The JNK signaling pathway is implicated in multiple physiological processes including cell transformation. There is growing evidence that JNK signaling is involved in oncogenesis. Nevertheless, the role that JNK plays in malignant transformation is still unclear. The aim of this thesis is to examine the role of JNK in malignant transformation. For this purpose, I used the Bcr/Abl oncogene as a transforming agent. Bcr/Abl is a leukemogenic oncogene that is created by reciprocal translocation between chromosome 9 and 22. The translocation breakpoint is variable and several different Bcr/Abl isoforms have been identified such as Bcr/AblP185 and Bcr/AblP210, whose expression is associated with different types of leukemia. Bcr/Abl activates the JNK signaling pathway in hematopoietic cells and increases AP-1 transcription activity. Furthermore, dominant negative approaches demonstrate that inhibition of c-Jun or JNK prevents Bcr/ Abl-induced cell transformation in vitro. These data implicate the JNK signaling pathway in Bcr/Abl transformation although the role that JNK might have in this process is unclear. Thus, I examined the importance of JNK signaling in Bcr/Abl-induced lymphoid or myeloid transformation. For this purpose I compared Bcr/AblP185- and Bcr/AblP210- induced transformation of wild-type and JNK1-deficient cells using three approaches: in vitro, in vivo and ex vivo. The results obtained with the in vitro approach suggest that both Bcr/AblP185 and Bcr/AblP210 require JNK activity to induce lymphoid transformation. While JNK1-deficiency inhibits Bcr/AblP210 oncogenic potential in lymphoid cells both in vitro and in vivo, pharmacological inhibition of JNK activity (JNK1 and/or JNK2) blocked Bcr/AblP185 induced malignant proliferation in vitro. The differential requirement for JNK observed in the two Bcr/Abl isoforms can be ascribed to the presence in Bcr/AblP210 of the Dbl domain which can activate the JNK pathway in vitro. In the case of Bcr/AblP210, JNK1 is critical for the survival of the ex vivo derived transformed lymphoblasts upon growth factor removal. This result correlates with the fact that mice reconstituted with Bcr/AblP210 transformed Jnk1-l- bone marrow showed normal malignant lymphoid expansion in the bone marrow yet they had reduced numbers of lymphoblast in the bloodstream and lacked peripheral organ infiltration. Thus JNK1 is essential for the survival of the transformed lymphoblast outside the bone marrow microenvironment in Bcr/AblP210induced lymphoid leukemia. Interestingly, while JNK1 is essential for lymphoid transformation, it is dispensable for the proliferation of transformed myeloblasts. Taken together these results indicate that the JNK signaling pathway plays an essential role in the survival of Bcr/AblP210 lymphoblasts and that JNK-deficiency decreases the leukomogenic potential of Bcr/AblP210 in vivo. Thus, cell survival mediated by JNK may contribute to the pathogenesis of proliferative diseases.
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Phelan, James D. B. S. "Transcriptional Control of Normal Lymphopoiesis and T-cell Neoplasia by Growth Factor Independent 1." University of Cincinnati / OhioLINK, 2012. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1337351444.

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Rodrigues, Fernanda Odrzywolek. "Avaliação dos níveis séricos de BDNF em pacientes pediátricos com neoplasia." reponame:Biblioteca Digital de Teses e Dissertações da UFRGS, 2012. http://hdl.handle.net/10183/56619.

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INTRODUÇÃO: O câncer infantil representa cerca de 0,5 a 3% de todas as neoplasias da população em geral. Do ponto de vista clínico, os tumores infantis crescem rapidamente e são mais invasivos que as neoplasias adultas, porém respondem melhor ao tratamento e são considerados de melhor prognóstico. As neurotrofinas e seus receptores (receptores de quinase relacionados à tropomiosina - Trk) são importantes reguladores da sobrevivência, desenvolvimento e plasticidade neuronal. Além disso, estão envolvidas no processo oncogênico, podendo facilitar ou suprimir o crescimento tumoral. O BDNF (brain-derived neurotrophic factor) é uma das neurotrofinas e possui ligação específica com o receptor TrkB, e também está envolvida em diferentes processos corporais. OBJETIVOS: Avaliar os níveis séricos de BDNF em pacientes pediátricos (crianças e adolescentes) com algum tipo de neoplasia e indivíduos sem doença, e avaliar a sua relação com sexo, idade, valor de plaquetas e sobrevida. MATERIAL E MÉTODOS: Estudo transversal com crianças e adolescentes com idade entre zero a 18 anos. Foram incluídos no estudo 114 pacientes, sendo 72 pacientes do grupo de crianças com neoplasia e 42 do grupo controle. A análise dos níveis séricos de BDNF foi realizada através da técnica de ELISA. O projeto foi aprovado pelo Comitê de Ética em Pesquisa do HCPA. RESULTADOS: As medianas (P 25-75) dos valores de BDNF foram 2,45 (0,76-5,23) pg/ml para o grupo com LLA, 0,45 (0,08-0,80) pg/ml para o grupo com LMA, 9,0 (3,14-14,7) pg/ml para o grupo com linfomas e tumores sólidos e 6,08 (2,60-9,35) pg/ml para o grupo controle. Não houve diferença entre os valores de BDNF quando comparados as varíaveis sexo e idade entre os diferentes grupos. Em relação aos valores de BDNF e plaquetas, houveram diferenças significativas entre os grupos de Leucemias e os demais grupos. Pacientes com neoplasia que tinham valores de BNDF menores que 4,00 pg/ml apresentaram uma menor sobrevida (p<0,05). CONCLUSÃO: Os resultados mostram diferenças significativas nos níveis de BDNF em pacientes com tumores infanto-juvenil, principalmente entre as diferentes neoplasias e até mesmo podendo ter influência na sobrevida destes pacientes. Porém mais estudos são necessários para investigar o papel das neurotrofinas nesta população, para quem sabe no futuro serem utilizadas como biomarcadores ou novos alvos terapêuticos.
BACKGROUND: The childhood cancer represents about 0.5 to 3% of all cancers of the general population. From a clinical standpoint, infant tumors grow quickly and are more invasive than the adult cancers, but respond better to treatment and are considered a better prognosis. The neurotrophins and their receptors (tropomyosin-related kinase - Trk) are important regulators of survival, development and neuronal plasticity. They are also involved in the oncogenic process, which can facilitate or suppress tumor growth. BDNF (Brain-derived neurotrophic factor) is a neurotrophin that has a specific binding with the receptor TrkB, and is also involved in different bodily processes. This study aimed to evaluate the serum levels of BDNF in pediatric patients (children and adolescents) with some type of cancer and healthy individuals, as well its relationship with gender, age, platelet value and survival. PATIENTS AND METHODS: Cross-sectional study with children and adolescents aged zero to 18 years. The study included 114 patients, 72 patients in the group of children with cancer and 42 control group. Analysis of the serum levels of BDNF was performed by ELISA. The project was approved by the Ethics Committee of HCPA. RESULTS: The median (P 25-75) values of BDNF were 2,45 (0,76-5,23) pg/ml for the group with ALL, 0,45 (0,08-0,80) pg/ml for the group with LMA, 9,0 (3,14-14,7) pg/ml for the group with lymphomas and solid tumors and 6,08 (2,60-9,35) pg/ml in the control group. There was no difference between the values of BDNF compared the gender and age among the different groups. Regarding the values of BDNF and platelets, there were significant differences between groups of patients diagnosed with leukemias and other groups. Patients with cancer who had BDNF values lower than 4,00 pg/ml had a lower survival curve (p<0,05). CONCLUSION: The results show significant differences in BDNF levels in patients with tumors, especially among different tumors and even may have an influence on patient survival. But more studies are needed to investigate the role of neurotrophins in this population, who knows in the future be used as biomarkers or new therapeutic targets.
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10

Ganazza, Mônica Aparecida 1982. "Estudo de doença residual mínima em leucemia linfóide aguda da criança e do adolescente." [s.n.], 2014. http://repositorio.unicamp.br/jspui/handle/REPOSIP/312738.

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Orientador: José Andrés Yunes
Tese (doutorado) - Universidade Estadual de Campinas, Faculdade de Ciências Médicas
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Resumo: A leucemia linfóide aguda (LLA) é o câncer mais comum da infância. Os atuais protocolos de tratamento da LLA levam à cura em até 80% dos casos e parte do sucesso se deve à aplicação de diferentes tratamentos para os pacientes estratificados em diferentes grupos de risco. Contudo, pacientes considerados em remissão podem apresentar conteúdo substancial de células neoplásicas, a chamada doença residual mínima (DRM), cuja proliferação está associada com a recaída da doença e que podem estar em níveis indetectáveis pelas técnicas convencionais de análise morfológica. O atual protocolo do Grupo Brasileiro de Tratamento da Leucemia Infantil (GBTLI-LLA-2009) utiliza as análises da DRM para estratificar os pacientes em grupos de risco e assim determinar seu tratamento. Desta maneira o presente estudo objetivou (1) estudar a DRM por método qualitativo e quantitativo (RQ-PCR) em amostras D35 de 120 pacientes prospectivos admitidos para tratamento com o protocolo GBTLI-LLA-2009 no Centro Boldrini entre dezembro de 2009 e julho de 2013 (2) determinar a freqüência e sensibilidade dos rearranjos gênicos de imunoglobulinas e receptores de células T (3) analisar a realocação dos pacientes em grupos de risco em três pontos do tratamento (D8, D15 e D35) (4) buscar associações entre resultados de DRM no D35 e variáveis clínico-biológicas dos pacientes (5) analisar a sobrevida global nos pacientes (6) analisar o grau de concordância entre os resultados obtidos por PCR qualitativo e RQ-PCR no D35. Para a DRM no D15 as análises foram realizadas por citometria de fluxo pela equipe multidisciplinar do Centro Boldrini, já para DRM no D35 as análises foram feitas por PCR qualitativo e RQ-PCR com o uso de primers para a região VDJ das imunoglobulinas e receptores de células T. Observou-se que pelo menos 1 rearranjo gênico foi detectado ao diagnóstico para 98% dos casos estudados através de PCR qualitativo. Os rearranjos mais frequentes ao diagnóstico foram IGH , IGK, TCRG e TCRD para os casos de LLA-B derivada e TCRG, TCRD e Sil-Tal e IGH para os casos de LLA-T. Os primers paciente específicos para RQ-PCR mais sensíveis (sensibilidade 1x10-4) foram aqueles envolvendo rearranjos IGH, TCRD, TCRG e IGK. Associação entre presença de DRM no D35 detectada por RQ-PCR e idade dos pacientes (grupo <1 e ?9 anos) foi observada. Presença de DRM ?10-3 no D35 se mostrou relacionada com sobrevida global em pacientes com LLA-B derivada classificados como BR após análises de DRM no D15. Casos de LLA-B derivada classificados como BR após o D15 em sua maioria não apresentaram DRM nos pontos analisados (D15 e D35) sugerindo que a análise da DRM nesses casos seja dispensável. Já para os casos LLA-B derivada classificados como AR após o D15, 7 pacientes considerados bons respondedores no D15 mostraram-se respondedores lentos no D35 ressaltando a importância da análise da DRM nesse ponto do tratamento. Para casos com LLA-T o número reduzido de pacientes impediu qualquer conclusão a respeito. As duas metodologias aplicadas para as análises da DRM no D35 obtiveram concordância de 80% e 100% para LLA-B derivada e LLA-T, respectivamente
Abstract: Acute lymphoblastic leukemia (ALL) is the most common pediatric cancer. The recent ALL treatment protocols can achieve the complete remission in 80% of cases and this success is due to different treatments for patients stratified into different risk groups. Therefore, patients considered in remission may have substantial contents of neoplasic cells, the minimal residual disease (MRD). The proliferation of such neoplasic cells is associated with disease relapse and they can be undected by conventional methods. The current protocol of the Brazilian Childhood Leukemia Treatment (GBTLI-LLA-2009) uses the analysis of MRD to stratify patients into risk groups and thus determine their treatment. Thus this study aimed to (1) study the MRD for qualitative and quantitative method (RQ-PCR) at D35 from 120 prospective patients admitted for treatment with protocol GBTLI-LLA-2009 at Centro Boldrini between December 2009 and July 2013 (2) determine the frequency and sensitivity of immunoglobulin and T cell receptor gene rearrangements (3) analysis of the relocation of patients into risk groups in three points of treatment (D8, D15 and D35) (4) find associations between results of MRD at D35 and D15 and clinical-biological characteristics of patients (5) analyze the overall survival in patients (6) to analyze the degree of agreement between the results obtained by qualitative PCR and RQ-PCR in D35. MRD analyzes at D15 were performed by flow cytometry by the multidisciplinary team of the Centro Boldrini, MRD at D35 analyzes were performed by qualitative PCR and RQ-PCR using primers for the VDJ region of the immunoglobulin and T cell receptors. At least one gene rearrangement was detected at diagnosis to 98% of the cases studied by qualitative PCR. The most frequent rearrangements at diagnosis were IGH, IGK, TCRG and TCRD for cases of B-ALL derived and TCRG, TCRD and Sil-Tal and IGH in cases of T-ALL. The most sensitive RQ-PCR patient specific primers (sensitivity 1x10-4) were those involving IGH, TCRD, TCRD and IGK rearrangements. Association between presence of MRD in D35 detected by RQ-PCR and age group (<1 and ? 9 years) was observed. Presence of MRD ? 10-3 in D35 showed to be related with overall survival in patients with B-ALL derived classified as BR after analysis of MRD in D15. Cases of B-ALL derived classified as low risk after the D15 mostly showed no MRD in the analyzed points (D15 and D35) suggesting that the analysis of these cases is dispensable. As for the B-ALL derived cases classified as AR after D15, 7 patients considered good responders in D15 proved to be slow responders in D35 emphasizing the importance of analyzing MRD at this point of treatment. For T-ALL cases the small number of patients did not allow any conclusion. Both methodologies for the analysis of DRM in D35 obtained 80% and 100% of agreement for B-ALL derived and T-ALL respectively
Doutorado
Ciencias Biomedicas
Doutora em Ciências Médicas
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Books on the topic "Neoplastic Leukemia"

1

Neoplastic diseases of the blood. 5th ed. New York: Springer, 2013.

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N, Emmons Foxwell, ed. Atlas of differential diagnosis in neoplastic hematopathology. 2nd ed. London: Informa Healthcare, 2008.

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The chromosomes in human cancer and leukemia. 2nd ed. New York: Elsevier, 1990.

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A handbook of essential drugs and regimens in hematological oncology. Chur: Harwood Academic Publishers, 1991.

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H, Wiernik Peter, ed. Neoplastic diseases of the blood. 3rd ed. New York: Churchill Livingstone, 1996.

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M, Knowles Daniel, ed. Neoplastic hematopathology. 2nd ed. Philadelphia: Lippincott Williams & Wilkins, 2001.

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M, Knowles Daniel, ed. Neoplastic hematopathology. Baltimore: Williams & Wilkins, 1992.

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H, Wiernik Peter, ed. Neoplastic diseases of the blood. 2nd ed. New York: Churchill Livingstone, 1991.

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Wiernik, Peter H., Janice P. Dutcher, and Morie A. Gertz. Neoplastic Diseases of the Blood. Springer, 2018.

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Wiernik, Peter H., Janice P. Dutcher, and Morie A. Gertz. Neoplastic Diseases of the Blood. Springer, 2019.

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Book chapters on the topic "Neoplastic Leukemia"

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Hasserjian, Robert P. "Chronic Myelogenous Leukemia." In Neoplastic Hematopathology, 193–211. Totowa, NJ: Humana Press, 2009. http://dx.doi.org/10.1007/978-1-60761-384-8_10.

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Bueso-Ramos, Carlos E. "Acute Myeloid Leukemia." In Neoplastic Hematopathology, 145–63. Totowa, NJ: Humana Press, 2009. http://dx.doi.org/10.1007/978-1-60761-384-8_7.

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Sheehan, Andrea M. "Lymphoblastic Leukemia and Lymphoma." In Neoplastic Hematopathology, 239–50. Totowa, NJ: Humana Press, 2009. http://dx.doi.org/10.1007/978-1-60761-384-8_13.

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Lorsbach, Robert B. "Mouse Models of Myeloid Leukemia." In Neoplastic Hematopathology, 597–610. Totowa, NJ: Humana Press, 2009. http://dx.doi.org/10.1007/978-1-60761-384-8_37.

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Jones, Dan. "Approaches to Classification of Lymphoma and Leukemia." In Neoplastic Hematopathology, 3–20. Totowa, NJ: Humana Press, 2009. http://dx.doi.org/10.1007/978-1-60761-384-8_1.

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Schlette, Ellen. "Chronic Lymphocytic Leukemia and Small Lymphocytic Lymphoma." In Neoplastic Hematopathology, 251–61. Totowa, NJ: Humana Press, 2009. http://dx.doi.org/10.1007/978-1-60761-384-8_14.

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You, M. James. "Mouse Models of Lymphoma and Lymphoid Leukemia." In Neoplastic Hematopathology, 583–96. Totowa, NJ: Humana Press, 2009. http://dx.doi.org/10.1007/978-1-60761-384-8_36.

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Ravandi, Farhad. "Treatment of Acute Myeloid Leukemia and Myelodysplastic Syndromes." In Neoplastic Hematopathology, 165–76. Totowa, NJ: Humana Press, 2009. http://dx.doi.org/10.1007/978-1-60761-384-8_8.

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Jhatakia, Sejal A., Darren S. Sigal, and Alan Saven. "Hairy Cell Leukemia." In Neoplastic Diseases of the Blood, 121–34. New York, NY: Springer New York, 2012. http://dx.doi.org/10.1007/978-1-4614-3764-2_10.

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Wiernik, Peter H., Robert E. Gallagher, and Martin S. Tallman. "Acute Promyelocytic Leukemia." In Neoplastic Diseases of the Blood, 403–53. New York, NY: Springer New York, 2012. http://dx.doi.org/10.1007/978-1-4614-3764-2_23.

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Conference papers on the topic "Neoplastic Leukemia"

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Tonelli, Gabriel Bessa Tibery, Larissa Santana Barros, Neslayne Louise Campiol, and Willian Caetano Rodrigues. "DETECÇÃO PRECOCE DAS MANIFESTAÇÕES ORAIS NA LEUCEMIA MIELOIDE AGUDA." In I Congresso Brasileiro de Hematologia Clínico-laboratorial On-line. Revista Multidisciplinar em Saúde, 2021. http://dx.doi.org/10.51161/rems/635.

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Introdução: a leucemia mieloide aguda (LMA) caracteriza-se por mutações genéticas que afetam as células tronco de origem mieloide, resultando na proliferação descontrolada de células neoplásicas e imaturas, os blastos. Estes acumulam-se rapidamente na medula óssea, devido à alta taxa de multiplicação e interferem na hematopoiese normal de células saudáveis. As manifestações orais da LMA são comuns e podem aparecer na fase precoce da doença, sendo indispensável neste cenário o papel da equipe multidisciplinar, na qual o odontólogo pode detectar os sinais de alerta na cavidade oral, suspeitar de leucemia e encaminhar ao Hematologista. Objetivo: por meio de uma revisão integrativa da literatura, avaliar a incidência das manifestações orais como forma de diagnóstico precoce da LMA por meio da equipe multidisciplinar. Material e métodos: levantamento de artigos indexados nas bases de dados PubMed, Lilacs e Scielo a partir de 2000; por meio dos seguintes descritores: Leukemia AND oral manifestations. Primariamente, obtiveram-se 430 referências. Após aplicação dos critérios de exclusão/inclusão, restaram 26 artigos analisados no presente estudo. Resultados: a LMA, caracterizada pelo comprometimento da linhagem mieloide, é uma neoplasia mais frequente na idade adulta, porém, cerca 25% dos casos são pediátricos. Sinais e sintomas orais primários manifestam-se em aproximadamente 90% dos casos e consistem basicamente em: ulcerações, petéquias, púrpuras, sangramento oral espontâneo, hiperplasia gengival (acompanhada ou não de necrose), lábios fissurados, além de infecções oportunistas recorrentes. O grave sarcoma mieloide, um tumor extramedular sólido, surge em apenas 5% dos casos. Alguns autores destacam que pacientes com sangramentos orais ou púrpuras apresentam tempo de sobrevida reduzido em relação aos demais. Tais acometimentos também podem aparecer na leucemia crônica, porém não são específicos como na LMA. Conclusão: Em casos de LMA, as manifestações orais são muito prevalentes e de extrema importância para o diagnóstico precoce por meio da equipe multidisciplinar de saúde.
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