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1. Hara N, Nishiyama T, Takizawa I, Saito T, Kitamura Y, Takahashi K: Decline of the red blood cell count in patients receiving androgen deprivation therapy for localized prostate cancer: impact of ADT on insulin-like growth factor-1 and erythropoiesis. Urology; 2010 Jun;75(6):1441-5
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Decline of the red blood cell count in patients receiving androgen deprivation therapy for localized prostate cancer: impact of ADT on insulin-like growth factor-1 and erythropoiesis.
  • OBJECTIVES: To elucidate the mechanism of blood hemoglobin loss in patients with prostate cancer during androgen deprivation therapy (ADT), and to examine the activity of the growth hormone (GH)/insulin-like growth factor-1 (IGF-1) axis during ADT, which plays an important role in hematopoiesis.
  • The hemoglobin concentration and RBC count declined after ADT compared with those before treatment (P<.001 for each).
  • IGF-1 in the bone marrow erythroid progenitor cells might be functionally inactivated during ADT.
  • [MeSH-major] Androgen Antagonists / adverse effects. Prostate-Specific Antigen / blood. Prostatic Neoplasms / blood. Prostatic Neoplasms / drug therapy. Somatomedins / analysis
  • [MeSH-minor] Aged. Antineoplastic Agents, Hormonal / adverse effects. Antineoplastic Agents, Hormonal / therapeutic use. Biomarkers / blood. Biopsy, Needle. Cohort Studies. Erythrocyte Count. Erythropoiesis / drug effects. Follow-Up Studies. Humans. Immunohistochemistry. Male. Middle Aged. Neoplasm Staging. Probability. Prospective Studies. Risk Assessment. Statistics, Nonparametric. Treatment Outcome

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  • [Copyright] Copyright (c) 2010 Elsevier Inc. All rights reserved.
  • [CommentIn] Urology. 2010 Oct;76(4):1020 [20932425.001]
  • (PMID = 20110105.001).
  • [ISSN] 1527-9995
  • [Journal-full-title] Urology
  • [ISO-abbreviation] Urology
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Androgen Antagonists; 0 / Antineoplastic Agents, Hormonal; 0 / Biomarkers; 0 / Somatomedins; EC 3.4.21.77 / Prostate-Specific Antigen
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2. Gambero S, Canalli AA, Traina F, Albuquerque DM, Saad ST, Costa FF, Conran N: Therapy with hydroxyurea is associated with reduced adhesion molecule gene and protein expression in sickle red cells with a concomitant reduction in adhesive properties. Eur J Haematol; 2007 Feb;78(2):144-51
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Therapy with hydroxyurea is associated with reduced adhesion molecule gene and protein expression in sickle red cells with a concomitant reduction in adhesive properties.
  • The effect of hydroxyurea therapy (HUT) on the adhesive properties of sickle cells and the expression of adhesion molecule genes by erythroid cells of SCA individuals is not yet fully understood.
  • The expressions of the CD36 gene and the VLA-4-integrin subunit genes, CD49d (alpha-subunit) and CD29 (beta-subunit), were compared in the reticulocytes of steady-state SCA patients and patients on HUT using real-time PCR.
  • [MeSH-major] Anemia, Sickle Cell / drug therapy. Cell Adhesion / drug effects. Cell Adhesion Molecules / biosynthesis. Gene Expression Regulation / drug effects. Hydroxyurea / therapeutic use
  • [MeSH-minor] Adult. Antigens, CD29 / biosynthesis. Antigens, CD29 / genetics. Antigens, CD36 / biosynthesis. Antigens, CD36 / genetics. Drug Evaluation. Female. Fibronectins / metabolism. Gene Expression Profiling. Humans. Integrin alpha4 / biosynthesis. Integrin alpha4 / genetics. Integrin alpha4beta1 / biosynthesis. Integrin alpha4beta1 / genetics. Lutheran Blood-Group System. Male. Middle Aged. Neoplasm Proteins / biosynthesis. Neoplasm Proteins / genetics. RNA, Messenger / biosynthesis. Reticulocytes / metabolism. Reticulocytes / pathology

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  • (PMID = 17313560.001).
  • [ISSN] 0902-4441
  • [Journal-full-title] European journal of haematology
  • [ISO-abbreviation] Eur. J. Haematol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Denmark
  • [Chemical-registry-number] 0 / Antigens, CD29; 0 / Antigens, CD36; 0 / BCAM protein, human; 0 / Cell Adhesion Molecules; 0 / Fibronectins; 0 / Integrin alpha4beta1; 0 / Lutheran Blood-Group System; 0 / Neoplasm Proteins; 0 / RNA, Messenger; 143198-26-9 / Integrin alpha4; X6Q56QN5QC / Hydroxyurea
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3. Ge Y, LaFiura KM, Dombkowski AA, Chen Q, Payton SG, Buck SA, Salagrama S, Diakiw AE, Matherly LH, Taub JW: The role of the proto-oncogene ETS2 in acute megakaryocytic leukemia biology and therapy. Leukemia; 2008 Mar;22(3):521-9
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  • [Title] The role of the proto-oncogene ETS2 in acute megakaryocytic leukemia biology and therapy.
  • ETS2 transcripts measured by real-time RT-PCR were 1.8- and 4.1-fold, respectively, higher in DS and non-DS megakaryoblasts than those in non-DS myeloblasts.
  • In a doxycycline-inducible erythroleukemia cell line, K562pTet-on/ETS2, induction of ETS2 resulted in an erythroid to megakaryocytic phenotypic switch independent of GATA1 levels.
  • These results suggest that ETS2 expression is linked to the biology of AMkL in both DS and non-DS children, and that ETS2 acts by regulating expression of hematopoietic lineage and transcription factor genes involved in erythropoiesis and megakaryopoiesis, and in chemotherapy sensitivities.

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  • (PMID = 18094719.001).
  • [ISSN] 1476-5551
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA092308; United States / NCI NIH HHS / CA / R01 CA92308; United States / NIEHS NIH HHS / ES / P30 ES06639; United States / NIEHS NIH HHS / ES / P30 ES006639; United States / NCI NIH HHS / CA / T32 CA009531; United States / NCI NIH HHS / CA / R01 CA120772
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / ETS2 protein, human; 0 / GATA1 Transcription Factor; 0 / GATA1 protein, human; 0 / Neoplasm Proteins; 0 / Proto-Oncogene Protein c-ets-2; 04079A1RDZ / Cytarabine; ZS7284E0ZP / Daunorubicin
  • [Other-IDs] NLM/ NIHMS505525; NLM/ PMC3809919
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4. Palmieri G, Montella L, Lastoria S: [Thymoma and somatostatin analogs. Biology, diagnostic and clinical practice]. Minerva Endocrinol; 2001 Sep;26(3):193-5
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • In the presence of locally advanced, metastatic or inoperable disease, combined strategies including chemotherapy, radiotherapy and surgery are now being evaluated.
  • Scintigraphy with 111In DTPA-D-Phe 1 octreotide was used for the first time in a relevant series of patients with thymic tumour (13 cases) by our research group.
  • The presence of somatostatin receptors (ss-R) assayed in vivo provided the rationale for the use of a treatment based on the octreotide analog in a patient with thymoma and aplasia of the erythroid series (pure red cell aplasia, PRCA) in whom a complete response for the tumour and the remission of anemia was obtained.
  • The efficacy of this treatment was confirmed by our series of patients with chemoresistant thymic tumour and by national and international confirmations.
  • These data, ranging from in vivo diagnosis to treatment and the in vitro study of receptor expression, confirm that somatostatin plays a major role in thymic tumours.
  • [MeSH-major] Octreotide / analogs & derivatives. Pentetic Acid / analogs & derivatives. Somatostatin / therapeutic use. Thymoma / drug therapy. Thymus Neoplasms / drug therapy
  • [MeSH-minor] Antineoplastic Agents, Hormonal / administration & dosage. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Humans. Indium Radioisotopes. Neoplasm Proteins / analysis. Neoplasm Proteins / metabolism. Neoplasm Staging. Prednisone / administration & dosage. Protein Isoforms / analysis. Protein Isoforms / metabolism. Radiopharmaceuticals. Receptors, Somatostatin / analysis. Receptors, Somatostatin / metabolism. Red-Cell Aplasia, Pure / drug therapy. Treatment Outcome

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  • (PMID = 11753243.001).
  • [ISSN] 0391-1977
  • [Journal-full-title] Minerva endocrinologica
  • [ISO-abbreviation] Minerva Endocrinol.
  • [Language] ita
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Hormonal; 0 / Indium Radioisotopes; 0 / Neoplasm Proteins; 0 / Protein Isoforms; 0 / Radiopharmaceuticals; 0 / Receptors, Somatostatin; 142694-57-3 / SDZ 215-811; 51110-01-1 / Somatostatin; 7A314HQM0I / Pentetic Acid; RWM8CCW8GP / Octreotide; VB0R961HZT / Prednisone
  • [Number-of-references] 10
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5. Flora RS, Brito-Babapulle F, Naresh KN: Aberrant positivity for CD79a in erythroid lineage cells--a finding observed in a subset of re-staging bone marrow trephine biopsies after treatment cell pain. Haematologica; 2007 Jun;92(6):855-6
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  • [Title] Aberrant positivity for CD79a in erythroid lineage cells--a finding observed in a subset of re-staging bone marrow trephine biopsies after treatment cell pain.
  • Aberrant expression of CD79a has been reported in neoplastic cells in peripheral T cell lymphoma, T-cell acute lymphoblastic leukemia and acute myeloid leukemia (especially those with t(8;21)).
  • In this report, we document the first report of CD79a positivity in erythroid precursor cells in bone marrow.
  • In all, we document this finding in five of 18 re-staging bone marrow trephine samples in patients of lymphoma treated with chemotherapy (one index case and 17 additional validation cases).
  • [MeSH-major] Antigens, CD79 / analysis. Erythroid Precursor Cells / pathology. Lymphoma / diagnosis
  • [MeSH-minor] Biopsy. Bone Marrow / pathology. Humans. Neoplasm Staging. Pain. Up-Regulation

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  • (PMID = 17550863.001).
  • [ISSN] 1592-8721
  • [Journal-full-title] Haematologica
  • [ISO-abbreviation] Haematologica
  • [Language] eng
  • [Publication-type] Letter
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / Antigens, CD79
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6. Zhang P, Singh A, Yegnasubramanian S, Esopi D, Kombairaju P, Bodas M, Wu H, Bova SG, Biswal S: Loss of Kelch-like ECH-associated protein 1 function in prostate cancer cells causes chemoresistance and radioresistance and promotes tumor growth. Mol Cancer Ther; 2010 Feb;9(2):336-46
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  • [Title] Loss of Kelch-like ECH-associated protein 1 function in prostate cancer cells causes chemoresistance and radioresistance and promotes tumor growth.
  • Loss-of-function mutations in the nuclear factor erythroid-2-related factor 2 (Nrf2) inhibitor Kelch-like ECH-associated protein 1 (Keap1) result in increased Nrf2 activity in non-small cell lung cancer and confer therapeutic resistance.
  • Very low levels of Keap1 mRNA were detected in DU-145 cells, which significantly increased by treatment with DNA methyltransferase inhibitor 5-aza-deoxycytidine.
  • The loss of Keap1 function led to an enhanced activity of Nrf2 and its downstream electrophile/drug detoxification pathway.
  • Inhibition of Nrf2 expression in DU-145 cells by RNA interference attenuated the expression of glutathione, thioredoxin, and the drug efflux pathways involved in counteracting electrophiles, oxidative stress, and detoxification of a broad spectrum of drugs.
  • Attenuation of Nrf2 function in DU-145 cells enhanced sensitivity to chemotherapeutic drugs and radiation-induced cell death.
  • In addition, inhibition of Nrf2 greatly suppressed in vitro and in vivo tumor growth of DU-145 prostate cancer cells.
  • Thus, targeting the Nrf2 pathway in prostate cancer cells may provide a novel strategy to enhance chemotherapy and radiotherapy responsiveness and ameliorate the growth and tumorigenicity, leading to improved clinical outcomes.

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  • (PMID = 20124447.001).
  • [ISSN] 1538-8514
  • [Journal-full-title] Molecular cancer therapeutics
  • [ISO-abbreviation] Mol. Cancer Ther.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / P50 CA058236; United States / NCI NIH HHS / CA / CA058236-07S20016; United States / NCI NIH HHS / CA / P30 CA006973; United States / NIEHS NIH HHS / ES / P30 ES003819-22; United States / NCI NIH HHS / CA / P50 CA058184; United States / NIEHS NIH HHS / ES / P30ES03819; United States / NCI NIH HHS / CA / CA058184-14A18045; United States / NCI NIH HHS / CA / P50 CA058236-07S20016; United States / NCI NIH HHS / CA / P50 CA58236; United States / NCI NIH HHS / PC / PC073533; United States / NCI NIH HHS / CA / P50 CA058184-14A18045; United States / NIEHS NIH HHS / ES / P30 ES003819
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Adaptor Proteins, Signal Transducing; 0 / Cytoskeletal Proteins; 0 / Intracellular Signaling Peptides and Proteins; 0 / KEAP1 protein, human; 0 / Keap1 protein, mouse; 0 / NF-E2-Related Factor 2; 0 / NFE2L2 protein, human; 0 / Reactive Oxygen Species
  • [Other-IDs] NLM/ NIHMS167673; NLM/ PMC2821808
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7. Danet-Desnoyers GA, Luongo JL, Bonnet DA, Domchek SM, Vonderheide RH: Telomerase vaccination has no detectable effect on SCID-repopulating and colony-forming activities in the bone marrow of cancer patients. Exp Hematol; 2005 Nov;33(11):1275-80
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • OBJECTIVES: The telomerase reverse transcriptase hTERT is a widely expressed tumor-associated antigen recognized by cytotoxic T lymphocytes (CTL).
  • We have previously shown that vaccination of cancer patients against hTERT induces functional anti-tumor CTL in vivo, but it is not known whether hTERT vaccination harms normal cells expressing the enzyme, especially hematopoietic stem cells and progenitors.
  • PATIENTS AND METHODS: We employed colony-forming cell (CFC) assays, long-term in vitro cultures, and nonobese diabetic/severe combined immunodeficient (NOD/SCID) repopulation studies to evaluate the effects of hTERT vaccination on hematopoietic progenitors and stem cells in cancer patients following treatment.
  • RESULTS: Using bone marrow samples obtained from cancer patients before and after vaccination, we found that there was no significant decline in the frequency of granulocyte, macrophage or erythroid CFCs using CFC assays or long-term in vitro cultures.
  • CONCLUSION: These findings suggest that induction of tumor-lytic hTERT-specific T cells in vivo by vaccination does not result in a detectable decline in hematopoietic potential despite the expression of hTERT and major histocompatibility complex class I in bone marrow progenitors and stem cells.
  • Thus, even for self-antigens such as telomerase, tumor immunity does not necessarily involve autoimmunity in normal tissues that share the target.
  • [MeSH-major] Cancer Vaccines / pharmacology. Stem Cells / drug effects. Telomerase / therapeutic use. Vaccination / methods
  • [MeSH-minor] Animals. Antigens, Neoplasm / immunology. Antigens, Neoplasm / therapeutic use. Bone Marrow / drug effects. Breast Neoplasms / therapy. Cells, Cultured. Female. Hematopoietic Stem Cells / drug effects. Histocompatibility Antigens Class I / drug effects. Humans. Male. Mice. Mice, Inbred NOD. Mice, SCID. Prostatic Neoplasms / therapy. T-Lymphocytes, Cytotoxic / drug effects. Treatment Outcome

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  • (PMID = 16263411.001).
  • [ISSN] 0301-472X
  • [Journal-full-title] Experimental hematology
  • [ISO-abbreviation] Exp. Hematol.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA84050
  • [Publication-type] Clinical Trial, Phase I; Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Antigens, Neoplasm; 0 / Cancer Vaccines; 0 / Histocompatibility Antigens Class I; EC 2.7.7.49 / Telomerase
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8. Rassidakis GZ, Georgakis GV, Oyarzo M, Younes A, Medeiros LJ: Lack of c-kit (CD117) expression in CD30+ lymphomas and lymphomatoid papulosis. Mod Pathol; 2004 Aug;17(8):946-53
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  • c-Kit receptor (CD117) is expressed by erythroid, megakaryocytic, and myeloid precursors and mature mast cells and has been reported to be expressed in CD30+ lymphomas such as Hodgkin's disease and anaplastic large-cell lymphoma.
  • Imatinib mesylate, a well-established inhibitor of bcr-abl tyrosine kinase, and currently used for the treatment of patients with chronic myeloid leukemia, also inhibits c-kit receptor kinase activity.
  • In view of the possible use of imatinib as experimental therapy for patients with c-kit-positive tumors, we assessed c-kit expression in CD30+ cell lines and lymphomas.
  • Furthermore, treatment with imatinib did not inhibit proliferation of cell lines in vitro.
  • Our data demonstrate that expression of c-kit receptor is exceedingly rare among CD30+ lymphomas and lymphomatoid papulosis, suggesting that c-kit receptor is unlikely to be an appropriate target for therapeutic options such as imatinib in patients with these tumors.
  • [MeSH-minor] Antigens, CD30 / analysis. Antineoplastic Agents / pharmacology. Benzamides. Cell Division / drug effects. Cell Line, Tumor. Flow Cytometry. Hodgkin Disease / genetics. Hodgkin Disease / metabolism. Hodgkin Disease / pathology. Humans. Imatinib Mesylate. Immunohistochemistry. Piperazines / pharmacology. Pyrimidines / pharmacology. RNA, Messenger / genetics. RNA, Messenger / metabolism. RNA, Neoplasm / genetics. RNA, Neoplasm / metabolism. Reverse Transcriptase Polymerase Chain Reaction

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  • (PMID = 15105813.001).
  • [ISSN] 0893-3952
  • [Journal-full-title] Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc
  • [ISO-abbreviation] Mod. Pathol.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD30; 0 / Antineoplastic Agents; 0 / Benzamides; 0 / Piperazines; 0 / Pyrimidines; 0 / RNA, Messenger; 0 / RNA, Neoplasm; 8A1O1M485B / Imatinib Mesylate; EC 2.7.10.1 / Proto-Oncogene Proteins c-kit
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9. Sada E, Abe Y, Ohba R, Tachikawa Y, Nagasawa E, Shiratsuchi M, Takayanagi R: Vitamin K2 modulates differentiation and apoptosis of both myeloid and erythroid lineages. Eur J Haematol; 2010 Dec;85(6):538-48
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  • [Title] Vitamin K2 modulates differentiation and apoptosis of both myeloid and erythroid lineages.
  • The effects of VK2 on primary myeloid and erythroid progenitors were examined.
  • Mobilized CD34-positive cells from peripheral blood were used for the examination of myeloid lineage cells, and erythroid progenitors purified from peripheral blood were used for erythroid lineage cells.
  • In erythroid progenitors, VK2 did not show a significant effect on differentiation.
  • However, VK2 exhibited an anti-apoptotic effect on erythroid progenitors under erythropoietin depletion.
  • This anti-apoptotic effect was restricted to normal erythroid progenitors and was not shown in erythroleukemic cell line AS-E2.
  • The major effect of VK2 on myeloid progenitors was promoting differentiation, whereas its anti-apoptotic effect seemed to be dominant in erythroid progenitors.
  • Although the detailed mechanism of VK2's effect on differentiation or apoptosis of hematopoietic progenitors remains unknown, the effect of VK2 therapy in patients with MDS could be partly explained by these mechanisms.
  • [MeSH-major] Apoptosis / drug effects. Cell Differentiation / drug effects. Erythroid Precursor Cells / metabolism. Leukemia, Myeloid, Acute / metabolism. Myelodysplastic Syndromes / metabolism. Myeloid Progenitor Cells / metabolism. Vitamin K 2 / pharmacology. Vitamins / pharmacology
  • [MeSH-minor] Antigens, Differentiation / biosynthesis. Female. Gene Expression Regulation, Leukemic / drug effects. Humans. Male. Neoplasm Proteins / biosynthesis


10. Oh S, Kim Y, Kim J, Kwon D, Lee E: Elevated pressure, a novel cancer therapeutic tool for sensitizing cisplatin-mediated apoptosis in A549. Biochem Biophys Res Commun; 2010 Aug 13;399(1):91-7
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  • [Title] Elevated pressure, a novel cancer therapeutic tool for sensitizing cisplatin-mediated apoptosis in A549.
  • Intensive cancer therapy strategies have thus far focused on sensitizing cancer cells to anticancer drug-mediated apoptosis to overcome drug resistance, and this strategy has led to more effective cancer therapeutics.
  • Cisplatin (cis-diamminedichloroplatinum(II), CDDP) is an effective anticancer drug used to treat many types of cancer, including non-small cell lung carcinoma (NSCLC), and can be used in combination with various chemicals to enhance cancer cell apoptosis.
  • Here, we introduce the use of elevated pressure (EP) in combination with CDDP for cancer treatment and explore the effects of EP on CDDP-mediated apoptosis in NSCLC cells.
  • The transcriptional levels of transporter proteins indicated that the mechanism by which EP-induced CDDP sensitization was intracellular drug accumulation.
  • The protein levels of some antioxidants, such as hemeoxygenase-1 (HO-1), glutathione (GSH) and glutathione peroxidase (Gpx), were decreased in A549 cells exposed to EP via the down-regulation of the transcription factor nuclear factor (erythroid-derived 2)-like 2 (Nrf-2).
  • Furthermore, normal human fibroblasts were resistant to EP treatment, with no elevated DNA damage or apoptosis.
  • Collectively, these data show that administration of EP is a potential adjuvant tool for CDDP-based chemosensitivity of lung cancer cells that may reduce drug resistance.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Carcinoma, Non-Small-Cell Lung / therapy. Cisplatin / therapeutic use. Drug Resistance, Neoplasm. Lung Neoplasms / therapy. Pressure. Stress, Mechanical
  • [MeSH-minor] Apoptosis. Cell Line, Tumor. DNA Damage. DNA Repair / genetics. Heme Oxygenase-1 / antagonists & inhibitors. Heme Oxygenase-1 / genetics. Humans. NF-E2-Related Factor 2 / antagonists & inhibitors

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  • [Copyright] 2010 Elsevier Inc. All rights reserved.
  • (PMID = 20643104.001).
  • [ISSN] 1090-2104
  • [Journal-full-title] Biochemical and biophysical research communications
  • [ISO-abbreviation] Biochem. Biophys. Res. Commun.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / NF-E2-Related Factor 2; 0 / NFE2L2 protein, human; EC 1.14.99.3 / HMOX1 protein, human; EC 1.14.99.3 / Heme Oxygenase-1; Q20Q21Q62J / Cisplatin
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11. Batova A, Shao LE, Diccianni MB, Yu AL, Tanaka T, Rephaeli A, Nudelman A, Yu J: The histone deacetylase inhibitor AN-9 has selective toxicity to acute leukemia and drug-resistant primary leukemia and cancer cell lines. Blood; 2002 Nov 1;100(9):3319-24
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  • [Title] The histone deacetylase inhibitor AN-9 has selective toxicity to acute leukemia and drug-resistant primary leukemia and cancer cell lines.
  • In colony-forming assays, primary T-cell acute lymphoblastic leukemia (T-ALL) cells were 3-fold more sensitive to AN-9 than the normal hematopoietic progenitors, erythroid burst-forming units and granulocyte/monocyte colony-forming units.
  • More strikingly, samples from 2 infants with t(4;11) ALL obtained at diagnosis and relapse each were the most sensitive to AN-9, with IC(50) values of 25 microM and 17 microM, respectively.
  • Collectively, our results suggest that AN-9 is a selective agent for hematopoietic malignancies that can circumvent the mechanisms of chemoresistance limiting most conventional chemotherapy.
  • [MeSH-major] Butyrates / pharmacology. Drug Resistance, Neoplasm. Enzyme Inhibitors / pharmacology. Histone Deacetylase Inhibitors. Leukemia / pathology. Neoplasm Proteins / antagonists & inhibitors. Neoplasms / pathology. Neoplastic Stem Cells / drug effects
  • [MeSH-minor] Acetylation / drug effects. Acute Disease. Apoptosis / drug effects. Cell Division / drug effects. Child. Cyclin-Dependent Kinase Inhibitor p21. Cyclins / biosynthesis. Cyclins / genetics. Doxorubicin / pharmacology. Drug Resistance, Multiple / genetics. Drug Screening Assays, Antitumor. Gene Expression Regulation, Leukemic / drug effects. Gene Expression Regulation, Neoplastic / drug effects. Genes, MDR. HL-60 Cells / drug effects. Hematopoietic Stem Cells / drug effects. Hematopoietic Stem Cells / enzymology. Histones / metabolism. Humans. Infant. Inhibitory Concentration 50. Leukemia, Myeloid / enzymology. Leukemia, Myeloid / genetics. Leukemia, Myeloid / pathology. Leukemia-Lymphoma, Adult T-Cell / enzymology. Leukemia-Lymphoma, Adult T-Cell / genetics. Leukemia-Lymphoma, Adult T-Cell / pathology. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / enzymology. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / genetics. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / pathology. Protein Processing, Post-Translational / drug effects. Transfection. Tumor Cells, Cultured / drug effects. Tumor Cells, Cultured / enzymology. Tumor Stem Cell Assay

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  • (PMID = 12384433.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA 79951; United States / NCRR NIH HHS / RR / M01 RR 00827
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Butyrates; 0 / CDKN1A protein, human; 0 / Cyclin-Dependent Kinase Inhibitor p21; 0 / Cyclins; 0 / Enzyme Inhibitors; 0 / Histone Deacetylase Inhibitors; 0 / Histones; 0 / Neoplasm Proteins; 122110-53-6 / pivalyloxymethyl butyrate; 80168379AG / Doxorubicin
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12. Asano Y, Niho Y: Treatment of myelodysplastic syndromes. Int J Clin Oncol; 2001 Apr;6(2):74-9
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  • [Title] Treatment of myelodysplastic syndromes.
  • The IPSS scoring system is useful to establish the appropriate treatment plan in MDS.
  • Serum Epo levels and need for transfusion serve as good predictors of the erythroid response to the combination of Epo and G-CSF.
  • Subgroups of MDS patients may respond favorably to immunosuppressive therapies such as CyA and ATG.
  • Low-dose chemotherapy may also improve peripheral blood counts.
  • High-dose chemotherapy may lead to complete remission in about half of MDS patients, but the duration of remission is often short.
  • The only proven curative therapy for MDS is allogeneic stem cell transplantation, resulting in an overall disease-free survival rate of about 40%.
  • Because the clinical features of patients with MDS are quite heterogeneous, the development of more accurate predictive models may be necessary to improve the efficacy of treatment.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Growth Substances / therapeutic use. Hematopoietic Stem Cell Transplantation. Immunosuppressive Agents / therapeutic use. Myelodysplastic Syndromes / drug therapy. Neoplasm Staging
  • [MeSH-minor] Granulocyte Colony-Stimulating Factor / therapeutic use. Humans. Karyotyping. Patient Care Planning. Prognosis. Risk Factors

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  • (PMID = 11706753.001).
  • [ISSN] 1341-9625
  • [Journal-full-title] International journal of clinical oncology
  • [ISO-abbreviation] Int. J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Growth Substances; 0 / Immunosuppressive Agents; 143011-72-7 / Granulocyte Colony-Stimulating Factor
  • [Number-of-references] 29
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13. Niitsu N, Umeda M, Honma Y: Myeloid and monocytoid leukemia cells have different sensitivity to differentiation-inducing activity of deoxyadenosine analogs. Leuk Res; 2000 Jan;24(1):1-9
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  • Monocytoid leukemia cells were more sensitive to the analogs than were erythroid or myeloid leukemia cells based on the inhibition of cell growth and induction of cell differentiation.
  • Monocytoid leukemia cells were highly sensitive to combined treatment with 2'-deoxycoformycin (dCF) and 9-beta-D-arabinofuranosyladenine (Ara A) for inducing cell differentiation.
  • These findings indicate that dCF + Ara A and CdA may be effective for the therapy of acute monocytoid and myeloid leukemia, respectively.
  • [MeSH-major] Antimetabolites, Antineoplastic / pharmacology. Cladribine / pharmacology. Leukemia, Myeloid / pathology. Monocytes / drug effects. Neoplastic Stem Cells / drug effects. Vidarabine / analogs & derivatives. Vidarabine / pharmacology
  • [MeSH-minor] Acute Disease. Adenosine Deaminase Inhibitors. Calcitriol / pharmacology. Cell Differentiation / drug effects. Deoxyadenosines / pharmacology. Dose-Response Relationship, Drug. Drug Synergism. Enzyme Inhibitors / pharmacology. HL-60 Cells / drug effects. Humans. K562 Cells / drug effects. Neoplasm Proteins / antagonists & inhibitors. Pentostatin / pharmacology. Tretinoin / pharmacology. Tumor Cells, Cultured / drug effects. U937 Cells / drug effects

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  • (PMID = 10634639.001).
  • [ISSN] 0145-2126
  • [Journal-full-title] Leukemia research
  • [ISO-abbreviation] Leuk. Res.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] ENGLAND
  • [Chemical-registry-number] 0 / Adenosine Deaminase Inhibitors; 0 / Antimetabolites, Antineoplastic; 0 / Deoxyadenosines; 0 / Enzyme Inhibitors; 0 / Neoplasm Proteins; 14365-44-7 / 5'-amino-5'-deoxyadenosine; 395575MZO7 / Pentostatin; 47M74X9YT5 / Cladribine; 5688UTC01R / Tretinoin; FA2DM6879K / Vidarabine; FXC9231JVH / Calcitriol; P2K93U8740 / fludarabine
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14. Richard RE, Wood B, Zeng H, Jin L, Papayannopoulou T, Blau CA: Expansion of genetically modified primary human hemopoietic cells using chemical inducers of dimerization. Blood; 2000 Jan 15;95(2):430-6
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  • The inability to deliver a therapeutic gene to a sufficient percentage of hematopoietic stem cells is the major obstacle to using gene therapy to treat blood disorders.
  • The cell type that emerged in suspension culture was erythroid.
  • [MeSH-major] Cytokines / pharmacology. Erythroid Precursor Cells / cytology. Genetic Therapy / methods. Hematopoietic Stem Cells / cytology. Immunophilins / genetics. Neoplasm Proteins. Receptors, Cytokine
  • [MeSH-minor] Animals. Antigens, CD34 / blood. Cell Culture Techniques / methods. Cell Division / drug effects. Cells, Cultured. Colony-Forming Units Assay. Dimerization. Fetal Blood / cytology. Genetic Vectors. Humans. Infant, Newborn. Mice. Point Mutation. Proto-Oncogene Proteins / physiology. Receptors, Thrombopoietin. Recombinant Proteins / biosynthesis. Retroviridae. Signal Transduction / drug effects. Tacrolimus Binding Proteins

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  • (PMID = 10627446.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Grant] United States / NIDDK NIH HHS / DK / 1R01DK5299701; United States / NIDDK NIH HHS / DK / 1R01DK57525; United States / NHLBI NIH HHS / HL / 5P01HL53750; etc
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] UNITED STATES
  • [Chemical-registry-number] 0 / Antigens, CD34; 0 / Cytokines; 0 / Neoplasm Proteins; 0 / Proto-Oncogene Proteins; 0 / Receptors, Cytokine; 0 / Receptors, Thrombopoietin; 0 / Recombinant Proteins; 143641-95-6 / MPL protein, human; EC 5.2.1.- / Tacrolimus Binding Proteins; EC 5.2.1.8 / Immunophilins
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15. Singh A, Boldin-Adamsky S, Thimmulappa RK, Rath SK, Ashush H, Coulter J, Blackford A, Goodman SN, Bunz F, Watson WH, Gabrielson E, Feinstein E, Biswal S: RNAi-mediated silencing of nuclear factor erythroid-2-related factor 2 gene expression in non-small cell lung cancer inhibits tumor growth and increases efficacy of chemotherapy. Cancer Res; 2008 Oct 1;68(19):7975-84
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  • [Title] RNAi-mediated silencing of nuclear factor erythroid-2-related factor 2 gene expression in non-small cell lung cancer inhibits tumor growth and increases efficacy of chemotherapy.
  • Nuclear factor erythroid-2-related factor 2 (Nrf2) is a redox-sensitive transcription factor that regulates the expression of electrophile and xenobiotic detoxification enzymes and efflux proteins, which confer cytoprotection against oxidative stress and apoptosis in normal cells.
  • In this study, we show that constitutive activation of Nrf2 in lung cancer cells promotes tumorigenicity and contributes to chemoresistance by up-regulation of glutathione, thioredoxin, and the drug efflux pathways involved in detoxification of electrophiles and broad spectrum of drugs.
  • RNAi-mediated reduction of Nrf2 expression in lung cancer cells induces generation of reactive oxygen species, suppresses tumor growth, and results in increased sensitivity to chemotherapeutic drug-induced cell death in vitro and in vivo.
  • Inhibiting Nrf2 expression using naked siRNA duplexes in combination with carboplatin significantly inhibits tumor growth in a subcutaneous model of lung cancer.
  • Thus, targeting Nrf2 activity in lung cancers, particularly those with Keap1 mutations, could be a promising strategy to inhibit tumor growth and circumvent chemoresistance.

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  • (PMID = 18829555.001).
  • [ISSN] 1538-7445
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] ENG
  • [Grant] United States / NIEHS NIH HHS / ES / ES003819-17; United States / NIEHS NIH HHS / ES / P30 ES003819-20; United States / NHLBI NIH HHS / HL / R01 HL081205; United States / NCI NIH HHS / CA / P50 CA058184-13; United States / NIEHS NIH HHS / ES / P30 ES003819-17; United States / NHLBI NIH HHS / HL / R01 HL081205-04; United States / NCI NIH HHS / CA / P50 CA058184; United States / NIEHS NIH HHS / ES / P30ES03819; United States / NCI NIH HHS / CA / CA104253-02; United States / NCI NIH HHS / CA / R01 CA104253; United States / NCI NIH HHS / CA / R01 CA104253-02; United States / NIEHS NIH HHS / ES / ES003819-20; United States / NIEHS NIH HHS / ES / P30 ES003819; United States / NHLBI NIH HHS / HL / HL081205-04
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Intracellular Signaling Peptides and Proteins; 0 / KEAP1 protein, human; 0 / NF-E2-Related Factor 2; 0 / RNA, Small Interfering
  • [Other-IDs] NLM/ NIHMS280693; NLM/ PMC3070411
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16. Singh A, Misra V, Thimmulappa RK, Lee H, Ames S, Hoque MO, Herman JG, Baylin SB, Sidransky D, Gabrielson E, Brock MV, Biswal S: Dysfunctional KEAP1-NRF2 interaction in non-small-cell lung cancer. PLoS Med; 2006 Oct;3(10):e420
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  • BACKGROUND: Nuclear factor erythroid-2 related factor 2 (NRF2) is a redox-sensitive transcription factor that positively regulates the expression of genes encoding antioxidants, xenobiotic detoxification enzymes, and drug efflux pumps, and confers cytoprotection against oxidative stress and xenobiotics in normal cells.
  • Increased expression of cellular antioxidants and xenobiotic detoxification enzymes has been implicated in resistance of tumor cells against chemotherapeutic drugs.
  • Evaluation of loss of heterozygosity at 19p13.2 revealed allelic losses in 61% of the NSCLC cell lines and 41% of the tumor samples.
  • Decreased KEAP1 activity in cancer cells induced greater nuclear accumulation of NRF2, causing enhanced transcriptional induction of antioxidants, xenobiotic metabolism enzymes, and drug efflux pumps.
  • Loss of KEAP1 function leading to constitutive activation of NRF2-mediated gene expression in cancer suggests that tumor cells manipulate the NRF2 pathway for their survival against chemotherapeutic agents.

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  • (PMID = 17020408.001).
  • [ISSN] 1549-1676
  • [Journal-full-title] PLoS medicine
  • [ISO-abbreviation] PLoS Med.
  • [Language] ENG
  • [Grant] United States / NIEHS NIH HHS / ES / P30 ES 038819; United States / NHLBI NIH HHS / HL / R01 HL081205-03; United States / NHLBI NIH HHS / HL / R01 HL081205; United States / NCI NIH HHS / CA / P50 CA058184; United States / NHLBI NIH HHS / HL / HL081205; United States / NHLBI NIH HHS / HL / HL081205-03
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Intracellular Signaling Peptides and Proteins; 0 / KEAP1 protein, human; 0 / NF-E2-Related Factor 2; 0 / NFE2L2 protein, human
  • [Other-IDs] NLM/ PMC1584412
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17. Lum BL, Kaubisch S, Fisher GA, Brown BW, Sikic BI: Effect of high-dose cyclosporine on etoposide pharmacodynamics in a trial to reverse P-glycoprotein (MDR1 gene) mediated drug resistance. Cancer Chemother Pharmacol; 2000;45(4):305-11
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  • [Title] Effect of high-dose cyclosporine on etoposide pharmacodynamics in a trial to reverse P-glycoprotein (MDR1 gene) mediated drug resistance.
  • PURPOSE: The consequences of using cyclosporine (CsA) therapy to modulate P-glycoprotein-mediated multidrug resistance include increased myelosuppression, hyperbilirubinemia, and altered disposition of the cytotoxin.
  • Serial plasma etoposide concentration-time samples were assayed by high-performance liquid chromatography (HPLC).
  • The percent decrease in white blood cell (WBC) count and the total or unbound etoposide AUC relationship was fitted to a sigmoid Emax model adapted for paired observations, where: % Decrease in WBC count =E(max) x PDRV(H+Z x delta)/(PDRV50 + Z x beta) + PDRVH + Z x delta In this equation, Z was the variable describing the two treatment groups (0 = no CsA and 1 = CsA).
  • The fitted parameters were PDRV50, the pharmacodynamic response variable (PDRV) producing 50% of the maximal response; parameter beta, which describes the effect of the treatment group on the PDRV50; parameter H (Hill constant), which defines the slope of the response curve and parameter delta, which describes the effect of the treatment group on parameter H.
  • This paralleled a 12% greater median percent decrease in WBC count during etoposide + CsA treatment (72% vs. 84%, P = 0.03).
  • The fitted parameter-estimates suggested that at equivalent unbound etoposide AUC values above 10 microg x h/ml, the sigmoid Emax model predicted a 5% greater WBC count suppression when CsA was added to the treatment regimen.
  • [MeSH-minor] Adult. Aged. Area Under Curve. Bone Marrow Diseases / blood. Bone Marrow Diseases / chemically induced. Chromatography, High Pressure Liquid. Drug Resistance, Neoplasm. Erythroid Precursor Cells / drug effects. Female. Humans. Infusions, Intravenous. Leukocyte Count / drug effects. Leukopenia / chemically induced. Male. Middle Aged

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  • (PMID = 10755319.001).
  • [ISSN] 0344-5704
  • [Journal-full-title] Cancer chemotherapy and pharmacology
  • [ISO-abbreviation] Cancer Chemother. Pharmacol.
  • [Language] eng
  • [Grant] United States / NCRR NIH HHS / RR / M01 RR00070; United States / NCI NIH HHS / CA / R01CA52168
  • [Publication-type] Clinical Trial; Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] GERMANY
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Phytogenic; 0 / Immunosuppressive Agents; 6PLQ3CP4P3 / Etoposide; 83HN0GTJ6D / Cyclosporine
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18. Magalhães IQ, Splendore A, Emerenciano M, Córdoba MS, Córdoba JC, Allemand PA, Ferrari I, Pombo-de-Oliveira MS: Transient neonatal myeloproliferative disorder without Down syndrome and detection of GATA1 mutation. J Pediatr Hematol Oncol; 2005 Jan;27(1):50-2
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  • [Title] Transient neonatal myeloproliferative disorder without Down syndrome and detection of GATA1 mutation.
  • The authors report an unusual case of a newborn without constitutional trisomy 21 who developed undifferentiated leukemia and subsequently achieved clinical and molecular remission without chemotherapy.
  • [MeSH-minor] Base Sequence. Erythroid-Specific DNA-Binding Factors. Female. GATA1 Transcription Factor. Humans. Infant, Newborn. Leukocytes / physiology. Mutation. Neoplasm Regression, Spontaneous

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  • (PMID = 15654280.001).
  • [ISSN] 1077-4114
  • [Journal-full-title] Journal of pediatric hematology/oncology
  • [ISO-abbreviation] J. Pediatr. Hematol. Oncol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / DNA-Binding Proteins; 0 / Erythroid-Specific DNA-Binding Factors; 0 / GATA1 Transcription Factor; 0 / GATA1 protein, human; 0 / Transcription Factors
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19. See HT, Thomas DA, Bueso-Ramos C, Kavanagh J: Secondary leukemia after treatment with paclitaxel and carboplatin in a patient with recurrent ovarian cancer. Int J Gynecol Cancer; 2006 Jan-Feb;16 Suppl 1:236-40
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  • [Title] Secondary leukemia after treatment with paclitaxel and carboplatin in a patient with recurrent ovarian cancer.
  • The occurrence of myelodysplastic syndrome (MDS) or acute myeloid leukemia (AML) has been reported after treatment with cytotoxic alkylating agent-based chemotherapy for solid tumors.
  • We report a patient with metastatic ovarian carcinoma treated with carboplatin and paclitaxel, who developed secondary acute erythroid leukemia.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / adverse effects. Leukemia, Erythroblastic, Acute / chemically induced. Liver Neoplasms / therapy. Neoplasms, Glandular and Epithelial / therapy. Ovarian Neoplasms / therapy
  • [MeSH-minor] Arm. Busulfan / administration & dosage. Carboplatin / administration & dosage. Carboplatin / adverse effects. Cytarabine / administration & dosage. Fatal Outcome. Female. Gynecologic Surgical Procedures. Humans. Idarubicin / administration & dosage. Leiomyosarcoma / surgery. Middle Aged. Neoplasm Recurrence, Local. Neoplasm, Residual. Neoplasms, Second Primary. Paclitaxel / administration & dosage. Paclitaxel / adverse effects. Reoperation. Stem Cell Transplantation. Vidarabine / administration & dosage. Vidarabine / analogs & derivatives

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  • (PMID = 16515597.001).
  • [ISSN] 1048-891X
  • [Journal-full-title] International journal of gynecological cancer : official journal of the International Gynecological Cancer Society
  • [ISO-abbreviation] Int. J. Gynecol. Cancer
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 04079A1RDZ / Cytarabine; BG3F62OND5 / Carboplatin; FA2DM6879K / Vidarabine; G1LN9045DK / Busulfan; P2K93U8740 / fludarabine; P88XT4IS4D / Paclitaxel; ZRP63D75JW / Idarubicin
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20. Ray S, Lu Y, Kaufmann SH, Gustafson WC, Karp JE, Boldogh I, Fields AP, Brasier AR: Genomic mechanisms of p210BCR-ABL signaling: induction of heat shock protein 70 through the GATA response element confers resistance to paclitaxel-induced apoptosis. J Biol Chem; 2004 Aug 20;279(34):35604-15
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  • Chronic myelogenous leukemia (CML) results from a t(9,22) translocation, producing the p210(BCR-ABL) oncoprotein, a tyrosine kinase that causes transformation and chemotherapy resistance.
  • To further understand mechanisms mediating chemotherapy resistance, we identified 556 differentially regulated genes in HL-60 cells stably expressing p210(BCR-ABL) versus those expressing an empty vector using cDNA macro- and oligonucleotide microarrays.
  • We suggest that down-regulation of the GATA-Hsp70 pathway may be useful in the treatment of chemotherapy-resistant CML.

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  • (PMID = 15155749.001).
  • [ISSN] 0021-9258
  • [Journal-full-title] The Journal of biological chemistry
  • [ISO-abbreviation] J. Biol. Chem.
  • [Language] ENG
  • [Grant] United States / NIAID NIH HHS / AI / R44 AI056869; United States / NIAID NIH HHS / AI / AI40218; United States / NCI NIH HHS / CA / CA56869; United States / NIEHS NIH HHS / ES / ES06676
  • [Publication-type] Journal Article; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Phytogenic; 0 / DNA-Binding Proteins; 0 / Erythroid-Specific DNA-Binding Factors; 0 / GATA1 Transcription Factor; 0 / GATA1 protein, human; 0 / HSP70 Heat-Shock Proteins; 0 / Transcription Factors; EC 2.7.10.2 / Fusion Proteins, bcr-abl; P88XT4IS4D / Paclitaxel
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21. Laurenti L, Chiusolo P, Garzia MG, Zini G, Sorà F, Piccirillo N, Piccioni P, Zollino M, Leone G, Sica S: Periodic morphologic, cytogenetic and clonality evaluation after autologous peripheral blood progenitor cell transplantation in patients with lymphoproliferative malignancies. Haematologica; 2002 Jan;87(1):59-66
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  • Twelve patients showed lineage dysplasia: six patients had dyserythropoiesis, 2 patients dysgranulopoiesis, one dysmegakaryocytopoiesis, two patients showed double lineage dysplasia (erythroid and granulocytic), and one patient showed dysgranulopoiesis at the first control acquiring dyserythropoiesis at the next follow-up.
  • INTERPRETATION AND CONCLUSIONS: The occurrence of MDS/sAML depends on a variety of risk factors such as the number and type of prior courses of chemo-radiotherapy, total body irradiation in conditioning regimen, cytogenetic and morphologic alterations prior to transplant.
  • [MeSH-major] Hematologic Neoplasms / therapy. Hematopoietic Stem Cell Transplantation
  • [MeSH-minor] Adult. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Bone Marrow / pathology. Cell Lineage. Chromosome Deletion. Chromosomes, Human, Pair 10 / ultrastructure. Chromosomes, Human, Pair 5 / ultrastructure. Combined Modality Therapy. DNA, Neoplasm / genetics. Erythropoiesis. Female. Follow-Up Studies. Graft Survival. Hematopoiesis. Hematopoietic Stem Cell Mobilization. Hodgkin Disease / drug therapy. Hodgkin Disease / genetics. Hodgkin Disease / pathology. Hodgkin Disease / therapy. Humans. Karyotyping. Leukemia, Lymphocytic, Chronic, B-Cell / drug therapy. Leukemia, Lymphocytic, Chronic, B-Cell / genetics. Leukemia, Lymphocytic, Chronic, B-Cell / pathology. Leukemia, Lymphocytic, Chronic, B-Cell / therapy. Lymphoma, Non-Hodgkin / drug therapy. Lymphoma, Non-Hodgkin / genetics. Lymphoma, Non-Hodgkin / pathology. Lymphoma, Non-Hodgkin / radiotherapy. Lymphoma, Non-Hodgkin / therapy. Male. Middle Aged. Multiple Myeloma / drug therapy. Multiple Myeloma / genetics. Multiple Myeloma / pathology. Multiple Myeloma / therapy. Neoplasm Proteins / genetics. Neoplastic Cells, Circulating. Receptors, Androgen / genetics. Retrospective Studies. Transplantation Conditioning. Transplantation, Autologous. Y Chromosome

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  • (PMID = 11801466.001).
  • [ISSN] 0390-6078
  • [Journal-full-title] Haematologica
  • [ISO-abbreviation] Haematologica
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / AR protein, human; 0 / DNA, Neoplasm; 0 / Neoplasm Proteins; 0 / Receptors, Androgen
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22. Axiak SM, Carreras JK, Hahn KA, Endicott MM, Parshley DE, King GK: Hematologic changes associated with half-body irradiation in dogs with lymphoma. J Vet Intern Med; 2006 Nov-Dec;20(6):1398-401
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  • BACKGROUND: Reports describe the technique and efficacy of half-body irradiation (HBI) of dogs with lymphoma, but few describe the distinctive toxicoses associated with the combination of HBI and chemotherapy.
  • HYPOTHESIS: HBI would transiently affect myelocytic and erythroid variables as assessed by serial analysis of complete blood counts.
  • Two HBI protocols were used, resulting in delivery of either 6 Gy or 8 Gy to each half of the body, 1 month apart.
  • Dogs received chemotherapy before, during, or after irradiation, or at multiple times.
  • Data were analyzed between collection periods by analysis of variance (ANOVA) RESULTS: The mean granulocyte count significantly (P < .01) decreased from 10,017 cells/microL (data range 3,001-20,170 cells/ microL) before the first radiation treatment to 3,250 cells/microL (820-4,400 cells/microL) at week 5 (P < .01).
  • No significant difference in toxicity was found between the 6 Gy and 8 Gy group.
  • Further studies are needed to elucidate the safety and role of HBI in the treatment of dogs with lymphoma.

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  • (PMID = 17186856.001).
  • [ISSN] 0891-6640
  • [Journal-full-title] Journal of veterinary internal medicine
  • [ISO-abbreviation] J. Vet. Intern. Med.
  • [Language] ENG
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents
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23. Richard RE, Blau CA: Small-molecule-directed mpl signaling can complement growth factors to selectively expand genetically modified cord blood cells. Stem Cells; 2003;21(1):71-8
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  • Efforts toward achieving gene therapy for blood disorders are plagued by low rates of gene transfer into hemopoietic stem cells.
  • One way to achieve selection employs genes that encode receptor-bearing fusion proteins capable of inducing cell growth in response to drugs called chemical inducers of dimerization (CIDs).
  • In contrast, human hemopoietic cells proliferate only transiently in response to the mpl signal (from differentiation of transduced erythroid and megakaryocytic progenitors), while human myeloid progenitors fail to respond.
  • These findings are relevant for the eventual clinical application of CID-regulated cell therapy.
  • [MeSH-major] Fetal Blood / cytology. Growth Substances / physiology. Myeloid Progenitor Cells / physiology. Neoplasm Proteins / physiology. Proto-Oncogene Proteins / physiology. Receptors, Cytokine / physiology. Signal Transduction / physiology. Tacrolimus / analogs & derivatives
  • [MeSH-minor] Antigens, CD34 / biosynthesis. Antigens, CD34 / immunology. Bone Marrow Cells / chemistry. Bone Marrow Cells / drug effects. Bone Marrow Cells / metabolism. Cell Differentiation / drug effects. Cell Differentiation / physiology. Cell Division / drug effects. Cell Division / physiology. Cell Line. Cells, Cultured. Genetic Vectors. Green Fluorescent Proteins. Humans. Immunomagnetic Separation / methods. Luminescent Proteins / biosynthesis. Luminescent Proteins / genetics. Receptors, Thrombopoietin. Retroviridae / genetics. Transduction, Genetic

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  • (PMID = 12529553.001).
  • [ISSN] 1066-5099
  • [Journal-full-title] Stem cells (Dayton, Ohio)
  • [ISO-abbreviation] Stem Cells
  • [Language] eng
  • [Grant] United States / NIDDK NIH HHS / DK / 1P01DK 55820; United States / NIDDK NIH HHS / DK / 1R01DK57525; United States / NIDDK NIH HHS / DK / 2P01DK47754; United States / NHLBI NIH HHS / HL / 2P01HL53750; United States / NIDDK NIH HHS / DK / 5R01DK 52997
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / AP20187; 0 / Antigens, CD34; 0 / Growth Substances; 0 / Luminescent Proteins; 0 / Neoplasm Proteins; 0 / Proto-Oncogene Proteins; 0 / Receptors, Cytokine; 0 / Receptors, Thrombopoietin; 143641-95-6 / MPL protein, human; 147336-22-9 / Green Fluorescent Proteins; WM0HAQ4WNM / Tacrolimus
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24. Acs G, Zhang PJ, McGrath CM, Acs P, McBroom J, Mohyeldin A, Liu S, Lu H, Verma A: Hypoxia-inducible erythropoietin signaling in squamous dysplasia and squamous cell carcinoma of the uterine cervix and its potential role in cervical carcinogenesis and tumor progression. Am J Pathol; 2003 Jun;162(6):1789-806
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  • [Title] Hypoxia-inducible erythropoietin signaling in squamous dysplasia and squamous cell carcinoma of the uterine cervix and its potential role in cervical carcinogenesis and tumor progression.
  • Tissue hypoxia is a characteristic property of cervical cancers that makes tumors resistant to chemo- and radiation therapy.
  • Acting via its receptor (EpoR), Epo up-regulates bcl-2 and inhibits apoptosis of erythroid cells and rescues neurons from hypoxic damage.
  • Our results suggest that increased expression of Epo and EpoR may play a significant role in cervical carcinogenesis and tumor progression.
  • Hypoxia-inducible Epo signaling may play a significant role in the aggressive behavior and treatment resistance of hypoxic cervical cancers.

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  • (PMID = 12759237.001).
  • [ISSN] 0002-9440
  • [Journal-full-title] The American journal of pathology
  • [ISO-abbreviation] Am. J. Pathol.
  • [Language] ENG
  • [Grant] United States / NINDS NIH HHS / NS / R01 NS037814; United States / NINDS NIH HHS / NS / NS37814
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Cyclin-Dependent Kinase Inhibitor p16; 0 / HIF1A protein, human; 0 / Hypoxia-Inducible Factor 1, alpha Subunit; 0 / Proto-Oncogene Proteins c-bcl-2; 0 / RNA, Messenger; 0 / Receptors, Erythropoietin; 0 / Recombinant Proteins; 0 / Transcription Factors; 11096-26-7 / Erythropoietin
  • [Other-IDs] NLM/ PMC1868129
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25. Delgado-Cañedo A, Chies JA, Nardi NB: Induction of fetal haemoglobin expression in erythroid cells--a model based on iron availability signalling. Med Hypotheses; 2005;65(5):932-6
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Induction of fetal haemoglobin expression in erythroid cells--a model based on iron availability signalling.
  • The K562 cell line has erythroid origin and is used for the study of fetal haemoglobin (HbF) production after treatment with several drugs, such as hydroxyurea, cisplatin and cytosine arabinoside (Ara C).
  • It represents an important tool for the study of cancer differentiation therapy and treatment of thalassaemia and sickle cell disease.
  • Particular attention was given to Ndrg1, expressed as early as 24 h after treatment, which can be regulated by iron and is involved with blocking of the cell cycle.
  • A review of the literature shows that, similar to doxorubicin and aclarubicin, most of the drugs used to induce HbF present some kind of effect on the iron signalling pathway, activating in the cells the machinery necessary for the incorporation of extracellular iron.
  • Considering these results, as well as the fact that in erythroid cells the synthesis of haemoglobin is of vital importance, we propose that the production of fetal haemoglobin in erythroid cells is highly dependent on the iron signalling pathway.
  • [MeSH-major] Aclarubicin / administration & dosage. Doxorubicin / administration & dosage. Fetal Hemoglobin / biosynthesis. Models, Biological. Neoplasm Proteins / metabolism. Signal Transduction / drug effects
  • [MeSH-minor] Antibiotics, Antineoplastic / administration & dosage. Cell Differentiation / drug effects. Dose-Response Relationship, Drug. Gene Expression Regulation, Neoplastic / drug effects. Humans. K562 Cells

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  • (PMID = 16054772.001).
  • [ISSN] 0306-9877
  • [Journal-full-title] Medical hypotheses
  • [ISO-abbreviation] Med. Hypotheses
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Scotland
  • [Chemical-registry-number] 0 / Antibiotics, Antineoplastic; 0 / Neoplasm Proteins; 74KXF8I502 / Aclarubicin; 80168379AG / Doxorubicin; 9034-63-3 / Fetal Hemoglobin
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