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  • 1
    Online Resource
    Online Resource
    Roles of cathelicidins in inflammation and bone loss
    Springer Science and Business Media LLC ; 2014
    In:  Odontology Vol. 102, No. 2 ( 2014-7), p. 137-146
    Details
    In: Odontology, Springer Science and Business Media LLC, Vol. 102, No. 2 ( 2014-7), p. 137-146
    Type of Medium: Online Resource
    ISSN: 1618-1247 , 1618-1255
    URL: Article
    DOI: 10.1007/s10266-014-0167-0
    Language: English
    Publisher: Springer Science and Business Media LLC
    Publication Date: 2014
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  • 2
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    Nation-Wide Survey of Relapsed Infantile Acute Lymphoblastic Leukemia In Japan: Treatment and Outcome From the Japanese Pediatric Leukemia/Lymphoma Study Group (JPLSG) MLL03 Study.
    American Society of Hematology ; 2010
    In:  Blood Vol. 116, No. 21 ( 2010-11-19), p. 1025-1025
    Details
    In: Blood, American Society of Hematology, Vol. 116, No. 21 ( 2010-11-19), p. 1025-1025
    Abstract: Abstract 1025 Introduction: Infantile acute lymphoblastic leukemia (ALL) is a rare leukemia subtype in infants with poor prognosis. Its outcome has gradually improved due to the development of treatment, including intensive chemotherapy or hematopoietic stem cell transplantation (SCT). However, prognosis of relapsed patients is extremely poor, which prompt us to establish the new treatment strategy for them. To establish the future treatment strategy for the relapsed cases, we here investigated the incidence of relapse, treatment, prognosis, and possible risk factors of relapsed cases with infantile ALL treated by the Japanese Pediatric Leukemia /Lymphoma Study Group (JPLSG) MLL03 study. Subjects: All relapsed cases with infantile ALL who underwent the MLL03 study between April 2004 and June 2009 were eligible for the study. The questionnaires were sent to all participants, asking the relapsed patients with infantile ALL by the MLL03 study. The questionnaires consisted of the time and site of relapse, treatment after relapse, presence or absence of remission prior to the second SCT, conditioning regimen for the second SCT, and age, white blood cell count, and presence or absence of central nervous system (CNS) infiltration at initial onset. Results: Total 63 patients were treated in this study period (mean follow-up, 31.8 months). Among them, 24 patients relapsed at any site after first complete remission (38%). These include 7 boys and 17 girls. Age at onset was less than 6 months in 19, and 6–12 months in 5. The overall survival (OS) rate of 24 patients was 60.2 ± 11.1% at 3 years; 44.6 ± 12.7% at 4 years, and 23.5 ± 13.4% at 5 years. Twenty-one of 24 patients (87.5%) relapsed after initial SCT; only three patients (12.5%) relapsed before SCT. Two patients relapsed early within 6 months after initial treatment terminally died. All four patients who relapsed at extramedullary site except CNS have survived, suggesting better prognosis. Patients diagnosed at age of less than 6 months also showed poor prognosis after relapse (5 year OS rate was 14.9 ± 13.0%). Presence or absence of remission prior to the second SCT was not a significant prognostic factor (28.3 ± 21.8% versus 15.6 ± 14.2%). Discussion: In the JPLSG MLL03 study, 38% of patients with infantile ALL relapsed. Only four patients relapsed prior to the initial SCT, indicating that the aim of the MLL03 study, to reduce the early relapse rate by performing the early SCT, could have been achieved. On the other hand, 87.5% of the patients relapsed after initial SCT in this study. Most of them were less than 6 months at onset. Several reasons for the high relapse rate after SCT should be considered, which include low graft-versus-leukemia (GVL) effect for infantile ALL, remained minimal residual disease (MRD) before SCT, or inappropriate conditioning regimen in this study. Since we have analyzed MRD before and after SCT in each patient treated by the MLL03 study, one reason could be resolved. In addition, the treatment strategy to induce GVL effect for infantile ALL should be established and we should reconsider the treatment strategy. Finally, appropriate treatment strategy for relapsed cases should be organized in the future. Disclosures: No relevant conflicts of interest to declare.
    Type of Medium: Online Resource
    ISSN: 0006-4971 , 1528-0020
    URL: Article
    DOI: 10.1182/blood.V116.21.1025.1025
    RVK:
    XA 33000
    RVK:
    XA 10000
    Language: English
    Publisher: American Society of Hematology
    Publication Date: 2010
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  • 3
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    Odontoblast death drives cell-rich zone-derived dental tissue regeneration
    Elsevier BV ; 2021
    In:  Bone Vol. 150 ( 2021-09), p. 116010-
    Details
    In: Bone, Elsevier BV, Vol. 150 ( 2021-09), p. 116010-
    Type of Medium: Online Resource
    ISSN: 8756-3282
    URL: Article
    DOI: 10.1016/j.bone.2021.116010
    Language: English
    Publisher: Elsevier BV
    Publication Date: 2021
    detail.hit.zdb_id: 1496324-3
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  • 4
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    Genetic abnormalities involved in t(12;21) TEL – AML1 acute lymphoblastic leukemia: Analysis by means of array‐based comparative genomic hybridization
    Wiley ; 2007
    In:  Cancer Science Vol. 98, No. 5 ( 2007-05), p. 698-706
    Details
    In: Cancer Science, Wiley, Vol. 98, No. 5 ( 2007-05), p. 698-706
    Abstract: The TEL (ETV6)–AML1 (RUNX1) chimeric gene fusion is the most common genetic abnormality in childhood acute lymphoblastic leukemias. Evidence suggests that this chimeric gene fusion constitutes an initiating mutation that is necessary but insufficient for the development of leukemia. In a search for additional genetic events that could be linked to the development of leukemia, we applied a genome‐wide array‐comparative genomic hybridization technique to 24 TEL–AML1 leukemia samples and two cell lines. It was found that at least two chromosomal imbalances were involved in all samples. Recurrent regions of chromosomal imbalance ( 〉 10% of cases) and representative involved genes were gain of chromosomes 10 (17%) and 21q (25%; RUNX1 ) and loss of 12p13.2 (87%; TEL ), 9p21.3 (29%; p16INK4a/ARF ), 9p13.2 (25%; PAX5 ), 12q21.3 (25%; BTG1 ), 3p21 (21%; LIMD1 ), 6q21 (17%; AIM1 and BLIMP1 ), 4q31.23 (17%; NR3C2 ), 11q22‐q23 (13%; ATM ) and 19q13.11‐q13.12 (13%; PDCD5 ). Enforced expression of TEL and to a lesser extent BTG1 , both single genes known to be located in their respective minimum common region of loss, inhibited proliferation of the TEL–AML1 cell line Reh. Together, these findings suggest that some of the genes identified as lost by array‐comparative genomic hybridization may partly account for the development of leukemia. ( Cancer Sci 2007; 98: 698–706)
    Type of Medium: Online Resource
    ISSN: 1347-9032 , 1349-7006
    URL: Issue
    URL: Article
    DOI: 10.1111/cas.2007.98.issue-5
    DOI: 10.1111/j.1349-7006.2007.00443.x
    Language: English
    Publisher: Wiley
    Publication Date: 2007
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  • 5
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    Sclerostin blockade promotes bone metastases of Wnt‐responsive breast cancer cells
    Wiley ; 2023
    In:  Cancer Science Vol. 114, No. 6 ( 2023-06), p. 2460-2470
    Details
    In: Cancer Science, Wiley, Vol. 114, No. 6 ( 2023-06), p. 2460-2470
    Abstract: The secreted protein sclerostin is primarily produced by osteocytes and suppresses osteoblast differentiation and function by inhibiting the canonical Wnt signaling pathway. Genetic and pharmacological inhibition of sclerostin has been shown to increase bone formation and an anti‐sclerostin antibody has been clinically approved for the treatment of osteoporosis. Canonical Wnt signaling is also involved in the progression of several types of cancers including breast cancer. Here, we studied the effects of sclerostin inhibition on the development of bone metastases of breast cancer using mouse models. TOPFLASH assay and real‐time PCR analysis of AXIN2 , a target of canonical Wnt signaling, revealed that, among four cell lines tested, MDA‐MB‐231 human breast cancer cells responded highly to the canonical Wnt ligand Wnt3a, whereas other cell lines exhibited marginal responses. Consistent with these results, treatment with an anti‐sclerostin antibody significantly increased the bone metastases of MDA‐MB‐231 but not those of other breast cancer cells. Immunohistochemical studies demonstrated that an anti‐sclerostin antibody induced intracellular accumulation of β‐catenin in bone‐colonized MDA‐MB‐231 cells. Suspension culture assays showed that Wnt3a accelerated the tumorsphere formation of MDA‐MB‐231 cells, whereas monolayer cell proliferation and migration were not affected. Furthermore, the numbers of osteoclasts and their precursor cells in bone metastases of MDA‐MB‐231 were significantly increased in mice treated with an anti‐sclerostin antibody. These results collectively suggest that sclerostin blockade activates canonical Wnt signaling in ligand‐responsive breast cancer cells metastasized to bone, thereby increasing bone metastases, likely to have been mediated at least in part by enhancing stem cell‐like properties of cancer cells and osteoclastogenesis.
    Type of Medium: Online Resource
    ISSN: 1347-9032 , 1349-7006
    URL: Issue
    URL: Article
    DOI: 10.1111/cas.v114.6
    DOI: 10.1111/cas.15765
    Language: English
    Publisher: Wiley
    Publication Date: 2023
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    detail.hit.zdb_id: 2111204-6
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  • 6
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    M2-like macrophage infiltration and transforming growth factor-β secretion during socket healing process in mice
    Elsevier BV ; 2021
    In:  Archives of Oral Biology Vol. 123 ( 2021-03), p. 105042-
    Details
    In: Archives of Oral Biology, Elsevier BV, Vol. 123 ( 2021-03), p. 105042-
    Type of Medium: Online Resource
    ISSN: 0003-9969
    URL: Article
    DOI: 10.1016/j.archoralbio.2021.105042
    RVK:
    XA 29550
    Language: English
    Publisher: Elsevier BV
    Publication Date: 2021
    detail.hit.zdb_id: 1496079-5
    SSG: 12
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  • 7
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    Defining Second-Hit Genetic Abnormalities Involved in the t(12; 21) TEL-AML1 Acute Lymphoblastic Leukemia by Array-Based Comparative Genomic Hybridization.
    American Society of Hematology ; 2005
    In:  Blood Vol. 106, No. 11 ( 2005-11-16), p. 2845-2845
    Details
    In: Blood, American Society of Hematology, Vol. 106, No. 11 ( 2005-11-16), p. 2845-2845
    Abstract: TEL (ETV6)-AML1 (RUNX1) chimeric gene fusion is the most common genetic abnormality in childhood acute lymphoblastic leukemias (ALL). Evidence suggests that this chimeric gene fusion usually occurs in utero during fetal hematopoiesis and most probably constitutes an initiating or first-hit mutation that is necessary but insufficient for the development of overt, clinical leukemia. In a search for additional secondary and postnatal genetic events that could be linked to leukemia development, we applied a genome- wide array- CGH technique to 24 TEL-AML1 leukemia samples and two cell lines (REH, KOPN41) and found that at least three chromosomal imbalances were involved in all patient samples and cell lines. Recurrent regions of chromosomal imbalances (found in & gt; 10% of clinical samples) were gain of chromosomes 10 (17 %) and 21q (25 %) and loss of chromosomes 2p11 (100 %), 12p13.2 (87 %), 9p21.3 (29 %), 9p13.2 (25 %), 12q21.3, (25 %), 3p21 (21 %), 6q21 (17 %), 4q31.23 (17 %), 11q22-q23 (13 %) and 19q13.11-q13.12 (13 %). The two cell lines showed gain of 21q22.12-qter and loss of 2p11.2, 9p21.3, 12p13.2, and 12q21.3. Among these, six regions of loss (2p11, 3p21, 4q31.23, 9p13.2, 12q21.3 and 19q13.12) have not been identified previously by conventional CGH in TEL-AML1 leukemia. Representative genes involved in the regions of loss were Igkappa (2p11), TEL (12p13.2), p16INK4a/ARF (9p21.3), Pax5 (9p13.2), BTG1 (12q21.3), LIMD1 (3p21), AIM1 and BLIMP1 (6q21), NR3C2 (4q31.23), ATM (11q22-q23), and PDCD5 (19q13.11-q13.12), while the region of gain at 21q contained RUNX1. These findings suggest that, in addition to TEL previously reported as deleted, genes involved in cell cycle regulation, p53 pathways and apoptosis are also often deleted. Our array-CGH obtained data may provide further insights into the molecular basis for the development of TEL-AML1 leukemia.
    Type of Medium: Online Resource
    ISSN: 0006-4971 , 1528-0020
    URL: Article
    DOI: 10.1182/blood.V106.11.2845.2845
    RVK:
    XA 33000
    RVK:
    XA 10000
    Language: English
    Publisher: American Society of Hematology
    Publication Date: 2005
    detail.hit.zdb_id: 1468538-3
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  • 8
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    Individual Pharmacokinetic Targeting of Busulfan in Allogeneic Hematopoietic Stem Cell Transplantation Is Essential for Infants with MLL Gene-Rearranged Acute Lymphoblastic Leukemia: A Report from the JPLSG MLL03 Study
    American Society of Hematology ; 2015
    In:  Blood Vol. 126, No. 23 ( 2015-12-03), p. 1915-1915
    Details
    In: Blood, American Society of Hematology, Vol. 126, No. 23 ( 2015-12-03), p. 1915-1915
    Abstract: Dose adjustment of busulfan (BU) based on individual pharmacokinetics (PK) has been established as an important clinical tool in conditioning of hematopoietic stem cell transplantation (HSCT). Wide interindividual variety of achievable BU concentration in infants by recommended formula is a problematic issue. Nevertheless, there is no sizable BU PK data in infants. We report here the characteristics of BU PK data in infants with MLL gene-rearranged acute lymphoblastic leukemia (MLL-r ALL) and its relevance to the outcome of HSCT. MLL03, a nationwide study conducted by the Japanese Pediatric Leukemia/Lymphoma Study Group (JPLSG), enrolled 62 infants with MLL-r ALL from 2004 to 2009 and tested whether an early intervention of allogeneic HSCT in first complete remission (1CR) could prevent early relapse and produce improved event-free survival (EFS) (Koh K, et al. Leukemia 2015). Protocol determined conditioning consisted of BU combined with etoposide and cyclophosphamide. Plasma BU concentration was measured by high performance liquid chromatography assay based on one-compartment model. The initial BU dose was determined according to an individual BU PK test measured one week prior to the start of HSCT conditioning, and further adjusted on the PK results. Among the 43 infants who received HSCT in 1CR, complete BU PK data were available in 30 cases (21 cases were transplanted from unrelated cord blood donor and 9 from family donor). Oral (PO) BU was given in 18 cases and intravenous (IV) BU in 12 cases. These 30 cases were analyzed for correlation with the clinical outcome. We set the target range of steady state concentration (Css) of BU calculated from PK within 600-900 ng/ml. As a result of BU PK test, the level of estimated Css in the group receiving PO-BU and IV-BU reached the range of 405-949 ng/ml and 484-1247 ng/ml, respectively; 61% of PO-BU group and 46% of IV-BU group were within the desired range. There was a trend of IV-BU group to attain higher targeted Css level with relatively lower dose of recommended formula, while higher dose of PO BU was necessary to achieve proper Css level. Thus, higher level of Css could be easily reached in the IV-BU group compared to the PO-BU group. After adjustment of BU dose based on the PK test results, no case showed abnormally high Css and one case showed extremely low Css than the targeted range despite twice as higher recommended PO BU dose were given. Despite wide diversity of PK data observed in each individual, permissible Css levels could be attained in most of the cases. All the cases achieved full engraftment. There was no statistical significance in the outcome including overall survival, EFS, relapse rate, and treatment-related mortality according to the level of Css nor BU formula. Sinusoidal obstruction syndrome (SOS) occurred in 6 cases (20%; two grade 3, three grade 2, and one grade 1), although Css levels of all the 6 cases did not exceed the upper limit (median 638 ng/ml, range 540-790 ng/ml). However, SOS occurred in another 5 cases out of 13 patients who did not undergo BU PK adjustment, with trend of more severe disease (38%; one grade 4, three grade 3, and one grade 2). We therefore consider that the BU dose adjustment based on PK test is useful to reduce both severity and incidence of SOS. Besides SOS, one case died of transfusion related lung injury. In conclusion, wide interindividual variety of BU PK was observed in infants with MLL-r ALL and dose adjustment of BU based on PK test would be essential for BU containing conditioning of allogeneic HSCT for infants in terms of both safety and efficacy. Disclosures Off Label Use: Off-label use of CliniMACS purified CD34+ cells.
    Type of Medium: Online Resource
    ISSN: 0006-4971 , 1528-0020
    URL: Article
    DOI: 10.1182/blood.V126.23.1915.1915
    RVK:
    XA 33000
    RVK:
    XA 10000
    Language: English
    Publisher: American Society of Hematology
    Publication Date: 2015
    detail.hit.zdb_id: 1468538-3
    detail.hit.zdb_id: 80069-7
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  • 9
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    The Vitamin D Receptor in Osteoblast-Lineage Cells Is Essential for the Proresorptive Activity of 1α,25(OH)2D3 In Vivo
    The Endocrine Society ; 2020
    In:  Endocrinology Vol. 161, No. 11 ( 2020-11-01)
    Details
    In: Endocrinology, The Endocrine Society, Vol. 161, No. 11 ( 2020-11-01)
    Abstract: We previously reported that daily administration of a pharmacological dose of eldecalcitol, an analog of 1α,25-dihydroxyvitamin D3 [1α,25(OH)2D3], increased bone mass by suppressing bone resorption. These antiresorptive effects were found to be mediated by the vitamin D receptor (VDR) in osteoblast-lineage cells. Using osteoblast-lineage-specific VDR conditional knockout (Ob-VDR-cKO) mice, we examined whether proresorptive activity induced by the high-dose 1α,25(OH)2D3 was also mediated by VDR in osteoblast-lineage cells. Administration of 1α,25(OH)2D3 (5 μg/kg body weight/day) to wild-type mice for 4 days increased the number of osteoclasts in bone and serum concentrations of C-terminal crosslinked telopeptide of type I collagen (CTX-I, a bone resorption marker). The stimulation of bone resorption was concomitant with the increase in serum calcium (Ca) and fibroblast growth factor 23 (FGF23) levels, and decrease in body weight. This suggests that a toxic dose of 1α,25(OH)2D3 can induce bone resorption and hypercalcemia. In contrast, pretreatment of wild-type mice with neutralizing anti-receptor activator of NF-κB ligand (RANKL) antibody inhibited the 1α,25(OH)2D3-induced increase of osteoclast numbers in bone, and increase of CTX-I, Ca, and FGF23 levels in serum. The pretreatment with anti-RANKL antibody also inhibited the 1α,25(OH)2D3-induced decrease in body weight. Consistent with observations in mice conditioned with anti-RANKL antibody, the high-dose administration of 1α,25(OH)2D3 to Ob-VDR-cKO mice failed to significantly increase bone osteoclast numbers, serum CTX-I, Ca, or FGF23 levels, and failed to reduce the body weight. Taken together, this study demonstrated that the proresorptive, hypercalcemic, and toxic actions of high-dose 1α,25(OH)2D3 are mediated by VDR in osteoblast-lineage cells.
    Type of Medium: Online Resource
    ISSN: 0013-7227 , 1945-7170
    URL: Article
    DOI: 10.1210/endocr/bqaa178
    Language: English
    Publisher: The Endocrine Society
    Publication Date: 2020
    detail.hit.zdb_id: 2011695-0
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  • 10
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    VDR in Osteoblast‐Lineage Cells Primarily Mediates Vitamin D Treatment‐Induced Increase in Bone Mass by Suppressing Bone Resorption
    Wiley ; 2017
    In:  Journal of Bone and Mineral Research Vol. 32, No. 6 ( 2017-06), p. 1297-1308
    Details
    In: Journal of Bone and Mineral Research, Wiley, Vol. 32, No. 6 ( 2017-06), p. 1297-1308
    Abstract: Long‐term treatment with active vitamin D [1α,25(OH) 2 D 3 ] and its derivatives is effective for increasing bone mass in patients with primary and secondary osteoporosis. Derivatives of 1α,25(OH) 2 D 3 , including eldecalcitol (ELD), exert their actions through the vitamin D receptor (VDR). ELD is more resistant to metabolic degradation than 1α,25(OH) 2 D 3 . It is reported that ELD treatment causes a net increase in bone mass by suppressing bone resorption rather than by increasing bone formation in animals and humans. VDR in bone and extraskeletal tissues regulates bone mass and secretion of osteotropic hormones. Therefore, it is unclear what types of cells expressing VDR preferentially regulate the vitamin D–induced increase in bone mass. Here, we examined the effects of 4‐week treatment with ELD (50 ng/kg/day) on bone using osteoblast lineage‐specific VDR conditional knockout ( Ob‐VDR‐cKO ) and osteoclast‐specific VDR cKO ( Ocl‐VDR‐cKO ) male mice aged 10 weeks. Immunohistochemically, VDR in bone was detected preferentially in osteoblasts and osteocytes. Ob‐VDR‐cKO mice showed normal bone phenotypes, despite no appreciable immunostaining of VDR in bone. Ob‐VDR‐cKO mice failed to increase bone mass in response to ELD treatment. Ocl‐VDR‐cKO mice also exhibited normal bone phenotypes, but normally responded to ELD. ELD‐induced FGF23 production in bone was regulated by VDR in osteoblast‐lineage cells. These findings suggest that the vitamin D treatment‐induced increase in bone mass is mediated by suppressing bone resorption through VDR in osteoblast‐lineage cells. © 2017 The Authors. Journal of Bone and Mineral Research Published by Wiley Periodicals Inc.
    Type of Medium: Online Resource
    ISSN: 0884-0431 , 1523-4681
    URL: Issue
    URL: Article
    DOI: 10.1002/jbmr.v32.6
    DOI: 10.1002/jbmr.3096
    RVK:
    XA 52230
    Language: English
    Publisher: Wiley
    Publication Date: 2017
    detail.hit.zdb_id: 2008867-X
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