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Eliasson, Pernilla
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Halvarsson, C., Rörby, E., Eliasson, P., Lang, S., Soneji, S. & Jönsson, J.-I. (2019). Putative Role of Nuclear Factor-Kappa B But Not Hypoxia-Inducible Factor-1α in Hypoxia-Dependent Regulation of Oxidative Stress in Hematopoietic Stem and Progenitor Cells. Antioxidants and Redox Signaling, 31(3), 211-226
Öppna denna publikation i ny flik eller fönster >>Putative Role of Nuclear Factor-Kappa B But Not Hypoxia-Inducible Factor-1α in Hypoxia-Dependent Regulation of Oxidative Stress in Hematopoietic Stem and Progenitor Cells
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2019 (Engelska)Ingår i: Antioxidants and Redox Signaling, ISSN 1523-0864, E-ISSN 1557-7716, Vol. 31, nr 3, s. 211-226Artikel i tidskrift (Refereegranskat) Published
Abstract [en]

Aims: Adaptation to low oxygen of hematopoietic stem cells (HSCs) in the bone marrow has been demonstrated to depend on the activation of hypoxia-inducible factor (HIF)-1α as well as the limited production of reactive oxygen species (ROS). In this study, we aimed at determining whether HIF-1α is involved in protecting HSCs from ROS.

Results: Oxidative stress was induced by DL-buthionine-(S,R)-sulfoximine (BSO)-treatment, which increases the mitochondrial ROS level. Hypoxia rescued Lineage-Sca-1+c-kit+ (LSK) cells from BSO-induced apoptosis, whereas cells succumbed to apoptosis in normoxia. Apoptosis in normoxia was inhibited with the antioxidant N-acetyl-L-cysteine or by overexpression of anti-apoptotic BCL-2. Moreover, stabilized expression of oxygen-insensitive HIFs could not protect LSK cells from oxidative stress-induced apoptosis at normoxia, neither could short hairpin RNA to Hif-1α inhibit the protective effects by hypoxia in LSK cells. Likewise, BSO treatment of LSK cells from Hif-1α knockout mice did not suppress the effects seen in hypoxia. Microarray analysis identified the nuclear factor-kappa B (NF-κB) pathway as a pathway induced by hypoxia. By using NF-κB lentiviral construct and DNA-binding assay, we found increased NF-κB activity in cells cultured in hypoxia compared with normoxia. Using an inhibitor against NF-κB activation, we could confirm the involvement of NF-κB signaling as BSO-mediated cell death was significantly increased in hypoxia after adding the inhibitor.

Innovation: HIF-1α is not involved in protecting HSCs and progenitors to elevated levels of ROS on glutathione depletion during hypoxic conditions.

Conclusion: The study proposes a putative role of NF-κB signaling as a hypoxia-induced regulator in early hematopoietic cells.

Ort, förlag, år, upplaga, sidor
Mary Ann Liebert, 2019
Nyckelord
hematopoiesis, hypoxia, oxidative stress, glutathione, mitochondria, NF-κB
Nationell ämneskategori
Cell- och molekylärbiologi Cellbiologi Immunologi
Identifikatorer
urn:nbn:se:liu:diva-156661 (URN)10.1089/ars.2018.7551 (DOI)000464553400001 ()30827134 (PubMedID)
Anmärkning

Funding agencies: Swedish Research Council; Swedish Cancer Foundation; Swedish Childrens Cancer Foundation; County Council of Ostergotland

Tillgänglig från: 2019-05-06 Skapad: 2019-05-06 Senast uppdaterad: 2019-10-17Bibliografiskt granskad
Halvarsson, C., Eliasson, P. & Jonsson, J.-I. (2012). Hypoxia-inducible factor (HIF)-1alpha is not required for hypoxia-mediated protection of hematopoietic stem cells to oxidative stress-induced cell death in FEBS JOURNAL, vol 279, issue SI, pp 203-203. In: FEBS JOURNAL (pp. 203-203). Wiley-Blackwell, 279(SI)
Öppna denna publikation i ny flik eller fönster >>Hypoxia-inducible factor (HIF)-1alpha is not required for hypoxia-mediated protection of hematopoietic stem cells to oxidative stress-induced cell death in FEBS JOURNAL, vol 279, issue SI, pp 203-203
2012 (Engelska)Ingår i: FEBS JOURNAL, Wiley-Blackwell , 2012, Vol. 279, nr SI, s. 203-203Konferensbidrag, Publicerat paper (Refereegranskat)
Abstract [en]

n/a

Ort, förlag, år, upplaga, sidor
Wiley-Blackwell, 2012
Serie
FEBS JOURNAL, ISSN 1742-464X
Nationell ämneskategori
Medicin och hälsovetenskap
Identifikatorer
urn:nbn:se:liu:diva-82053 (URN)000308128601487 ()
Tillgänglig från: 2012-10-01 Skapad: 2012-09-28 Senast uppdaterad: 2012-10-01
Tang, Y.-j., Halvarsson, C., Eliasson, P. & Jönsson, J.-I. (2012). Letter: Hypoxic and normoxic in vitro cultures maintain similar numbers of long-term reconstituting hematopoietic stem cells from mouse bone marrow [Letter to the editor]. Experimental Hematology, 40(11), 879-881
Öppna denna publikation i ny flik eller fönster >>Letter: Hypoxic and normoxic in vitro cultures maintain similar numbers of long-term reconstituting hematopoietic stem cells from mouse bone marrow
2012 (Engelska)Ingår i: Experimental Hematology, ISSN 0301-472X, E-ISSN 1873-2399, Vol. 40, nr 11, s. 879-881Artikel i tidskrift, Letter (Övrigt vetenskapligt) Published
Abstract [en]

n/a

Ort, förlag, år, upplaga, sidor
Elsevier, 2012
Nationell ämneskategori
Medicin och hälsovetenskap
Identifikatorer
urn:nbn:se:liu:diva-85627 (URN)10.1016/j.exphem.2012.07.005 (DOI)000310182400001 ()
Tillgänglig från: 2012-11-26 Skapad: 2012-11-26 Senast uppdaterad: 2018-10-18
Nordigården, A., Zetterblad, J., Trinks, C., Green, H., Eliasson, P., Druid, P., . . . Jönsson, J.-I. (2011). Irreversible pan-ERBB inhibitor canertinib elicits anti-leukaemic effects and induces the regression of FLT3-ITD transformed cells in mice. British Journal of Haematology, 155(2), 198-208
Öppna denna publikation i ny flik eller fönster >>Irreversible pan-ERBB inhibitor canertinib elicits anti-leukaemic effects and induces the regression of FLT3-ITD transformed cells in mice
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2011 (Engelska)Ingår i: British Journal of Haematology, ISSN 0007-1048, E-ISSN 1365-2141, Vol. 155, nr 2, s. 198-208Artikel i tidskrift (Refereegranskat) Published
Abstract [en]

Recent findings have indicated that tyrosine kinase inhibitors (TKIs) targeting the ERBB receptor family display anti-leukaemic effects, despite the lack of receptor expression on human leukaemic cells. The occurrence of activating mutations in the gene encoding FMS-like tyrosine kinase 3 (FLT3) in patients with acute myeloid leukaemia (AML) has rendered inhibition of this receptor a promising therapeutic target. Due to possibility of cross-reactivity, we investigated the effect of the irreversible pan-ERBB inhibitor canertinib (CI-1033) on leukaemic cells expressing FLT3. The drug had anti-proliferative and apoptotic effects on primary AML cells and human leukaemic cell lines expressing mutated FLT3. In several AML patient samples, a blast cell population expressing FLT3-internal tandem duplication (ITD) was eradicated by canertinib. Canertinib inhibited receptor autophosphorylation and kinase activity of both mutated and FLT3 ligand stimulated wildtype FLT3, leading to inhibition of the PI3-kinase and MAP kinase pathways. Apoptotic induction was dependent on pro-apoptotic BH3-only protein BCL2L11/BIM because siRNA silencing attenuated apoptosis. Moreover, the drug induced regression of cells expressing FLT3-ITD in a murine in vivo-transplantation model at previously described tolerated doses. These results indicate that canertinib, as an irreversible TKI, could constitute a novel treatment regimen in patients with mutated or overexpressed FLT3.

Ort, förlag, år, upplaga, sidor
Blackwell Publishing, 2011
Nyckelord
acute myeloid leukaemia, apoptosis, signalling, drugs, murine model, leukaemia therapy
Nationell ämneskategori
Medicin och hälsovetenskap
Identifikatorer
urn:nbn:se:liu:diva-72031 (URN)10.1111/j.1365-2141.2011.08819.x (DOI)000296063400006 ()
Anmärkning
Funding Agencies|Swedish Cancer Foundation||Swedish Childrens Cancer Foundation||Swedish Research Council||County Council of Ostergotland||Cancer Foundation of Ostergotland||Ollie and Elof Ericssons Foundation||Tillgänglig från: 2011-11-11 Skapad: 2011-11-11 Senast uppdaterad: 2017-12-08
Eliasson, P., Rehn, M., Hammar, P., Larsson, P., Sirenko, O., A Flippin, L., . . . Jönsson, J.-I. (2010). Hypoxia mediates low cell-cycle activity and increases the proportion of long-term reconstituting hematopoietic stem cells during in vitro culture. Experimental Hematology, 38(4), 301-310
Öppna denna publikation i ny flik eller fönster >>Hypoxia mediates low cell-cycle activity and increases the proportion of long-term reconstituting hematopoietic stem cells during in vitro culture
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2010 (Engelska)Ingår i: Experimental Hematology, ISSN 0301-472X, E-ISSN 1873-2399, Vol. 38, nr 4, s. 301-310Artikel i tidskrift (Refereegranskat) Published
Abstract [en]

Objective. Recent evidence suggests that hematopoietic stem cells (HSCs) in the bone marrow (BM) are located in areas where the environment is hypoxic. Although previous studies have demonstrated positive effects by hypoxia, its role in HSC maintenance has not been fully elucidated, neither has the molecular mechanisms been delineated. Here, we have investigated the consequence of in vitro incubation of HSCs in hypoxia prior to transplantation and analyzed the role of hypoxia-inducible factor (HIF)-1 alpha. Materials and Methods. HSC and progenitor populations isolated from mouse BM were cultured in 20% or 1% O-2, and analyzed for effects on cell cycle, expression of cyclin-dependent kinase inhibitors genes, and reconstituting ability to lethally irradiated mice. The involvement of HIF-1 alpha was studied using methods of protein stabilization and gene silencing. Results. When long-term FLT3(-)CD34(-)Lin(-)Sca-1(+)c-Kit(+) (LSK) cells were cultured in hypoxia, cell numbers were significantly reduced in comparison to normoxia. This was due to a decrease in proliferation and more cells accumulating in G(0). Moreover, the proportion of HSCs with long-term engraftment potential was increased. Whereas expression of the cyclin-dependent kinase inhibitor genes p21(cip1), p27(Kip1), and p57(Kip2) increased in LSK cells by hypoxia, only p21(cip1) was upregulated in FLT3(-)CD34(-)LSK cells. We could demonstrate that expression of p27(KiP1) and p57(Kip2) was dependent of HIF-1 alpha. Surprisingly, overexpression of constitutively active HIF-1 alpha or treatment with the HIF stabilizer agent FG-4497 led to a reduction in HSC reconstituting ability. Conclusions. Our results imply that hypoxia, in part via HIF-1 alpha, maintains HSCs by decreasing proliferation and favoring quiescence.

Ort, förlag, år, upplaga, sidor
Elsevier, 2010
Nationell ämneskategori
Medicin och hälsovetenskap
Identifikatorer
urn:nbn:se:liu:diva-54780 (URN)10.1016/j.exphem.2010.01.005 (DOI)000276054300005 ()
Anmärkning

Original Publication: Pernilla Eliasson, Matilda Rehn, Petter Hammar, Peter Larsson, Oksana Sirenko, Lee A Flippin, Jorg Cammenga and Jan-Ingvar Jönsson, Hypoxia mediates low cell-cycle activity and increases the proportion of long-term reconstituting hematopoietic stem cells during in vitro culture, 2010, EXPERIMENTAL HEMATOLOGY, (38), 4, 301-310. http://dx.doi.org/10.1016/j.exphem.2010.01.005 Copyright: Elsevier Science B.V., Amsterdam. http://www.elsevier.com/

On the day of the defence date the title of this article was "Hypoxia, via hypoxia-inducible factor (HIF)-1, mediates low cell cycle activity and preserves the engraftment potential of mouse hematopoietic stem cells" and one of the authors is no longer included in the article.

When finally published online the title of this article changed name to Hypoxia mediates low cell-cycle activity and increases the proportion of long-term-reconstituting hematopoietic stem cells during in vitro culture.

Tillgänglig från: 2010-04-09 Skapad: 2010-04-09 Senast uppdaterad: 2017-12-12Bibliografiskt granskad
Eliasson, P. & Jönsson, J.-I. (2010). The Hematopoietic Stem Cell Niche: Low in Oxygen but a Nice Place to be. Journal of Cellular Physiology, 222(1), 17-22
Öppna denna publikation i ny flik eller fönster >>The Hematopoietic Stem Cell Niche: Low in Oxygen but a Nice Place to be
2010 (Engelska)Ingår i: Journal of Cellular Physiology, ISSN 0021-9541, E-ISSN 1097-4652, Vol. 222, nr 1, s. 17-22Artikel, forskningsöversikt (Refereegranskat) Published
Abstract [en]

The enormous regenerative capacity of the blood system to sustain functionally mature cells are generated from highly proliferative, short-lived progenitors, which in turn arise from a rare population of pluripotent and self-renewing hematopoietic stem cells (HSC). In the bone marrow, these stem cells are kept in a low proliferative, relatively quiescent state in close proximity to stromal cells and osteoblasts, forming specialized niches. The interaction in particular to bone is crucial to prevent exhaustion of HSCs from uncontrolled cell-cycle entry and to excessive proliferation. In addition, the niche and its components protect stem cells from stress, such as accumulation of reactive oxygen species and DNA damage. One of the key issues is to identify conditions to increase the number of HSCs, either in vivo or during ex vivo growth cultures. This task has been very difficult to resolve and most attempts have been unsuccessful. However, the mechanistic insights to HSC self-renewal and preservation are gradually increasing and there is now hope that future research will enable scientists and clinicians to modulate the process. In this review, we will focus on the molecular mechanisms of self-renewal and HSC maintenance in the light of novel findings that HSCs reside at the lowest end of an oxygen gradient. Hypoxia appears to regulate hematopoiesis in the bone marrow by maintaining important HSC functions, such as cell cycle control, survival, metabolism, and protection against oxidative stress. To improve the therapeutic expansion of HSCs we need to learn more about the molecular mechanisms of hypoxia-mediated regulation.

Nationell ämneskategori
Medicin och hälsovetenskap
Identifikatorer
urn:nbn:se:liu:diva-52904 (URN)10.1002/jcp.21908 (DOI)
Tillgänglig från: 2010-01-13 Skapad: 2010-01-12 Senast uppdaterad: 2017-12-12
Nordigården, A., Kraft, M., Eliasson, P., Labi, V., Lam, E.-F. W. F., Villunger, A. & Jönsson, J.-I. (2009). BH3-only protein Bim more critical than Puma in tyrosine kinase inhibitor-induced apoptosis of human leukemic cells and transduced hematopoietic progenitors carrying oncogenic FLT3.. Blood, 113(10), 2302-2311
Öppna denna publikation i ny flik eller fönster >>BH3-only protein Bim more critical than Puma in tyrosine kinase inhibitor-induced apoptosis of human leukemic cells and transduced hematopoietic progenitors carrying oncogenic FLT3.
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2009 (Engelska)Ingår i: Blood, ISSN 0006-4971, E-ISSN 1528-0020, Vol. 113, nr 10, s. 2302-2311Artikel i tidskrift (Refereegranskat) Published
Abstract [en]

Constitutively activating internal tandem duplications (ITD) of FLT3 (FMS-like tyrosine kinase 3) are the most common mutations in acute myeloid leukemia (AML) and correlate with poor prognosis. Receptor tyrosine kinase inhibitors targeting FLT3 have developed as attractive treatment options. Because relapses occur after initial responses, identification of FLT3-ITD–mediated signaling events are important to facilitate novel therapeutic interventions. Here, we have determined the growth-inhibitory and proapototic mechanisms of 2 small molecule inhibitors of FLT3, AG1295 or PKC412, in hematopoietic progenitor cells, human leukemic cell lines, and primary AML cells expressing FLT3-ITD. Inactivation of the PI3-kinase pathway, but not of Ras–mitogen-activated protein (MAP) kinase signaling, was essential to elicit cytotoxic responses. Both compounds induced up-regulation of proapoptotic BH3-only proteins Bim and Puma, and subsequent cell death. However, only silencing of Bim, or its direct transcriptional activator FOXO3a, abrogated apoptosis efficiently. Similar findings were made in bone marrow cells from gene-targeted mice lacking Bim and/or Puma infected with FLT3-ITD and treated with inhibitor, where loss of Puma only provided transient protection from apoptosis, but loss of Bim preserved clonal survival upon FLT3-ITD inhibition.

 

Ort, förlag, år, upplaga, sidor
Washington, D.C: The American Society of Hematology, 2009
Nationell ämneskategori
Cell- och molekylärbiologi
Identifikatorer
urn:nbn:se:liu:diva-52728 (URN)10.1182/blood-2008-07-167023 (DOI)
Tillgänglig från: 2010-01-11 Skapad: 2010-01-11 Senast uppdaterad: 2018-01-12
Eliasson, P. (2009). Live and Let Die: Critical regulation of survival in normal and malignant hematopoietic stem and progenitor cells. (Doctoral dissertation). Linköping: Linköping University Electronic Press
Öppna denna publikation i ny flik eller fönster >>Live and Let Die: Critical regulation of survival in normal and malignant hematopoietic stem and progenitor cells
2009 (Engelska)Doktorsavhandling, sammanläggning (Övrigt vetenskapligt)
Abstract [en]

The hematopoietic stem cell (HSC) is characterized by its ability to self-renew and produce all mature blood cells throughout the life of an organism. This is tightly regulated to maintain a balance between survival, proliferation, and differentiation. The HSCs are located in specialized niches in the bone marrow thought to be low in oxygen, which is suggested to be involved in the regulation of HSC maintenance, proliferation, and migration. However, the importance of hypoxia in the stem cell niche and the molecular mechanisms involved remain fairly undefined. Another important regulator of human HSCs maintenance is the tyrosine kinase receptor FLT3, which triggers survival of HSCs and progenitor cells. Mutations in FLT3 cause constitutively active signaling. This leads to uncontrolled survival and proliferation, which can result in development of acute myeloid leukemia (AML). One of the purposes with this thesis is to investigate how survival, proliferation and self-renewal in normal HSCs are affected by hypoxia. To study this, we used both in vitro and in vivo models with isolated Lineage-Sca-1+Kit+ (LSK) and CD34-Flt3-LSK cells from mouse bone marrow. We found that hypoxia maintained an immature phenotype. In addition, hypoxia decreased proliferation and induced cell cycle arrest, which is the signature of HSCs with long term multipotential capacity. A dormant state of HSCs is suggested to be critical for protecting and preventing depletion of the stem cell pool. Furthermore, we observed that hypoxia rescues HSCs from oxidative stress-induced cell death, implicating that hypoxia is important in the bone marrow niche to limit reactive oxidative species (ROS) production and give life-long protection of HSCs. Another focus in this thesis is to investigate downstream pathways involved in tyrosine kinase inhibitor-induced cell death of primary AML cells and cell lines expressing mutated FLT3. Our results demonstrate an important role of the PI3K/AKT pathway to mediate survival signals from FLT3. We found FoxO3a and its target gene Bim to be key players of apoptosis in cells carrying oncogenic FLT3 after treatment with tyrosine kinase inhibitors. In conclusion, this thesis highlights hypoxic-mediated regulation of normal HSCs maintenance and critical effectors of apoptosis in leukemic cells expressing mutated FLT3.

Ort, förlag, år, upplaga, sidor
Linköping: Linköping University Electronic Press, 2009. s. 93
Serie
Linköping University Medical Dissertations, ISSN 0345-0082 ; 1160
Nyckelord
hematopoietic stem cells, hypoxia, self-renewal, survival, acute myeloid leukemia, FLT3
Nationell ämneskategori
Biokemi och molekylärbiologi Hematologi
Identifikatorer
urn:nbn:se:liu:diva-52932 (URN)978-91-7393-470-1 (ISBN)
Disputation
2009-12-11, Berzeliussalen, Hälsouniversitetet, Campus US, Linköpings universitet, Linköping, 09:00 (Engelska)
Opponent
Handledare
Anmärkning

On the day of the defence date the title of article II was "Hypoxia, via hypoxia-inducible factor (HIF)-1, mediates low cell cycle activity and preserves the engraftment potential of mouse hematopoietic stem cells" and one of the authors is no longer included in the article.

Tillgänglig från: 2010-01-19 Skapad: 2010-01-13 Senast uppdaterad: 2018-09-11Bibliografiskt granskad
Eliasson, P., Karlsson, R. & Jönsson, J.-I. (2006). Hypoxia Expands Primitive Hematopoietic Progenitor Cells from Mouse Bone Marrow During In Vitro Culture and Preserves the Colony-Forming Ability. Journal of Stem Cells, 1(4), 247-257
Öppna denna publikation i ny flik eller fönster >>Hypoxia Expands Primitive Hematopoietic Progenitor Cells from Mouse Bone Marrow During In Vitro Culture and Preserves the Colony-Forming Ability
2006 (Engelska)Ingår i: Journal of Stem Cells, ISSN 1556-8539, Vol. 1, nr 4, s. 247-257Artikel i tidskrift (Refereegranskat) Published
Abstract [en]

Self-renewal is a prerequisite for the maintenance of hematopoietic stem cells (HSCs) in the bone marrow throughout adult life. Cytokines are mainly providing pro-survival signals of HSC, whereas low oxygen levels (hypoxia) were recently shown to influence self-renewal. In contrast, the effects on other progenitor cell types is not clear. In the present work, we have analyzed whether hypoxia has any effects on mouse multipotent progenitors. When bone marrow-derived Lin-Sca1+c-kit+ (LSK) cells were kept in hypoxic cultures (1% O2 ) for 4 days together with cytokines, the numbers of colony forming high-proliferative progenitors (HPP-CFC) and precursors for cobble-stone forming cells (CAFC) were increased compared to normoxic conditions. A similar effect was seen with pre-CFCmulti from unfractionated bone marrow, whereas more committed progenitors (CFU-GM) were expanded better in normoxia compared to hypoxia. The observed increase in numbers of primitive colony-forming progenitor cells was associated with maintenance of the c-kit/Sca-1 phenotype and a preferential expansion of immature  blast-like appearing cells. The results suggest that a major function of hypoxia is to regulate differentiation by increased self-renewal. Furthermore, in cultures of limited cytokine supply, survival of the stem cell-like cell line FDCP-mix was increased during hypoxia. Thus, hypoxia allows for better survival and self-renewal of multipotent progenitors and HSCs from adult bone marrow. Such culture conditions may have beneficial clinical implications for ex vivo purposes and may improve the yields of stem cells and early progenitors.

Ort, förlag, år, upplaga, sidor
Nova Science Publishers, Inc., 2006
Nyckelord
Hematopoiesis, Stem cells, Progenitor, Hypoxia, Survival, Self-renewal
Nationell ämneskategori
Medicin och hälsovetenskap
Identifikatorer
urn:nbn:se:liu:diva-17713 (URN)
Anmärkning

Original Publication: Pernilla Eliasson, Richard Karlsson and Jan-Ingvar Jönsson, Hypoxia Expands Primitive Hematopoietic Progenitor Cellsfrom Mouse Bone Marrow During In Vitro Culture and Preserves the Colony-Forming Ability, 2006, Journal of Stem Cells, (1), 4, 247-257. https://www.novapublishers.com/catalog/editorial.php?products_id=3730 Copyright: Nova Science Publishers https://www.novapublishers.com/

Tillgänglig från: 2009-04-16 Skapad: 2009-04-16 Senast uppdaterad: 2018-05-29Bibliografiskt granskad
Eliasson, P., Andersson, P., Willander, K., Linderholm, M., Söderkvist, P. & Jönsson, J.-I. (2006). Letter: Absence of hot spot mutations of the PIK3CA gene in acute myeloid leukaemia [Letter to the editor]. European Journal of Haematology, 77(1), 86-87
Öppna denna publikation i ny flik eller fönster >>Letter: Absence of hot spot mutations of the PIK3CA gene in acute myeloid leukaemia
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2006 (Engelska)Ingår i: European Journal of Haematology, ISSN 0902-4441, E-ISSN 1600-0609, Vol. 77, nr 1, s. 86-87Artikel i tidskrift, Letter (Övrigt vetenskapligt) Published
Abstract [en]

[No abstract available]

Nationell ämneskategori
Medicin och hälsovetenskap
Identifikatorer
urn:nbn:se:liu:diva-37786 (URN)10.1111/j.0902-4441.2006.t01-1-EJH2605.x (DOI)38625 (Lokalt ID)38625 (Arkivnummer)38625 (OAI)
Tillgänglig från: 2009-10-10 Skapad: 2009-10-10 Senast uppdaterad: 2017-12-13Bibliografiskt granskad
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