About: Deborah L. White

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An Entity of Type : wikibase:Item, within Data Space : wikidata.demo.openlinksw.com associated with source document(s)

researcher

Attributes	Values
rdf:type	Item
field of work	wds:Q39640654-6343aa68-4dfb-05cc-87d5-4d48bcaf8245
field of work	pathology
description	researcher (en) 연구원 (ko) গবেষক (bn) 研究者 (ja) ഗവേഷക (ml) дослідниця (uk) эрдэмтэн (mn) वैज्ञानिक (hi) изилдөөчү (ky) 研究者 (zh) հետազոտող (hy) researcher (en-ca) researcher (en-gb) researcher (en-us) hulumtuese (sq) taighdeoir (ga) onderzoekster uit Australië (nl) investigadora australiana (es) investigadora australiana (ast) Avustralyalı araştırmacı (tr) chercheuse australienne (fr) ikertzaile australiarra (eu) investigadora australiana (ca) investigadora australiana (gl) investigadora australiana (pt) ricercatrice australiana (it)
rdfs:label	Deborah L White (nl) Deborah L White (sl) Deborah L. White (ca) Deborah L. White (en) Deborah L. White (es) Deborah L. White (fr) Deborah L. White (ga) Deborah L. White (sq)
skos:prefLabel	Deborah L White (nl) Deborah L White (sl) Deborah L. White (ca) Deborah L. White (en) Deborah L. White (es) Deborah L. White (fr) Deborah L. White (ga) Deborah L. White (sq)
name	Deborah L White (nl) Deborah L White (sl) Deborah L. White (ca) Deborah L. White (en) Deborah L. White (es) Deborah L. White (fr) Deborah L. White (ga) Deborah L. White (sq)
Scopus author ID	wds:Q39640654-9DCAB637-28FB-4F26-BF96-1DAFBB421567
Scopus author ID	8860729800
given name	wds:Q39640654-873AD956-62F5-47BC-AA42-B2F1DDF196E5
given name	Deborah
instance of	wds:Q39640654-7AFC8D24-40AF-4A03-9AC9-78529BDED020
instance of	Homo sapiens
skos:altLabel	DL White (en) Deborah White (en)
occupation	wds:Q39640654-2DD7D480-F141-46D3-8736-13A4B41D2BC6
employer	wds:Q39640654-298726A2-0FE8-4709-9C7D-2B64718FF884 wds:Q39640654-31ba965b-4113-341c-234c-245a7b4b2b1c wds:Q39640654-38DBE61A-D5F9-405D-BCB9-A04C69F54B74
sex or gender	wds:Q39640654-FFBFC975-8B83-46EA-BE30-FA90C1B85CD6
country of citizenship	wds:Q39640654-fe21f092-45cc-a481-92d0-149c0118c8ec
educated at	wds:Q39640654-075ecb5e-494f-2481-49c1-f0e1e73206a3 wds:Q39640654-d5625da0-43a8-b5ed-057f-702fbd699898
family name	wds:Q39640654-8E31D7E4-C930-4CE6-A3CE-3CB796E142B2
occupation	researcher
employer	South Australian Health and Medical Research Institute SA Pathology University of Adelaide
sex or gender	female organism
country of citizenship	Australia
educated at	University of Adelaide University of South Australia
family name	White
ORCID iD	wds:Q39640654-9E047A82-E503-4184-9344-BBB7B7128E2D
ORCID iD	https://orcid.org/0000-0003-4844-333X
ORCID iD	0000-0003-4844-333X
is about of	https://www.wikidata.org/wiki/Special:EntityData/Q39640654
is author of	BCR–ABL1 lymphoblastic leukaemia is characterized by the deletion of Ikaros TIDEL-II: first-line use of imatinib in CML with early switch to nilotinib for failure to achieve time-dependent molecular targets SHP-1 expression accounts for resistance to imatinib treatment in Philadelphia chromosome-positive cells derived from patients with chronic myeloid leukemia Targetable kinase-activating lesions in Ph-like acute lymphoblastic leukemia Monoclonal antibody targeting of IL-3 receptor α with CSL362 effectively depletes CML progenitor and stem cells Sustained inhibition of STAT5, but not JAK2, is essential for TKI-induced cell death in chronic myeloid leukemia. Safety and efficacy of imatinib cessation for CML patients with stable undetectable minimal residual disease: results from the TWISTER study. Impact of early dose intensity on cytogenetic and molecular responses in chronic- phase CML patients receiving 600 mg/day of imatinib as initial therapy Interaction of the efflux transporters ABCB1 and ABCG2 with imatinib, nilotinib, and dasatinib. Tyrosine kinase inhibitor resistance in chronic myeloid leukemia cell lines: investigating resistance pathways Measurement of in vivo BCR-ABL kinase inhibition to monitor imatinib-induced target blockade and predict response in chronic myeloid leukemia. Chronic phase chronic myeloid leukemia patients with low OCT-1 activity randomized to high-dose imatinib achieve better responses and have lower failure rates than those randomized to standard-dose imatinib Which TKI? An embarrassment of riches for chronic myeloid leukemia patients OCT-1 activity measurement provides a superior imatinib response predictor than screening for single-nucleotide polymorphisms of OCT-1. Low GFI1 expression in white blood cells of CP-CML patients at diagnosis is strongly associated with subsequent blastic transformation In vitro sensitivity to imatinib-induced inhibition of ABL kinase activity is predictive of molecular response in patients with de novo CML. Most CML patients who have a suboptimal response to imatinib have low OCT-1 activity: higher doses of imatinib may overcome the negative impact of low OCT-1 activity

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