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1 n carcinomas) and cAC10 (specific to CD30 on hematological malignancies).
2 y in the contexts of development, aging, and hematological malignancy.
3 ts, suggesting that they might predispose to hematological malignancy.
4 ve been clinically used for the treatment of hematological malignancy.
5 Multiple myeloma (MM) is an age-dependent hematological malignancy.
6 al therapeutic targets in treating LSC-based hematological malignancy.
7 cycle regulation, degraded HSC function, and hematological malignancy.
8 ce for genetic susceptibility to this B-cell hematological malignancy.
9 ncer and represents the second most frequent hematological malignancy.
10 iological model for VRE BSI in patients with hematological malignancy.
11 i-VRE antimicrobial therapy in patients with hematological malignancy.
12 transplant recommendations for melanoma and hematological malignancies.
13 pathogenesis of several myeloid and lymphoid hematological malignancies.
14 tuximab, is an established means of treating hematological malignancies.
15 -HSCT) is a potentially curative therapy for hematological malignancies.
16 duced prolonged neutropenia in patients with hematological malignancies.
17 a promising therapeutic target for specific hematological malignancies.
18 iseases, cancer mortality, and high risk for hematological malignancies.
19 or patients with recurrent and/or refractory hematological malignancies.
20 rtant therapy for patients with a variety of hematological malignancies.
21 l targeted epigenetic therapies for treating hematological malignancies.
22 promising diagnostic tool for patients with hematological malignancies.
23 mal epigenetic control to the development of hematological malignancies.
24 are associated with many diseases, including hematological malignancies.
25 veral phase 1 trials of cancer patients with hematological malignancies.
26 es the functional implications for different hematological malignancies.
27 Activating JAK2 mutants cause hematological malignancies.
28 components of the RNA splicing machinery in hematological malignancies.
29 ed compared with control samples in multiple hematological malignancies.
30 ssociation between paternal age at birth and hematological malignancies.
31 gs of invasive mold disease in patients with hematological malignancies.
32 tors could prove useful for the treatment of hematological malignancies.
33 y been approved for the treatment of several hematological malignancies.
34 protect HSC pool integrity, guarding against hematological malignancies.
35 65 (56%) had solid tumors, and 140 (47%) had hematological malignancies.
36 -mC, 5-hmC, and their enzymatic modifiers in hematological malignancies.
37 elop novel epigenetic therapies for treating hematological malignancies.
38 d be prioritized for targeting in a range of hematological malignancies.
39 t anticancer drugs against various solid and hematological malignancies.
40 or autoimmune and inflammatory disorders and hematological malignancies.
41 in the blood of individuals without apparent hematological malignancies.
42 profiles, and expression changes underlying hematological malignancies.
43 nity in patients with bone marrow failure or hematological malignancies.
44 etic cell differentiation and causal role in hematological malignancies.
45 olic interventions in ALL and possibly other hematological malignancies.
46 with both developmental growth disorders and hematological malignancies.
47 e for the expression of CCL5 and CCR5 in non-hematological malignancies.
48 ns in a population of patients with advanced hematological malignancies.
49 arious diseases and is approved for treating hematological malignancies.
50 me, miR-22 transgenic mice developed MDS and hematological malignancies.
51 ination chemotherapies, especially targeting hematological malignancies.
52 ation of patients with high-risk or advanced hematological malignancies.
53 olecular mechanism of CQ in the treatment of hematological malignancies.
54 in key chromatin modifiers, most notably in hematological malignancies.
55 systolic dysfunction (LVSD) in patients with hematological malignancies.
56 enic viruses with IRF4 in the development of hematological malignancies.
57 agents for the treatment of solid tumors and hematological malignancies.
58 l blood increasingly guides clinical care in hematological malignancies.
59 y of cell survival control in epithelial and hematological malignancies.
60 nsplantation (BMT), an effective therapy for hematological malignancies.
61 exin may have tumor suppressor properties in hematological malignancies.
62 of cancers and are particularly prominent in hematological malignancies.
63 st overexpressed miRNAs in several solid and hematological malignancies.
64 all types of carcinomas and various types of hematological malignancies.
65 suppressor function in both solid tumors and hematological malignancies.
66 or impediment to the successful treatment of hematological malignancies.
67 role of the bone marrow microenvironment in hematological malignancies.
68 in targeting glycolysis for the treatment of hematological malignancies.
69 nged understanding of the molecular basis of hematological malignancies.
70 FAO inhibitors as a therapeutic strategy in hematological malignancies.
71 e clinically active in both solid tumors and hematological malignancies.
72 m stem cell to mature tissue, similar to the hematological malignancies.
73 (HSCT) have been shown to cure patients with hematological malignancies.
74 in patients with small cell lung cancer and hematological malignancies.
75 nd no significantly increased risk for other hematological malignancies.
76 l tools to treat or suppress oncogene-driven hematological malignancies.
77 olecular basis of certain cancers, including hematological malignancies.
78 cancer agents for the treatment of solid and hematological malignancies.
79 mulated the development of vaccines to treat hematological malignancies.
80 nsplantation (BMT), an effective therapy for hematological malignancies.
81 tic system to study blood cell formation and hematological malignancies.
82 eneic transplantation to a growing number of hematological malignancies.
83 herapy target for the treatment of solid and hematological malignancies.
84 have been implicated in the pathogenesis of hematological malignancies.
85 cancer agents for the treatment of solid and hematological malignancies.
86 ay represent a novel therapeutic strategy in hematological malignancies.
87 (MV-Edm) had antineoplastic efficacy against hematological malignancies.
88 ied via deep sequencing of 185 patients with hematological malignancies.
89 s a driver in many types of solid tumors and hematological malignancies.
90 apeutic agents in the treatment of solid and hematological malignancies.
91 ibition of BTK is useful in the treatment of hematological malignancies.
92 ltiple signaling pathways, and contribute to hematological malignancies.
93 s treated with recently introduced drugs for hematological malignancies.
94 ighly expressed in multiple solid tumors and hematological malignancies.
95 ge and is associated with increased risks of hematological malignancies.
96 ears been approved for the treatment of some hematological malignancies.
97 t as potential novel therapeutic targets for hematological malignancies.
98 -round-blue cell tumors, and unexpectedly in hematological malignancies.
99 by bone marrow failure and predisposition to hematological malignancies.
100 s, in individuals without clear diagnosis of hematological malignancies.
101 tive for selected HIV-infected patients with hematological malignancies.
102 ptional dynamics during hematopoiesis and in hematological malignancies.
103 the only treatment option for several severe hematological malignancies.
104 ave already been performed in the setting of hematological malignancies.
105 icacy of selinexor in patients with advanced hematological malignancies.
106 TET2 and DNMT3A) are frequently observed in hematological malignancies(1-3) and clonal hematopoiesis
107 robes, we analyzed 204 patients with diverse hematological malignancies accompanied by clonal chromos
109 Despite its success in treating melanoma and hematological malignancies, adoptive cell therapy (ACT)
110 Myelodysplastic syndrome is an important hematological malignancy affecting the expanding aged po
113 their cancer management: 15 of 28 (54%) with hematological malignancies and 27 of 63 (43%) with solid
114 in all calculations, including 28 (31%) with hematological malignancies and 63 (69%) with solid tumor
115 ated as a therapeutic agent for treatment of hematological malignancies and autoimmune diseases.
116 ted mortality and morbidity in patients with hematological malignancies and bone marrow transplants.
117 ine samples from 71 patients with underlying hematological malignancies and found that the urine GM/c
119 table mortality, especially in patients with hematological malignancies and in hematopoietic stem cel
120 I3Kdelta) is an appealing target for several hematological malignancies and inflammatory diseases.
121 re Food and Drug Administration-approved for hematological malignancies and inhibit class II and/or c
122 f the most frequently mutated genes in human hematological malignancies and is a critical factor for
123 her CT imaging findings in 100 patients with hematological malignancies and possible invasive mold di
124 activity play critical roles in treatment of hematological malignancies and refractory autoimmune dis
125 3 is frequently activated in human solid and hematological malignancies and remains a challenging the
126 implicated in numerous pathologies including hematological malignancies and rheumatoid arthritis.
127 expression and regulation of TET proteins in hematological malignancies and solid tumors, and discuss
132 103 clinical variables from patients with hematological malignancies and subsequent alloSCT were c
133 tional Cancer Institute hosted a workshop on hematological malignancies and the marrow microenvironme
135 are settings, especially among patients with hematological malignancies and those who are immunocompr
136 s to define the mutational landscape driving hematological malignancies and underscore the utility of
137 te for dCK-inhibitor based therapies against hematological malignancies and, potentially, other cance
138 f common, low-penetrance susceptibility to a hematological malignancy and new insights into disease c
139 cell non-Hodgkin lymphoma is the most common hematological malignancy and represents a substantial cl
140 ce of certain autoimmune diseases, increased hematological malignancies, and elevated incidence of ag
141 H signaling, its role in the pathobiology of hematological malignancies, and its potential as a thera
142 t decade have these cells been identified in hematological malignancies, and more recently in solid t
143 ly to induce synthetic sickness/lethality in hematological malignancies, and possibly in other cancer
145 lators are targets for dysregulation in many hematological malignancies, and that patterns of histone
146 d clinical course, the evolution to advanced hematological malignancies, and the accessibility of neo
147 nly 9 patients (27%) had a family history of hematological malignancy, and 15 (46%) had a personal hi
148 ars old, had undergone allogeneic HSCT for a hematological malignancy, and had available pretransplan
150 disorders, including autoimmune diseases and hematological malignancies, are at risk of developing os
152 ase hematopoietic cell kinase (HCK) triggers hematological malignancies as a tumor cell-intrinsic onc
153 ce for genetic susceptibility to this B-cell hematological malignancy, as well as insight into the bi
154 e small, but significant, risks of solid and hematological malignancies associated with increased rad
155 ffect has been understudied in patients with hematological malignancies at non-critical-care units.
156 lability of blood products for patients with hematological malignancies at Uganda Cancer Institute.
158 regulation of several mitotic events, and in hematological malignancies, AURKA and AURKB hyperexpress
159 n profiling has been applied to a variety of hematological malignancies, autoimmune disorders, and in
160 ls play critical roles in protection against hematological malignancies but can acquire a dysfunction
161 rative therapy for high-risk and/or advanced hematological malignancies but remains limited by graft-
162 eting lymphocytes has shown great promise in hematological malignancies, but clinical efficacy agains
163 have demonstrated promising results against hematological malignancies, but have encountered signifi
164 ntation (allo-BMT) is a curative therapy for hematological malignancies, but is associated with signi
165 an important curative therapy for high-risk hematological malignancies, but the development of sever
166 Expression of c-Myb is often increased in hematological malignancies, but the underlying mechanism
167 are understood to play fundamental roles in hematological malignancies by acting as oncogenes or tum
169 ere was no clear linear trend in the risk of hematological malignancies by either paternal or materna
170 tem cell transplantation (allo-SCT) can cure hematological malignancies by inducing alloreactive T ce
171 c the cell and temporally specific origin of hematological malignancies by targeting oncogenes into s
172 tylation or DNA methylation are approved for hematological malignancies by the US Food and Drug Admin
173 ars, it has become increasingly evident that hematological malignancies can alter their microenvironm
174 tures of ALPS as well as a predisposition to hematological malignancies can be caused by a heterozygo
175 The biological and clinical behaviors of hematological malignancies can be influenced by the acti
176 ell leukemia/lymphoma (ATL) is an aggressive hematological malignancy caused by human T-cell leukemia
177 s (MDS) are a heterogeneous group of chronic hematological malignancies characterized by dysplasia, i
178 the role of cytokines of the IL-1 family in hematological malignancies, chemotherapy-induced intesti
179 d be active in mantle cell lymphoma (MCL), a hematological malignancy clinically responsive to mTOR i
180 P = .002); survival was reduced in cases of hematological malignancies compared with diabetes mellit
182 eneic hematopoietic cell transplantation for hematological malignancies conditioned with TLI and depl
183 eneic hematopoietic cell transplantation for hematological malignancies conditioned with TLI and depl
185 ingly, although there are multiple described hematological malignancies, DC cancers are rarely observ
186 e asparagine from the blood, because several hematological malignancies depend on extracellular aspar
187 Acute promyelocytic leukemia (APL) is a hematological malignancy driven by a chimeric oncoprotei
188 s in solid tumors are not as extensive as in hematological malignancies due to several technical and
189 mong patients undergoing allogeneic HSCT for hematological malignancy, early administration of azithr
190 oach has been a paradigm in treating certain hematological malignancies, efforts to translate this su
191 In contrast, the function of heparanase in hematological malignancies (except myeloma) was not inve
193 f NK cells developing in three patients with hematological malignancies given umbilical cord blood tr
194 tor interferon regulatory factor 4 (IRF4) in hematological malignancies has been increasingly recogni
195 40 years, the approach to classification of hematological malignancies has evolved from descriptive
196 the glycolytic pathway for the treatment of hematological malignancies has sufficient rationale give
197 gulate T cell activation versus tolerance to hematological malignancies have been underexplored.
202 hosphorylation underlies the pathogenesis of hematological malignancies; however, the extent to which
203 Comparison of these findings to mutations in hematological malignancies identified several recurrentl
204 urrently being tested in clinical trials for hematological malignancies, impairs PDA tumorigenesis by
206 mples that alteration of the BMM can lead to hematological malignancies in mice, we describe, without
207 ffect has been understudied in patients with hematological malignancies in noncritical care units.
208 h broad antitumor activity against solid and hematological malignancies in phases 2 and 3 clinical tr
209 from both solid epithelial cancers and some hematological malignancies in which FAK inhibitors have
210 plicated in inflammatory diseases as well as hematological malignancies in which the AKT pathway is o
213 genes in mixed lineage leukemia (MLL)-based hematological malignancies, in the control of induced ge
214 (HSCT) is a critically important therapy for hematological malignancies, inborn errors of metabolism,
215 ells have been highly successful in treating hematological malignancies, including acute and chronic
216 r of these cells is often used for high-risk hematological malignancies, including acute myeloid leuk
218 e in cell survival and proliferation in many hematological malignancies, including multiple myeloma (
219 e a role in the treatment of diseases beyond hematological malignancies, including solid tumors and a
220 lts demonstrate that the presence of SV40 in hematological malignancies is associated with promoter m
221 ion of the mechanisms of immune tolerance in hematological malignancies is critical to inform the dev
222 d tumors, the importance of Trk signaling in hematological malignancies is underexplored and warrants
223 invasive mold disease (IMD) in patients with hematological malignancy is not standardized and is a ch
224 Z has shown remarkable antitumor activity in hematological malignancies, it has been less effective i
225 n has shown remarkable antitumor activity in hematological malignancies, it has been less effective i
226 ancer, with studies of both solid tumors and hematological malignancies leading to the development of
227 topoietic stem cell donors for patients with hematological malignancies, leukemia-associated mutation
228 nsplantation (BMT) as a curative therapy for hematological malignancies lies in the successful separa
229 effective in the treatment of children with hematological malignancies, marrow failure, immunodefici
230 atients with erythema migrans and underlying hematological malignancy more often had signs of dissemi
231 ction (septicemia, pneumonia, tuberculosis), hematological malignancy (non-Hodgkin's lymphoma, leukem
232 tion (infection, neurological condition, and hematological malignancy), nor by cumulative number of p
233 ultiple myeloma (MM), a bone marrow-resident hematological malignancy of plasma cells, has remained l
235 ibodies are widely used for the treatment of hematological malignancies or autoimmune disease but may
236 le 84 (52.5%) individuals had a diagnosis of hematological malignancies or chronic myeloproliferative
237 rnative approach for patients with high-risk hematological malignancies or marrow failure syndromes.
240 ast cancer (OR, 1.48; 95% CI, 1.11 to 1.96), hematological malignancies (OR, 1.70; 95% CI, 1.13 to 2.
241 m exposure (OR: 3.23; 95% CI: 1.67-6.25) and hematological malignancies (OR: 2.85; 95% CI: 1.10-7.41)
244 mples obtained from 33 cases with underlying hematological malignancies receiving induction chemother
245 ection is associated with increased risk for hematological malignancies, related lymphoproliferative
246 B virus (HBV) infection who are treated for hematological malignancies remain at risk for HBV reacti
247 studied in solid cancers, their functions in hematological malignancies remain poorly understood.
251 phoblastic leukemia (T-ALL) is an aggressive hematological malignancy resulting from the dysregulatio
252 ing glucose consumption for the treatment of hematological malignancies seems to be a promising field
253 no differences in the incidence of solid and hematological malignancies, serious infections, graft fa
254 tes with increased mortality rates, risk for hematological malignancy, smoking behavior, telomere len
256 nepithelial cancer cell lines, as well as in hematological malignancies such as multiple myeloma, and
257 preferentially induces apoptosis in various hematological malignancies, suggesting that EZH2 may be
258 ymphoblastic lymphoma (T-LBL) are aggressive hematological malignancies that are currently treated wi
259 istration for the treatment of the subset of hematological malignancies that are dependent on the ext
260 tion of tumor types in terms of solid versus hematological malignancies that can be best targeted wit
263 g regimens used when performing BMT to treat hematological malignancies, the reduced intensity condit
264 ous treatments were reported in a variety of hematological malignancies, there were a number of prese
265 ments are also involved in rearrangements in hematological malignancies; three are putative tumor sup
266 ted a multicenter, phase 1 study in advanced hematological malignancies to assess the safety, efficac
268 antimicrobial stewardship interventions in a hematological malignancy unit: monthly antibiotic cyclin
269 ype 2 and in cancer immunotherapy trials for hematological malignancies using chimeric antigen recept
271 ell surface of various tumor cells including hematological malignancies, was identified as an activat
272 antigen negative) receiving chemotherapy for hematological malignancies, we conducted a meta-analysis
274 resses miR-155 and develops miR-155-addicted hematological malignancy, we describe here a multi-step
276 Lymphoma is the most common type of canine hematological malignancy where the multicentric (cMCL) f
277 plays a profound role in the pathogenesis of hematological malignancies, which is often the result of
278 -line-associated bacteremia in patients with hematological malignancies who are hospitalized for cyto
279 line-associated bacteremia in patients with hematological malignancies who are hospitalized for cyto
280 nrandomized trial involving 36 patients with hematological malignancies who had clinical suspicion of
281 lid tumor patients and 6,652 patients with a hematological malignancy who were admitted between 2009
282 underlying diseases (65% without underlying hematological malignancy) who had BALF galactomannan (GM
284 rms of immunotherapy, redirecting T cells to hematological malignancies with bispecific antibodies (B
285 sing therapeutic target for the treatment of hematological malignancies with DDR defects, where ATM/p
286 dentical related donors for the treatment of hematological malignancies with end-stage renal failure.
287 had unprecedented impact in the treatment of hematological malignancies with few therapeutic options.
288 has shown considerable efficacy in treating hematological malignancies with induction of programmed
289 sults, we conclude that, as in solid tumors, hematological malignancies with MSI are also associated
290 cell-targeted BsAbs for the immunotherapy of hematological malignancies with special focus on conduct
292 phoblastic leukemia (T-ALL) is an aggressive hematological malignancy with a dismal prognosis in pati
294 cell (PDC) neoplasm (BPDCN) is an aggressive hematological malignancy with a poor prognosis that deri
295 cute Myeloid Leukemia (AML) is an aggressive hematological malignancy with abnormal progenitor self-r
296 phoblastic leukemia (T-ALL) is an aggressive hematological malignancy with an increased incidence in
297 ith a solid tumor and 13,538 patients with a hematological malignancy with an unplanned ICU admission
299 equently in acute myeloid leukemia and other hematological malignancies, with the majority ( approxim
300 with resolved HBV receiving chemotherapy for hematological malignancies without antiviral prophylaxis