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1 n carcinomas) and cAC10 (specific to CD30 on hematological malignancies).
2 al therapeutic targets in treating LSC-based hematological malignancy.
3 cycle regulation, degraded HSC function, and hematological malignancy.
4 ce for genetic susceptibility to this B-cell hematological malignancy.
5 iological model for VRE BSI in patients with hematological malignancy.
6 i-VRE antimicrobial therapy in patients with hematological malignancy.
7 ome for patients with this universally fatal hematological malignancy.
8 y in the contexts of development, aging, and hematological malignancy.
9 ts, suggesting that they might predispose to hematological malignancy.
10 ve been clinically used for the treatment of hematological malignancy.
11 Multiple myeloma (MM) is an age-dependent hematological malignancy.
12 t anticancer drugs against various solid and hematological malignancies.
13 in the blood of individuals without apparent hematological malignancies.
14 profiles, and expression changes underlying hematological malignancies.
15 nity in patients with bone marrow failure or hematological malignancies.
16 etic cell differentiation and causal role in hematological malignancies.
17 olic interventions in ALL and possibly other hematological malignancies.
18 with both developmental growth disorders and hematological malignancies.
19 e for the expression of CCL5 and CCR5 in non-hematological malignancies.
20 ns in a population of patients with advanced hematological malignancies.
21 arious diseases and is approved for treating hematological malignancies.
22 me, miR-22 transgenic mice developed MDS and hematological malignancies.
23 ination chemotherapies, especially targeting hematological malignancies.
24 ation of patients with high-risk or advanced hematological malignancies.
25 olecular mechanism of CQ in the treatment of hematological malignancies.
26 in key chromatin modifiers, most notably in hematological malignancies.
27 systolic dysfunction (LVSD) in patients with hematological malignancies.
28 enic viruses with IRF4 in the development of hematological malignancies.
29 agents for the treatment of solid tumors and hematological malignancies.
30 y of cell survival control in epithelial and hematological malignancies.
31 ptional dynamics during hematopoiesis and in hematological malignancies.
32 nsplantation (BMT), an effective therapy for hematological malignancies.
33 exin may have tumor suppressor properties in hematological malignancies.
34 of cancers and are particularly prominent in hematological malignancies.
35 st overexpressed miRNAs in several solid and hematological malignancies.
36 the only treatment option for several severe hematological malignancies.
37 all types of carcinomas and various types of hematological malignancies.
38 suppressor function in both solid tumors and hematological malignancies.
39 or impediment to the successful treatment of hematological malignancies.
40 role of the bone marrow microenvironment in hematological malignancies.
41 in targeting glycolysis for the treatment of hematological malignancies.
42 nged understanding of the molecular basis of hematological malignancies.
43 ave already been performed in the setting of hematological malignancies.
44 FAO inhibitors as a therapeutic strategy in hematological malignancies.
45 e clinically active in both solid tumors and hematological malignancies.
46 m stem cell to mature tissue, similar to the hematological malignancies.
47 (HSCT) have been shown to cure patients with hematological malignancies.
48 in patients with small cell lung cancer and hematological malignancies.
49 nd no significantly increased risk for other hematological malignancies.
50 l tools to treat or suppress oncogene-driven hematological malignancies.
51 olecular basis of certain cancers, including hematological malignancies.
52 cancer agents for the treatment of solid and hematological malignancies.
53 mulated the development of vaccines to treat hematological malignancies.
54 nsplantation (BMT), an effective therapy for hematological malignancies.
55 tic system to study blood cell formation and hematological malignancies.
56 eneic transplantation to a growing number of hematological malignancies.
57 herapy target for the treatment of solid and hematological malignancies.
58 have been implicated in the pathogenesis of hematological malignancies.
59 cancer agents for the treatment of solid and hematological malignancies.
60 ay represent a novel therapeutic strategy in hematological malignancies.
61 (MV-Edm) had antineoplastic efficacy against hematological malignancies.
62 may also be useful in the treatment of other hematological malignancies.
63 genic conversion of transcription factors in hematological malignancies.
64 D26/DPPIV in the treatment of selected human hematological malignancies.
65 -tumor effects against a number of different hematological malignancies.
66 lines and 44% of the cell lines derived from hematological malignancies.
67 se in treating patients with CD40-expressing hematological malignancies.
68 d seems to act as a tumor suppressor gene in hematological malignancies.
69 rrow transplantation (BMT) for patients with hematological malignancies.
70 entially in the growth of human biphenotypic hematological malignancies.
71 current translocation reported in a range of hematological malignancies.
72 icacy of selinexor in patients with advanced hematological malignancies.
73 q, a region strongly associated with various hematological malignancies.
74 es are one of the most common alterations in hematological malignancies.
75 4A in the major types of adult and pediatric hematological malignancies.
76 o pesticides have increased risks of various hematological malignancies.
77 pathogenesis of several myeloid and lymphoid hematological malignancies.
78 tuximab, is an established means of treating hematological malignancies.
79 -HSCT) is a potentially curative therapy for hematological malignancies.
80 a promising therapeutic target for specific hematological malignancies.
81 iseases, cancer mortality, and high risk for hematological malignancies.
82 or patients with recurrent and/or refractory hematological malignancies.
83 rtant therapy for patients with a variety of hematological malignancies.
84 l targeted epigenetic therapies for treating hematological malignancies.
85 promising diagnostic tool for patients with hematological malignancies.
86 mal epigenetic control to the development of hematological malignancies.
87 are associated with many diseases, including hematological malignancies.
88 veral phase 1 trials of cancer patients with hematological malignancies.
89 Activating JAK2 mutants cause hematological malignancies.
90 components of the RNA splicing machinery in hematological malignancies.
91 s, in individuals without clear diagnosis of hematological malignancies.
92 ed compared with control samples in multiple hematological malignancies.
93 ssociation between paternal age at birth and hematological malignancies.
94 gs of invasive mold disease in patients with hematological malignancies.
95 tors could prove useful for the treatment of hematological malignancies.
96 y been approved for the treatment of several hematological malignancies.
97 protect HSC pool integrity, guarding against hematological malignancies.
98 tive for selected HIV-infected patients with hematological malignancies.
99 65 (56%) had solid tumors, and 140 (47%) had hematological malignancies.
100 -mC, 5-hmC, and their enzymatic modifiers in hematological malignancies.
101 elop novel epigenetic therapies for treating hematological malignancies.
102 d be prioritized for targeting in a range of hematological malignancies.
103 robes, we analyzed 204 patients with diverse hematological malignancies accompanied by clonal chromos
105 Myelodysplastic syndrome is an important hematological malignancy affecting the expanding aged po
107 ion of susceptibility for hematotoxicity and hematological malignancy among workers with a history of
108 their cancer management: 15 of 28 (54%) with hematological malignancies and 27 of 63 (43%) with solid
109 in all calculations, including 28 (31%) with hematological malignancies and 63 (69%) with solid tumor
110 ted mortality and morbidity in patients with hematological malignancies and bone marrow transplants.
111 in 11 cell lines derived from patients with hematological malignancies and demonstrated that six out
112 ine samples from 71 patients with underlying hematological malignancies and found that the urine GM/c
114 table mortality, especially in patients with hematological malignancies and in hematopoietic stem cel
115 I3Kdelta) is an appealing target for several hematological malignancies and inflammatory diseases.
116 re Food and Drug Administration-approved for hematological malignancies and inhibit class II and/or c
117 f the most frequently mutated genes in human hematological malignancies and is a critical factor for
118 her CT imaging findings in 100 patients with hematological malignancies and possible invasive mold di
119 activity play critical roles in treatment of hematological malignancies and refractory autoimmune dis
120 implicated in numerous pathologies including hematological malignancies and rheumatoid arthritis.
121 expression and regulation of TET proteins in hematological malignancies and solid tumors, and discuss
125 p73 is a frequent event in specific types of hematological malignancies and suggest that epigenetic s
126 tional Cancer Institute hosted a workshop on hematological malignancies and the marrow microenvironme
128 are settings, especially among patients with hematological malignancies and those who are immunocompr
129 te for dCK-inhibitor based therapies against hematological malignancies and, potentially, other cance
130 f common, low-penetrance susceptibility to a hematological malignancy and new insights into disease c
131 cell non-Hodgkin lymphoma is the most common hematological malignancy and represents a substantial cl
132 myeloablative preparative regimen to treat a hematological malignancy and to provide allotolerance fo
133 ce of certain autoimmune diseases, increased hematological malignancies, and elevated incidence of ag
134 tive therapeutics for in vivo eradication of hematological malignancies, and ex vivo purging of cance
135 H signaling, its role in the pathobiology of hematological malignancies, and its potential as a thera
136 t decade have these cells been identified in hematological malignancies, and more recently in solid t
137 ly to induce synthetic sickness/lethality in hematological malignancies, and possibly in other cancer
140 lators are targets for dysregulation in many hematological malignancies, and that patterns of histone
141 d clinical course, the evolution to advanced hematological malignancies, and the accessibility of neo
142 and p16INK4A characterize different types of hematological malignancy, and alterations in these tumor
143 ars old, had undergone allogeneic HSCT for a hematological malignancy, and had available pretransplan
144 ltiple myeloma (MM) is a presently incurable hematological malignancy, and novel biologically based t
145 factors, which is rearranged in a variety of hematological malignancies; and KIP1, the gene encoding
146 ematological malignancies, but whether these hematological malignancies are associated with MMR defic
148 disorders, including autoimmune diseases and hematological malignancies, are at risk of developing os
150 ase hematopoietic cell kinase (HCK) triggers hematological malignancies as a tumor cell-intrinsic onc
151 ce for genetic susceptibility to this B-cell hematological malignancy, as well as insight into the bi
152 e small, but significant, risks of solid and hematological malignancies associated with increased rad
153 n profiling has been applied to a variety of hematological malignancies, autoimmune disorders, and in
154 splantation (BMT) is currently restricted to hematological malignancies because of a lack of antitumo
155 have demonstrated promising results against hematological malignancies, but have encountered signifi
156 ntation (allo-BMT) is a curative therapy for hematological malignancies, but is associated with signi
157 Expression of c-Myb is often increased in hematological malignancies, but the underlying mechanism
160 ere was no clear linear trend in the risk of hematological malignancies by either paternal or materna
161 tem cell transplantation (allo-SCT) can cure hematological malignancies by inducing alloreactive T ce
162 c the cell and temporally specific origin of hematological malignancies by targeting oncogenes into s
163 tylation or DNA methylation are approved for hematological malignancies by the US Food and Drug Admin
164 ars, it has become increasingly evident that hematological malignancies can alter their microenvironm
165 tures of ALPS as well as a predisposition to hematological malignancies can be caused by a heterozygo
166 The biological and clinical behaviors of hematological malignancies can be influenced by the acti
167 elated volunteer donors for the treatment of hematological malignancy can be optimized by complete an
168 s (MDS) are a heterogeneous group of chronic hematological malignancies characterized by dysplasia, i
169 the role of cytokines of the IL-1 family in hematological malignancies, chemotherapy-induced intesti
170 d be active in mantle cell lymphoma (MCL), a hematological malignancy clinically responsive to mTOR i
171 P = .002); survival was reduced in cases of hematological malignancies compared with diabetes mellit
173 eneic hematopoietic cell transplantation for hematological malignancies conditioned with TLI and depl
174 eneic hematopoietic cell transplantation for hematological malignancies conditioned with TLI and depl
176 ingly, although there are multiple described hematological malignancies, DC cancers are rarely observ
177 e asparagine from the blood, because several hematological malignancies depend on extracellular aspar
178 Acute promyelocytic leukemia (APL) is a hematological malignancy driven by a chimeric oncoprotei
179 s in solid tumors are not as extensive as in hematological malignancies due to several technical and
180 mong patients undergoing allogeneic HSCT for hematological malignancy, early administration of azithr
181 umor suppressor gene alterations do occur in hematological malignancies, especially structural altera
182 In contrast, the function of heparanase in hematological malignancies (except myeloma) was not inve
183 use of these agents in both solid tumors and hematological malignancies, few have addressed their eff
185 f NK cells developing in three patients with hematological malignancies given umbilical cord blood tr
186 tor interferon regulatory factor 4 (IRF4) in hematological malignancies has been increasingly recogni
187 40 years, the approach to classification of hematological malignancies has evolved from descriptive
188 the glycolytic pathway for the treatment of hematological malignancies has sufficient rationale give
189 gulate T cell activation versus tolerance to hematological malignancies have been underexplored.
190 hosphorylation underlies the pathogenesis of hematological malignancies; however, the extent to which
191 ions in patients with chemotherapy-resistant hematological malignancies; however, the selection of th
192 Comparison of these findings to mutations in hematological malignancies identified several recurrentl
193 urrently being tested in clinical trials for hematological malignancies, impairs PDA tumorigenesis by
195 h broad antitumor activity against solid and hematological malignancies in phases 2 and 3 clinical tr
197 genes in mixed lineage leukemia (MLL)-based hematological malignancies, in the control of induced ge
198 (HSCT) is a critically important therapy for hematological malignancies, inborn errors of metabolism,
199 isk, especially for increased mortality from hematological malignancies including acute myeloid leuke
200 ells have been highly successful in treating hematological malignancies, including acute and chronic
201 r of these cells is often used for high-risk hematological malignancies, including acute myeloid leuk
202 effective therapeutic agents for a number of hematological malignancies, including cutaneous T-cell l
204 e in cell survival and proliferation in many hematological malignancies, including multiple myeloma (
205 e a role in the treatment of diseases beyond hematological malignancies, including solid tumors and a
206 lts demonstrate that the presence of SV40 in hematological malignancies is associated with promoter m
207 ion of the mechanisms of immune tolerance in hematological malignancies is critical to inform the dev
208 Z has shown remarkable antitumor activity in hematological malignancies, it has been less effective i
209 n has shown remarkable antitumor activity in hematological malignancies, it has been less effective i
210 ancer, with studies of both solid tumors and hematological malignancies leading to the development of
211 nsplantation (BMT) as a curative therapy for hematological malignancies lies in the successful separa
212 effective in the treatment of children with hematological malignancies, marrow failure, immunodefici
213 atients with erythema migrans and underlying hematological malignancy more often had signs of dissemi
214 ction (septicemia, pneumonia, tuberculosis), hematological malignancy (non-Hodgkin's lymphoma, leukem
215 ight monoclonal antibodies were tested on 10 hematological malignancies of various histological types
217 rnative approach for patients with high-risk hematological malignancies or marrow failure syndromes.
219 idence for methylation in any other types of hematological malignancies or solid tumors examined.
220 ast cancer (OR, 1.48; 95% CI, 1.11 to 1.96), hematological malignancies (OR, 1.70; 95% CI, 1.13 to 2.
221 m exposure (OR: 3.23; 95% CI: 1.67-6.25) and hematological malignancies (OR: 2.85; 95% CI: 1.10-7.41)
222 mples obtained from 33 cases with underlying hematological malignancies receiving induction chemother
223 ection is associated with increased risk for hematological malignancies, related lymphoproliferative
224 B virus (HBV) infection who are treated for hematological malignancies remain at risk for HBV reacti
225 studied in solid cancers, their functions in hematological malignancies remain poorly understood.
226 ptor in other types of cancer, especially in hematological malignancies, remains to be fully elucidat
230 ing glucose consumption for the treatment of hematological malignancies seems to be a promising field
231 no differences in the incidence of solid and hematological malignancies, serious infections, graft fa
232 tes with increased mortality rates, risk for hematological malignancy, smoking behavior, telomere len
234 nepithelial cancer cell lines, as well as in hematological malignancies such as multiple myeloma, and
235 preferentially induces apoptosis in various hematological malignancies, suggesting that EZH2 may be
236 istration for the treatment of the subset of hematological malignancies that are dependent on the ext
237 agent for scintigraphic detection of various hematological malignancies that express IL-2 alpha recep
240 g regimens used when performing BMT to treat hematological malignancies, the reduced intensity condit
241 ous treatments were reported in a variety of hematological malignancies, there were a number of prese
242 ments are also involved in rearrangements in hematological malignancies; three are putative tumor sup
243 ted a multicenter, phase 1 study in advanced hematological malignancies to assess the safety, efficac
245 ype 2 and in cancer immunotherapy trials for hematological malignancies using chimeric antigen recept
246 in a group of multitransfused patients with hematological malignancy was studied using a reverse tra
247 ell surface of various tumor cells including hematological malignancies, was identified as an activat
248 antigen negative) receiving chemotherapy for hematological malignancies, we conducted a meta-analysis
251 individuals and patients with CML and other hematological malignancies were screened for high-titer
252 nrandomized trial involving 36 patients with hematological malignancies who had clinical suspicion of
253 lid tumor patients and 6,652 patients with a hematological malignancy who were admitted between 2009
255 rms of immunotherapy, redirecting T cells to hematological malignancies with bispecific antibodies (B
256 sing therapeutic target for the treatment of hematological malignancies with DDR defects, where ATM/p
257 has shown considerable efficacy in treating hematological malignancies with induction of programmed
258 sults, we conclude that, as in solid tumors, hematological malignancies with MSI are also associated
259 cell-targeted BsAbs for the immunotherapy of hematological malignancies with special focus on conduct
261 cell (PDC) neoplasm (BPDCN) is an aggressive hematological malignancy with a poor prognosis that deri
262 phoblastic leukemia (T-ALL) is an aggressive hematological malignancy with an increased incidence in
263 ith a solid tumor and 13,538 patients with a hematological malignancy with an unplanned ICU admission
264 equently in acute myeloid leukemia and other hematological malignancies, with the majority ( approxim
265 with resolved HBV receiving chemotherapy for hematological malignancies without antiviral prophylaxis
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