ライフサイエンスコーパス: hematologic

1 en experienced dose-limiting toxicities (all hematologic).

2 ter 1980 the CIR of active TB was highest in hematologic (219/100,000 population, IRR=26), head and n

3 re association of congenital hemangioma with hematologic abnormalities and verifies somatic activatin

4 ic blood-cell clone in persons without other hematologic abnormalities, is common among older persons

5 They are rarely associated with transient hematologic abnormalities, which are typically less seve

6 ompared the renoprotective, hemodynamic, and hematologic activities and survival effects of identical

7 ction, both requiring hospitalization) and 2 hematologic adverse effects (grade 4 neutropenia and thr

8 ar-plantar erythrodysesthesia (8% v 4%), and hematologic adverse events (3% v 22%).

9 experienced more grade 3 and 4 drug-related hematologic adverse events (AEs) and fewer nonhematologi

10 With the exception of hematologic adverse events and PN, other grade 3 or 4 to

11 Hematologic adverse events are common during continuous

12 Grade 3 or greater overall hematologic adverse events were associated with V732I (O

13 topenia (22%) were the most common grade 3-4 hematologic adverse events.

14 er, these therapies result in an increase in hematologic adverse events.

15 Vital signs and hematologic and biochemical parameters were monitored be

16 The remaining hematologic and biochemical results were normal.

17 ed dose (MTD), recommended phase 2 dose, and hematologic and clinical response.

18 cific T lymphocytes has been correlated with hematologic and cytogenetic remissions in patients with

19 hours posttreatment, the overall pattern of hematologic and immunologic changes suggest that posttre

20 HCT) is a potentially curative treatment for hematologic and immunologic diseases.

21 Toxic effects were primarily hematologic and included neutropenia (grade 3, n = 20 [3

22 ps in knowledge about gestational changes in hematologic and iron variables and regulatory aspects of

23 in patients receiving volasertib were mainly hematologic and manageable.

24 ajor diagnostic criteria in combination with hematologic and morphological abnormalities.

25 TC deficiency can produce the hematologic and neurologic complications after birth, wh

26 Because G6PD is expressed by a variety of hematologic and nonhematologic cells, a broader clinical

27 CLARA cycles were associated with higher hematologic and nonhematologic toxicity than HDAC cycles

28 ial and alternating groups exhibited similar hematologic and nonhematologic toxicity.

29 only, 23%; (3) organ R/P only, 32%; (4) both hematologic and organ R/P, 31%; and (5) suboptimal respo

30 ing body weight, analyzing blood samples for hematologic and renal toxicity (hemoglobin, leukocytes,

31 up to 95%, with a low incidence of long-term hematologic and renal toxicity, have been reported.

32 ctive TB decreased by 3 fold and 6.5 fold in hematologic and solid cancers respectively before and af

33 between hematopoietic stem cells (as well as hematologic and solid tumor cells) and their protective

34 Blood chemistry, hematologic, and body mass correlates of psychological s

35 cacy of ipilimumab in patients with relapsed hematologic cancer after allogeneic HSCT.

36 Multiple myeloma (MM) is a plasma B-cell hematologic cancer that causes significant skeletal morb

37 and is associated with an increased risk of hematologic cancer.

38 Sensitivity was lower for hematologic cancers (69%, 95% CI: 41, 89) and melanoma (

39 umab was feasible in patients with recurrent hematologic cancers after allogeneic HSCT, although immu

40 or ascertaining incident cancers, other than hematologic cancers and melanoma, in multistate cohort s

41 After excluding hematologic cancers and melanoma, sensitivity was 94% (9

42 Patients with hematologic cancers and those who died after 2004 were m

43 ovides guidelines for clinical management of hematologic cancers during the perinatal period, which w

44 led to an increased incidence of subsequent hematologic cancers, and CH-PD was associated with short

45 cells has demonstrated high success rates in hematologic cancers, but results against solid malignanc

46 ers an increased risk for the development of hematologic cancers.

47 h as islets, liver, skin, and most solid and hematologic cancers.

48 lineage restricted, non-essential targets in hematologic cancers.

49 ll transplantation (HSCT) permits relapse of hematologic cancers.

50 nt, as it is overexpressed in many solid and hematologic cancers.

51 However, due to the scarcity of CCSCs among hematologic cells in the blood and the complexity of the

52 All patients achieved a molecular or hematologic complete remission (CR) after T-cell therapy

53 can be used in future simulation studies of hematologic complications of T2DM patients.

54 mes are usually identified when they develop hematologic complications such as severe bone marrow fai

55 cted from the medical records, including any hematologic complications that occurred within 3 months

56 primary therapy for bulky disease, profound hematologic compromise, or constitutional symptoms attri

57 Unlike most hematologic conditions in which the diagnosis is intenti

58 (TLR) activation contributes to premalignant hematologic conditions, such as myelodysplastic syndrome

59 of 3 prior lines of therapy, with a previous hematologic CR in only 5 patients.

60 characterized by cerebellar ataxia, variable hematologic cytopenias, and predisposition to marrow fai

61 Hematologic defects that can be corrected with an alloge

62 rge and were alive and in remission of their hematologic disease after a follow-up of 18 (range, 5-30

63 uired severe aplastic anemia (SAA) is a rare hematologic disease associated with significant morbidit

64 to analyze the impact of CMV reactivation on hematologic disease relapse in the current era.

65 CMV reactivation had no preventive effect on hematologic disease relapse irrespective of diagnosis.

66 d does not seem to confer protection against hematologic disease relapse.

67 arameters out of normal range as a result of hematologic disease should be included in trials.

68 nd, but diagnostic criteria for MDS or other hematologic diseases are not fulfilled, a condition term

69 type I, which is seen exclusively in clonal hematologic diseases, and type II/III, which is called m

70 uring an immune response and in premalignant hematologic diseases, such as MDS.

71 berrant PKA signaling in the pathogenesis of hematologic diseases.

72 netic subgroup, age, and history of previous hematologic disorder or antineoplastic therapy.

73 n with and without ovarian cancer (none with hematologic disorder).

74 ophil number and survival are common to both hematologic disorders and chronic inflammatory diseases.

75 oplasms (MPNs) are a group of related clonal hematologic disorders characterized by excess accumulati

76 consequence, many human leukemias and other hematologic disorders do not robustly engraft in these c

77 a curative therapy for several nonmalignant hematologic disorders through the provision of donor-der

78 treatment of patients with life-threatening hematologic disorders.

79 underpinnings of nonmalignant and malignant hematologic disorders.

80 aim of this study was to analyze persistent hematologic dysfunction (PHD) after PRRT with (177)Lu-DO

81 mplications for transcription factor-related hematologic dysfunctions.

82 gnificance (MGUS) is, in many ways, a unique hematologic entity.

83 0.0%; P = .02), translating into a prolonged hematologic event-free survival (hemEFS; median, 46.1 vs

84 nclusions: Individuals living in the US with hematologic, head and neck, and lung cancers had a 9-fol

85 Individuals living in the US with hematologic, head and neck, and lung cancers had a 9-fol

86 acy of CTPA in a larger cohort including non-hematologic immunocompromised patients.

87 Toxicity was predominantly hematologic in nature but was not statistically higher i

88 59 patients (56%), and the most common were hematologic, including anemia (15%), neutropenia (11%),

89 ence gap that is related to whether changing hematologic indexes in otherwise asymptomatic pregnant w

90 cy on the basis of megaloblastic anemia as a hematologic indicator in persons >/=4 y of age (e.g., se

91 Pertinent hematologic laboratory investigations revealed a white b

92 omised, distributed into solid tumors (122), hematologic malignancies (106), and nonmalignant immunos

93 monstrated tremendous success in eradicating hematologic malignancies (e.g., CD19 CARs in leukemias).

94 Forty-three patients with high-risk hematologic malignancies (median age, 43 years) were enr

95 Twenty-two patients developed hematologic malignancies (posttransplant lymphoprolifera

96 investigate the risk and outcomes of second hematologic malignancies (SHMs) in a population-based co

97 22 primary patient samples from a variety of hematologic malignancies against a panel of 48 drug comb

98 ) patients, including 18 (36%) patients with hematologic malignancies and 5 (10%) patients with solid

99 One hundred patients were studied, 50 with hematologic malignancies and 50 with solid tumors.

100 bispecific antibodies (bsAb) show promise in hematologic malignancies and are also being evaluated in

101 and systemic diseases such as B-cell lineage hematologic malignancies and connective tissue disorders

102 hereditary cancer syndromes with associated hematologic malignancies and contribute to clinically ef

103 d higher rates of spontaneous tumors, mainly hematologic malignancies and hepatocellular adenomas and

104 activation-dampening molecule participate in hematologic malignancies and may serve as a key determin

105 and tumor models, representing a variety of hematologic malignancies and solid tumor indications.

106 ch can impact outcome through progression to hematologic malignancies and through cell-non-autonomous

107 ients age 70 years or older who had solid or hematologic malignancies and underwent a geriatric asses

108 Patients with hematologic malignancies are at highest risk even when e

109 ogies, more hereditary cancer syndromes with hematologic malignancies are being described.

110 individuals with germ line predisposition to hematologic malignancies are diagnosed with increasing f

111 Hematologic malignancies are driven by combinations of g

112 p spontaneous bone marrow failure or diverse hematologic malignancies by 6 months of age.

113 Many patients with hematologic malignancies cannot tolerate hematopoietic c

114 scades, functioning as a tumor suppressor in hematologic malignancies driven by those pathways.

115 and are often activated in solid tumors and hematologic malignancies due to intratumoral hypoxia and

116 entially curative treatment for a variety of hematologic malignancies due to the well-recognized graf

117 The incidence of hematologic malignancies during pregnancy is 0.02%.

118 nt of chronic HCV infection in patients with hematologic malignancies has evolved rapidly as safe and

119 inical trials in patients with mIDH advanced hematologic malignancies have demonstrated compelling cl

120 ibits potent antileukemic effects on several hematologic malignancies including chronic myeloid leuke

121 Development of hematologic malignancies is driven by mutations that may

122 Advancement of many solid tumors and hematologic malignancies is frequently characterized by

123 n HSCs invariably lead to the development of hematologic malignancies or bone marrow failure syndrome

124 ddress platelet transfusion in patients with hematologic malignancies or solid tumors or in those who

125 ome inhibitors, and to demonstrate that many hematologic malignancies predominantly express immunopro

126 The diagnosis of hematologic malignancies relies on multidisciplinary wor

127 rived acute myeloid leukemia (AML) and other hematologic malignancies such as myelofibrosis (MF) in m

128 yndrome was not more frequently related with hematologic malignancies than classic neutrophilic Sweet

129 syndrome is more frequently associated with hematologic malignancies than classic Sweet syndrome.

130 R) T cells can produce durable remissions in hematologic malignancies that are not responsive to stan

131 (VitD) deficiency is common in patients with hematologic malignancies undergoing allogeneic transplan

132 domized clinical trial among 160 adults with hematologic malignancies undergoing autologous/allogenei

133 although mortality from prostate cancer and hematologic malignancies was noted in the American Cance

134 rmline mutations in children and adults with hematologic malignancies was previously underappreciated

135 Those with hematologic malignancies were at highest risk (odds rati

136 Nonmalignant immunosuppression and hematologic malignancies were independently associated w

137 , but much less immunogenic in patients with hematologic malignancies where the immune system is supp

138 thods We randomly assigned 160 patients with hematologic malignancies who underwent autologous or all

139 Among patients with hematologic malignancies who underwent hematopoietic ste

140 y produced TPO (a microenvironment factor in hematologic malignancies) or c-MPL-targeted pharmacologi

141 residents (n = 1,792; 52% allogeneic and 90% hematologic malignancies) were frequency matched by demo

142 Solid cancer, pneumonia in hematologic malignancies, and do-not-resuscitate status

143 evidence for mortality from prostate cancer, hematologic malignancies, and kidney cancer.

144 ) signaling and are used in the treatment of hematologic malignancies, block BCR-mediated lytic induc

145 extracranial embryonal tumors, brain tumors, hematologic malignancies, carcinomas, and gonadal tumors

146 ical scenarios of HCV-infected patients with hematologic malignancies, focusing on diagnosis, clinica

147 ated with worse survival in most subtypes of hematologic malignancies, in a dose-response fashion.

148 T-cell therapeutics in patients with B-cell hematologic malignancies, in light of differences in CAR

149 currently also under investigation in other hematologic malignancies, including acute lymphoblastic

150 ve uncovered a spectrum of mutations in many hematologic malignancies, including acute myeloid leukem

151 ation of variants associated with hereditary hematologic malignancies, including the importance of an

152 In other hematologic malignancies, particularly leukemias, the ab

153 ndition, such as severe infections, solid or hematologic malignancies, trauma, or obstetric calamitie

154 International Consensus Meeting of Prenatal Hematologic Malignancies, which took place in Leuven, Be

155 ved HBV infection receiving chemotherapy for hematologic malignancies.

156 ly produce positive results in patients with hematologic malignancies.

157 y of duvelisib in 210 patients with advanced hematologic malignancies.

158 drug response in 86 patients with refractory hematologic malignancies.

159 nce, survival, and outcomes in patients with hematologic malignancies.

160 tification of novel treatment strategies for hematologic malignancies.

161 in personalized management of patients with hematologic malignancies.

162 own about these disparities in patients with hematologic malignancies.

163 linical relevance of CH in patients with non-hematologic malignancies.

164 actors have emerged as a hallmark of several hematologic malignancies.

165 Some are associated with predisposition to hematologic malignancies.

166 hich -DNMT3A- is frequently mutated in human hematologic malignancies.

167 f malignancies arising in donors including 3 hematologic malignancies.

168 risk of developing AML and CML but no other hematologic malignancies.

169 therapeutic target for the treatment of non-hematologic malignancies.

170 or in combination, in both solid tumors and hematologic malignancies.

171 ay increase treatment options for aggressive hematologic malignancies.

172 s among the most frequently mutated genes in hematologic malignancies.

173 ection afflicting patients with diabetes and hematologic malignancies.

174 e measures are appropriate for patients with hematologic malignancies.

175 tumors, and similar evidence has emerged in hematologic malignancies.

176 n important role in detection and staging of hematologic malignancies.

177 therapeutically beneficial, particularly for hematologic malignancies.

178 imab vedotin efficacy in other CD30-positive hematologic malignancies.

179 is a promising approach for the treatment of hematologic malignancies.

180 blastic leukemia and lymphoma, but not other hematologic malignancies.

181 advances have been made in various areas of hematologic malignancies.

182 ent of patients affected by diverse forms of hematologic malignancies.

183 ation (BMT) is used with curative intent for hematologic malignancies.

184 eased significantly over time, especially in hematologic malignancies.

185 might be an attractive new approach to treat hematologic malignancies.

186 ranslocations are a genomic hallmark of many hematologic malignancies.

187 ociated with a higher risk of early death in hematologic malignancies.

188 of 3 approaches to molecular diagnostics in hematologic malignancies: indication-specific single gen

189 factors were associated with ICU admission: hematologic malignancy (odds ratio, 1.51; 95% CI, 1.26-1

190 Primary myelofibrosis (PMF) is a clonal hematologic malignancy characterized by BM fibrosis, ext

191 Hairy cell leukemia is an uncommon hematologic malignancy characterized by pancytopenia and

192 Acute myeloid leukemia (AML) is a deadly hematologic malignancy characterized by the uncontrolled

193 Diagnosis of an inherited predisposition to hematologic malignancy informs choice of therapy, risk o

194 Multiple myeloma (MM) is an age-related hematologic malignancy of clonal bone marrow plasma cell

195 y recognized form of GN, but its relation to hematologic malignancy remains poorly understood.

196 The recognition that patients with inherited hematologic malignancy syndromes may present without cla

197 c leukemia (T-ALL) is a highly proliferative hematologic malignancy that results from the transformat

198 gamma in late-stage clinical development for hematologic malignancy treatment.

199 erved during this same period in an adjacent hematologic malignancy unit, which followed the same inf

200 nts and Methods A total of 681 patients with hematologic malignancy who underwent transplantation in

201 Acute Myeloid Leukemia (AML) is a hematologic malignancy with a poor prognosis.

202 eukemia (AML) is a genetically heterogeneous hematologic malignancy, which is initiated and driven by

203 coccus (VRE) is an important complication of hematologic malignancy.

204 atch) and survival after transplantation for hematologic malignancy.

205 icts the aggressive clinical outcome of this hematologic malignancy.

206 frailty and its relevance for patients with hematologic malignancy.

207 I, 2.00-3.76; P < .001), and the presence of hematologic malignant neoplasm was associated with 1.74

208 patients, especially in SOTRs and those with hematologic malignant neoplasm, but not patients with HI

209 3 subgroups: SOTRs and patients with HIV or hematologic malignant neoplasm.

210 rognosis solid tumors, whereas patients with hematologic malignant neoplasms or less severe illness s

211 s with human immunodeficiency virus (HIV) or hematologic malignant neoplasms, increases the risk of d

212 deficiency may produce severe neurologic and hematologic manifestations.

213 t can result in the impairment of endocrine, hematologic, musculoskeletal, renal, respiratory, periph

214 had systemic mastocytosis with an associated hematologic neoplasm, and 16 had mast-cell leukemia.

215 At diagnosis or relapse of most hematologic neoplasms, malignant cells are often easily

216 1) in hematopoietic cell transplantation for hematologic neoplasms.

217 e 3/4 treatment-emergent adverse events were hematologic (neutropenia [49.7%], anemia [33.0%], and th

218 d the therapeutic was well tolerated without hematologic, nonhematologic, and cardiac toxicities.

219 In 2015, we asked a national cohort of hematologic oncologists about the acceptability of eight

220 In this large national cohort of hematologic oncologists, standard EOL quality measures w

221 sment for frailty increasingly important for hematologic oncologists.

222 toxicities consisted primarily of reversible hematologic or electrolyte abnormalities, including neut

223 re population statistical cutoffs for either hematologic or iron status but are not bioindicators of

224 mised and immunocompromised distributed into hematologic or solid malignancies and nonmalignant immun

225 e of iron status with health outcomes beyond hematologic outcomes, and 4) the balance of benefit and

226 (dFLC) has been established as an invaluable hematologic parameter in systemic amyloid light chain (A

227 stic models are mainly based on clinical and hematologic parameters, but innovative models that inclu

228 lerability and response were evaluated using hematologic parameters, renal scintigraphy, clinical dat

229 The most common grade 3 or 4 AEs were hematologic, particularly thrombocytopenia (45%).

230 alyses identified solid cancer, pneumonia in hematologic patients, and do-not-resuscitate status as i

231 to be more sensitive and specific for IPA in hematologic patients.

232 my 7, mutational status had no effect on the hematologic phenotype.

233 d 252 637 population controls unselected for hematologic phenotypes.

234 Median hematologic progression-free survival was 14.8 months; 1

235 Associated conditions were hematologic, prothrombotic, neoplastic, immune, and expo

236 whole-exome sequence association analyses of hematologic quantitative traits in 15,459 community-dwel

237 ings reveal a biomechanical answer to an old hematologic question regarding how glucocorticoids and c

238 nger time to develop organ progression after hematologic R/P (24.2 vs 3.2 months, P = .007).

239 were (1) clinical suspicion of R/P, 10%; 92) hematologic R/P only, 23%; (3) organ R/P only, 32%; (4)

240 with respect to complete remission with full hematologic recovery (34% vs. 16%, P<0.001) and with res

241 remission with full, partial, or incomplete hematologic recovery (44% vs. 25%, P<0.001).

242 s complete remission (CR) or CR with partial hematologic recovery (CRh) during the first two cycles.

243 including complete remission with incomplete hematologic recovery) and overall survival.

244 remission with full, partial, or incomplete hematologic recovery, or death, 0.55; 95% CI, 0.43 to 0.

245 nd almost all patients eventually experience hematologic relapse and progression of organ involvement

246 rsus-host disease in the patient treated for hematologic relapse.

247 a parallel Italian study validated this new hematologic remission parameter.

248 ter therapy, lead to clonal expansion during hematologic remission, and eventually lead to relapsed d

249 Complete or very good partial hematologic remissions occurred in six of 22 treated cry

250 Overall, hematologic response (HR) was 50% in 24 evaluable patien

251 mg/L showed a higher proportion of complete hematologic response after first-line therapy compared t

252 was associated with markedly higher rates of hematologic response among patients with severe aplastic

253 Hematologic response assessed with adapted criteria pred

254 We propose the appreciation of dFLC in hematologic response assessment for all patients with a

255 This strategy should allow for hematologic response assessment while avoiding the risk

256 The primary outcome was complete hematologic response at 6 months.

257 essed before and after SCT and compared with hematologic response criteria and bone marrow biopsies.

258 The validated criteria of hematologic response in light-chain (AL) amyloidosis are

259 his subgroup of patients and to define novel hematologic response parameters.

260 The overall hematologic response rate to daratumumab was 76%, includ

261 Overall, the hematologic response rate was 52% in patients treated at

262 Hematologic response to treatment at various time points

263 Hematologic response was observed in 68% of patients (ve

264 Clinical features, hematologic response, and overall survival (OS) were ana

265 MFC may have a role in the definition of hematologic response.

266 ent was generally well tolerated and induced hematologic responses in patients for whom prior AML the

267 Hematologic responses occurred in 19 of 24 patients (79%

268 Deeper hematologic responses translate into improved outcomes,

269 effective agent that produced rapid and deep hematologic responses without unexpected toxicity in our

270 Hematologic status, renal function, and serum prostate-s

271 t Foxa3 likely regulates the HSC response to hematologic stress.

272 Patients' characteristics and hematologic tests data at initial diagnosis were collect

273 ized after thorough assessment for potential hematologic toxic effects and drug-drug interactions.

274 rred in (19 [40%] of 48 patients), including hematologic toxicities (19 [40%]), hyperglycemia (12 [25

275 xperienced transient fevers and the expected hematologic toxicities from lymphodepletion pretreatment

276 Grade 3/4 hematologic toxicities occurred in 42% of the patients a

277 Grade 3/4 hematologic toxicities occurred in 42% of the patients a

278 Grade 3 and grade 4 hematologic toxicities were more common in group B, with

279 Significantly higher hematologic toxicity ( P < .001) and more infectious com

280 de should be given with close monitoring for hematologic toxicity (grade B) with dose reduction as ne

281 on (P = 0.021, n = 5/group) without subacute hematologic toxicity (n = 3/group).

282 ostic biomarker of overall survival (OS) and hematologic toxicity and as a tool for response assessme

283 PA(0)]octreotide scan, tumor load, grade 3-4 hematologic toxicity during treatment, estimated absorbe

284 sing biomarker for prognostication of OS and hematologic toxicity in late-stage mCRPC patients receiv

285 Clinical outcomes were OS and occurrence of hematologic toxicity of grades 2-5.

286 status on the basis of concern of excessive hematologic toxicity or poor outcomes may not be justifi

287 Acute hematologic toxicity was also not correlated with treatm

288 Hematologic toxicity was more pronounced with MPR-R, esp

289 Hematologic toxicity was more severe for patients receiv

290 No relevant hematologic toxicity was observed.

291 Prostate-specific antigen response and hematologic toxicity were measured at least every 4 wk.

292 The frequencies of severe grade 3 or 4 hematologic toxicity, infection, CNS events, and toxic d

293 Regarding hematologic toxicity, no statistically significant diffe

294 on of marrow may induce short- and long-term hematologic toxicity.

295 leukemia (AML) models at the cost of severe hematologic toxicity.

296 wo arms and to correlate absorbed doses with hematologic toxicity.

297 owever, associated with gastrointestinal and hematologic toxicity.

298 The primary endpoint was >/= grade 3 non-hematologic toxicity.

299 ine BSI was prognostic for the occurrence of hematologic toxicity; patients with a BSI of greater tha

300 characterization of genetic loci influencing hematologic traits.