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1                                              HDT as consolidation therapy for relapsed ESFT seems to
2 stic model provides a basis for risk-adapted HDT.
3 py with ICE with the intent of administering HDT/ASCT to those patients with chemosensitive disease w
4 emotherapy, with the intent of administering HDT/ASCT to those with chemosensitive disease.
5                                        After HDT, hematopoietic recovery to critical levels of granul
6 tiparameter flow cytometry at day +100 after HDT/ASCT (hazard ratio 8.0; P = .005) were the only inde
7 ries of 241 patients in CR at day +100 after HDT/ASCT who were enrolled in the Spanish GEM2000 (n = 1
8 n whom cytogenetic data were available after HDT.
9    All patients who achieved BCR or CR after HDT-ASCT (ACR) were identified.
10 fore could optimise the chance of cure after HDT/ASCT.
11 ents with MDS-CAs, its detection early after HDT was associated with longer time interval from diagno
12 nts in CR at risk of early progression after HDT/ASCT in whom novel treatments should be investigated
13 older age, and lower platelet recovery after HDT; persistent MDS-CAs were predicted by CD34 yield of
14                              Rituximab after HDT and HCT is feasible, and these phase 2 data support
15  patients who experienced relapse soon after HDT suggest that more aggressive induction chemotherapy
16 ML, at a median follow-up of 5.9 years after HDT.
17          Therefore, dose-dense induction and HDT/ASCT are a rational up-front strategy in transplanta
18 n response rates between the two study arms (HDT, n = 261 patients; SDT, n = 255 patients).
19 ttering from chemisorption of the Lewis base HDT on the atom-scale junction caused a normalized imped
20 d after salvage chemotherapy (ST) and before HDT-ASCT by modern criteria.
21 nts received reinduction chemotherapy before HDT and HSCR.
22 We hypothesized that patients with CR before HDT-ASCT (BCR) will have their disease burden reduced fu
23 els of abnormal cells can be detected before HDT and may predict which patients are at increased risk
24 of clonally abnormal cells were found before HDT in 20 of 20 tMDS/sAML patients screened, compared wi
25        An intensive induction regimen before HDT and ASCT was not associated with improved survival a
26 oma should be a negative FDG-PET scan before HDT/ASCT.
27 ntense second-line chemotherapy, followed by HDT and ASCT, are reported.
28             Dose-dense induction followed by HDT/ASCT was well tolerated and led to long-term PFS in
29 ezomib/thalidomide/dexamethasone followed by HDT/ASCT; n = 276).
30 , adriamycin, and dexamethasone) followed by HDT/ASCT; n = 319] and GEM2005<65y (randomized induction
31  HD-RIT and 53% and 29%, respectively, for C-HDT.
32 the HD-RIT group and.086 at 7 years in the C-HDT group.
33 as 3.7% in the HD-RIT group and 11% in the C-HDT group.
34 n = 27) or conventional high-dose therapy (C-HDT) (n = 98) and autologous hematopoietic stem cell tra
35         HD-RIT may improve outcomes versus C-HDT in patients with relapsed FL.
36                      Patients treated with C-HDT received total body irradiation plus chemotherapy (7
37  0.5, P =.03) versus patients treated with C-HDT.
38 sease (HD) with high-dose chemoradiotherapy (HDT) and autologous stem cell transplantation (ASCT) res
39 o had undergone high-dose chemoradiotherapy (HDT) with autologous stem cell rescue for Hodgkin's dise
40                 High-dose chemoradiotherapy (HDT) with autologous stem cell transplantation (ASCT) is
41 olidated by up-front high-dose chemotherapy (HDT) and autologous stem-cell transplantation (ASCT) in
42 one or two cycles of high-dose chemotherapy (HDT) followed by autologous HSCR.
43                      High-dose chemotherapy (HDT) plus autologous stem cell transplantation (ASCT) is
44 rove PFS after high-dose radio-chemotherapy (HDT) and ASCT.
45        Four patients who completed the first HDT course did not complete the second, and there were t
46   Treatment-related mortality with the first HDT cycle was 2% in younger and 8% among older subjects,
47 uivalent to a population fluctuation of five HDT molecules.
48 rtion of patients who achieve a CR following HDT, although other biologic characteristics of the tumo
49 9.8 +/- 4.6 for sitting, and 6.6 +/- 2.5 for HDT.
50  every 12 h, day 1) before consideration for HDT/ASCT.
51 mpedance was measured while hexadecanethiol (HDT) was chemisorbed onto the atom-scale junction.
52 ting, or HDT (P >/= 0.11), except for IOP in HDT (P = 0.04).
53     Patients then received tandem courses of HDT/SCR, 4 to 6 weeks apart.
54         Four patients received two cycles of HDT and HSCR.
55  12 years) were assessable, and 70 cycles of HDT/SCR were completed.
56 nistic nature of the different mechanisms of HDT over short timescales means their contribution to ba
57 or understanding the evolutionary origins of HDT.
58 significantly, justifying further pursuit of HDT, especially toward curing non-triangle up13 MM.
59                                   The use of HDT with ABMT has been shown to improve survival in mult
60 ts who lose their CR status within 1 year of HDT/ASCT (unsustained CR) have poor prognosis.
61                     Clinical utility data on HDT benefit in these patients and other special subsets
62 o 1998, 218 patients with HL were treated on HDT with ASCR salvage protocols.
63 in ICP, IOP, or TLCPD in supine, sitting, or HDT (P >/= 0.11), except for IOP in HDT (P = 0.04).
64 s would not have participated in the pivotal HDT trials.
65 occurred infrequently, monitoring after post-HDT consolidation chemotherapy appears warranted.
66 rapy 2 and Total Therapy 3 that applied post-HDT consolidation chemotherapy (suggesting possible post
67 ation chemotherapy (suggesting possible post-HDT damage).
68 mg/L, C-reactive protein </= 4 mg/L, and pre-HDT standard chemotherapy </= 12 months.
69 DT platelet count (likely resulting from pre-HDT damage), whereas late-onset MDS-CAs were noted among
70 ger time interval from diagnosis and low pre-HDT platelet count (likely resulting from pre-HDT damage
71                                 No other pre-HDT-ASCT risk factors significantly impacted PFS or OS.
72 ents transplanted with negative FDG-PET, pre-HDT/ASCT after 1 or 2 SLT programs, had an EFS of > 80%,
73                            Several promising HDT candidates are being evaluated, but major advancemen
74 nts treated with RHCVAD (n = 83, 50%), RCHOP+HDT/ASCR (n = 34, 20%), RCHOP (n = 29, 17%), or RHCVAD+H
75 l survival (OS) between the RHCVAD and RCHOP+HDT/ASCR (P = .98).
76       RCHOP was inferior to RHCVAD and RCHOP+HDT/ASCR, which had similar PFS and OS.
77 stine, adriamycin, and dexamethasone), RCHOP+HDT/ASCR (rituximab, cyclophosphamide, doxorubicin, vinc
78 eatment as per protocol proceeded to receive HDT/ASCT.
79 tients) subtypes of B-cell lymphoma received HDT followed by a purged autologous graft.
80         Because all 13 patients who received HDT also had responsive relapse, we performed a multivar
81 , 0.29; 95% CI, 0.13 to 0.66), and receiving HDT (relative risk, 0.26; 95% CI, 0.08 to 0.85).
82 s (high-dose therapy) with stem-cell rescue (HDT/SCR) in rapid sequence.
83 n = 34, 20%), RCHOP (n = 29, 17%), or RHCVAD+HDT/ASCR (n = 21, 13%).
84 therapy/autologous stem cell rescue), RHCVAD+HDT/ASCR, or RCHOP.
85                              CR and a second HDT cycle applied within 6 months both extended event-fr
86 nd older subjects with both first and second HDT.
87 o significant difference in response to SLT, HDT, event-free or overall survival based on the cell of
88 nts for most deaths among patients surviving HDT and ASCR.
89                                     A tandem HDT/SCR regimen for high-risk neuroblastoma is a feasibl
90 ve patients receiving melphalan-based tandem HDT.
91                     Our results suggest that HDT with HSCR is an effective treatment for patients wit
92                                          The HDT and SDT regimens used in S9321 yielded comparable re
93  and OS durations did not differ between the HDT and SDT arms, with 7-year estimates of PFS of 17% an
94 vercome by incorporating novel agents in the HDT/ASCT setting.
95 ) corresponding to three orientations of the HDT moiety.
96 ) corresponding to three orientations of the HDT moiety.
97 rmine eligibility for HER2-directed therapy (HDT) in breast cancer.
98 tudy of PIXY321 following high-dose therapy (HDT) and autologous bone marrow transplantation (ABMT) w
99 ficacy and toxicity after high-dose therapy (HDT) and autologous hematopoietic cell transplantation (
100 therapy (SLT) followed by high-dose therapy (HDT) and autologous stem cell transplantation (ASCT) to
101                           High-dose therapy (HDT) and autologous stem-cell transplantation (ASCT) are
102 atopoietic cell-supported high-dose therapy (HDT) effected higher complete response rates and extende
103                           High-dose therapy (HDT) has increased complete remission (CR) rates and sur
104 me to standard treatment, high-dose therapy (HDT) has usually been limited to patients up to 65 years
105 d the relative benefit of high-dose therapy (HDT) is controversial.
106 oma who were eligible for high-dose therapy (HDT) were enrolled onto the trial.
107 lating factors (CSFs), or high-dose therapy (HDT) with autologous bone marrow support (ABMT).
108 3,077 patients undergoing high-dose therapy (HDT).
109 pine, sitting, and 9 degrees head-down tilt (HDT) positions.
110 e, sitting, and in 9 degrees head-down tilt (HDT).
111 n, longer time interval from MM diagnosis to HDT, older age, and lower platelet recovery after HDT; p
112 ville score of 1 or 2) proceeded directly to HDT/ASCT; those with persistent abnormalities on PET rec
113 CI 13-40) were PET-negative and proceeded to HDT/ASCT.
114 evidence of disease progression proceeded to HDT/ASCT; those with progressive disease were study fail
115 29 patients with rel/ref DLBCL proceeding to HDT-ASCT, with ST response assessment by FDG-PET accordi
116 termine whether the depth of the response to HDT-ASCT leads to an improvement in time to progression
117                     Horizontal DNA transfer (HDT) is a pervasive mechanism of diversification in many
118 therapy and autologous stem-cell transplant (HDT/ASCT) for patients with relapsed or refractory Hodgk
119 y with autologous stem-cell transplantation (HDT-ASCT) is now almost standard therapy for many patien
120 y plus autologous stem-cell transplantation (HDT-ASCT).
121 herapy/autologous stem cell transplantation (HDT/ASCT) and novel agents has significantly improved su
122 herapy/autologous stem cell transplantation (HDT/ASCT) is a surrogate for prolonged survival in multi
123 t peripheral blood stem cells to support two HDT cycles (CD34 > 5 x 10(6)/kg) were available in 83% o
124 e or non-Hodgkin's lymphoma (NHL) undergoing HDT and ABMT received PIXY321 post-ABMT in doses that ra
125                          Patients undergoing HDT with stem cell rescue are at an increased risk of t-
126 ly descended bacterial population undergoing HDT through transmission of mobile genetic elements (MGE
127                     A total of 115 underwent HDT/ASCT, with 90 in complete remission at 3 months post
128 nt in the majority of patients who underwent HDT and ABMT for lymphoid malignancies.
129 relatively good outcome can be achieved with HDT and PSCT, even in patients with a significant marrow
130 on, patients proceeded to consolidation with HDT/ASCT.
131 her major responses were primarily seen with HDT-ASCT, but insights into the biology of MM have led t

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