ライフサイエンスコーパス: lapatinib

1 1 and HER2-targeting agents (trastuzumab and lapatinib).

2 esponse of two EGFR inhibitors (afatinib and lapatinib).

3 in the presence of the HER2 kinase inhibitor lapatinib.

4 ponses to the HER2-targeted kinase inhibitor lapatinib.

5 the pro-apoptotic effects of trastuzumab and lapatinib.

6 ity of the cancer cells to a HER2 inhibitor, lapatinib.

7 to dampen sensitivity of the cancer cells to lapatinib.

8 diate resistance to the ERBB2-targeted agent lapatinib.

9 who have previously received trastuzumab and lapatinib.

10 diarrhea, fatigue, and rash associated with lapatinib.

11 iants in 1,194 patients randomly assigned to lapatinib.

12 hronic exposure to the ErbB kinase inhibitor lapatinib.

13 single agent or combination of foretinib and lapatinib.

14 in C, doxorubicin, cisplatin, sorafenib, and lapatinib.

15 served more frequently in patients receiving lapatinib.

16 regulin (P = 0.026) predicted sensitivity to lapatinib.

17 , which were then exposed to trastuzumab and lapatinib.

18 sponse to the HER2 tyrosine kinase inhibitor lapatinib.

19 with chemotherapy plus either trastuzumab or lapatinib.

20 between the direct effects of cetuximab and lapatinib.

21 tched to erlotinib, gefitinib, afatinib, and lapatinib.

22 gistically enhances the apoptotic effects of lapatinib.

23 in arm C, patients received trastuzumab and lapatinib 1,000 mg PO daily.

24 ned (1:1) to receive lapatinib-capecitabine (lapatinib 1,250 mg per day; capecitabine 2,000 mg/m(2) p

25 28 and every 4 weeks thereafter, and either lapatinib 1,500 mg or placebo daily.

26 d by 2 mg weekly; in arm B patients received lapatinib 1,500 mg orally (PO) daily; and in arm C, pati

27 months of letrozole 2.5 mg orally daily plus lapatinib 1,500 mg orally daily or placebo.

28 ence in PFS (hazard ratio [HR] of placebo to lapatinib, 1.04; 95% CI, 0.82 to 1.33; P = .37); median

29 per week (4 mg/kg loading, then 2 mg/kg) and lapatinib 1000 mg once per day for 12 weeks.

30 mg/kg loading dose followed by 2 mg/kg), or lapatinib (1000 mg) plus trastuzumab (same dose as for s

31 OR CORRECTED], subsequent doses 2 mg/kg), or lapatinib (1000 mg) plus trastuzumab.

32 aily on days 1-14 on each 21-day cycle, plus lapatinib 1250 mg orally once daily on days 1-21).

33 2 mg/kg intravenously) weekly until surgery, lapatinib (1250 mg orally) daily until surgery, or weekl

34 nts occurred in 149 (99%) patients receiving lapatinib, 142 (96%) patients receiving trastuzumab, and

35 FINDINGS: 154 patients received lapatinib, 149 trastuzumab, and 152 the combination.

36 s with EGFR-positive CTCs were recruited and lapatinib 1500 mg daily was administered, in a standard

37 ere randomly assigned (1:1) to receive daily lapatinib (1500 mg) or daily placebo for 12 months.

38 r and randomly assigned them to receive oral lapatinib (1500 mg), intravenous trastuzumab (4 mg/kg lo

39 m in diameter were randomly assigned to oral lapatinib (1500 mg), intravenous trastuzumab (loading do

40 r-enzyme alterations were more frequent with lapatinib (27 [17.5%]) and lapatinib plus trastuzumab (1

41 no significant difference in pCR between the lapatinib (38 of 154 patients [24.7%, 18.1-32.3]) and th

42 (488 patients treated with capecitabine plus lapatinib, 490 patients treated with trastuzumab emtansi

43 ly until surgery, or weekly trastuzumab plus lapatinib (750 mg orally) daily until surgery.

44 overall survival was 93% (95% CI 87-96) for lapatinib, 90% (84-94) for trastuzumab, and 95% (90-98)

45 , TBK1/IKKepsilon inhibition cooperated with lapatinib, a HER2/EGFR1-targeted drug, to accelerate apo

46 mab, and following subsequent treatment with lapatinib, a splicing mutation in GAS6 (growth arrest-sp

47 trastuzumab (TZ), a monoclonal antibody, and lapatinib, a tyrosine kinase inhibitor, have proved high

48 TZ and lapatinib ability to block extracellular signal-regulate

49 ib and the FDA-approved ErbB1/2-directed TKI lapatinib abrogated proliferation and increased sensitiv

50 HER2 blockade consisting of trastuzumab and lapatinib added to paclitaxel, considering tumor and mic

51 previously treated with both trastuzumab and lapatinib (advanced setting) and a taxane (any setting)

52 Further, lapatinib, AEE788, and canertinib were docked to TbLBPKs

53 Purpose To establish whether maintenance lapatinib after first-line chemotherapy is beneficial in

54 us trastuzumab improves outcomes relative to lapatinib alone in heavily pretreated, human epidermal g

55 se-dependent, and inhibited by erlotinib and lapatinib, although to differing extents.

56 Lapatinib, an approved epidermal growth factor receptor

57 were randomized to letrozole with or without lapatinib, an epidermal growth factor receptor (EGFR)/HE

58 rmore, ErbB2-directed RNAi or treatment with lapatinib, an ErbB2/EGFR small-molecule inhibitor used f

59 Lapatinib, an inhibitor of HER2 and EGFR, was more effec

60 bined with the EGFR/HER2 dual-targeting drug lapatinib, an Src-targeting combinatorial regimen preven

61 adverse events were similar in both arms (6% lapatinib and 5% placebo).

62 e response) were observed (70% for letrozole-lapatinib and 63% for letrozole-placebo).

63 occurred in 99 (6%) of 1573 patients taking lapatinib and 77 (5%) of 1574 patients taking placebo, w

64 Lapatinib and CBL0137 synergistically inhibited the prol

65 d MET targeting by small-molecule inhibitors lapatinib and foretinib, respectively, both in in-vitro

66 Lapatinib and imatinib may cause clinically significant

67 Lapatinib and indirubin-3'-monoxime showed moderate hCOX

68 r-positive/HER2-negative patients, letrozole-lapatinib and letrozole-placebo resulted in a similar ov

69 del is used to quantify two different drugs, lapatinib and nevirapine, in dosed tissues from nonclini

70 Previous studies showed that lapatinib and obatoclax interact in a greater-than-addit

71 Lapatinib and obatoclax killed multiple CNS tumor isolat

72 Lapatinib and obatoclax killed multiple tumor cell types

73 Altogether, our data show that lapatinib and obatoclax therapy could be of use in the t

74 cient rho-zero cells were radiosensitized by lapatinib and obatoclax treatment.

75 n plays an essential role in cell killing by lapatinib and obatoclax, as well as radiosensitization b

76 Lapatinib and obatoclax-initiated autophagy depended on

77 Importantly, lapatinib and palbociclib strictly block de novo synthes

78 The overall survival for lapatinib and placebo was 12.6 (95% CI, 9.0 to 16.2) and

79 The median PFS for lapatinib and placebo was 4.5 (95% CI, 2.8 to 5.4) and 5

80 The rate of grade 3 to 4 adverse events for lapatinib and placebo was 8.6% versus 8.1% ( P = .82).

81 sine kinase inhibitors, including erlotinib, lapatinib and sunitinib.

82 toma cells between the EGFR kinase inhibitor lapatinib and the anticancer compound YM155 that is pres

83 was significantly higher in the group given lapatinib and trastuzumab (78 of 152 patients [51.3%; 95

84 icant 4.5-month median OS advantage with the lapatinib and trastuzumab combination and support dual H

85 hosphamide treatment, and of the addition of lapatinib and trastuzumab combined after doxorubicin plu

86 val did not significantly differ between the lapatinib and trastuzumab groups (HR 0.86, 95% CI 0.45-1

87 ent-free survival did not differ between the lapatinib and trastuzumab groups (HR 1.06, 95% CI 0.66-1

88 Early use of lapatinib and trastuzumab is active in human epidermal g

89 breast cancer showed that the combination of lapatinib and trastuzumab significantly improved rates o

90 mice by inhibition of the HER2 pathway with lapatinib and trastuzumab to block all homo- and heterod

91 ere consistent with known safety profiles of lapatinib and trastuzumab.

92 and 2B17) by four TKIs (axitinib, imatinib, lapatinib and vandetanib) were characterized by using he

93 Neo-ALTTO (Neoadjuvant Lapatinib and/or Trastuzumab Treatment Optimisation) enr

94 ancer who were enrolled onto the Neoadjuvant Lapatinib and/or Trastuzumab Treatment Optimization tria

95 The NeoALTTO trial (Neoadjuvant Lapatinib and/or Trastuzumab Treatment Optimization) ran

96 attributed to flucloxacillin, ximelagatran, lapatinib, and amoxicillin-clavulanate.

97 advanced setting, including trastuzumab and lapatinib, and previous taxane therapy in any setting, w

98 The 4-anilinoquinazolines canertinib and lapatinib, and the pyrrolopyrimidine AEE788 killed blood

99 sed (trastuzumab) vs a small molecule-based (lapatinib) anti-HER2 therapy.

100 The increase in ALT case incidence in the lapatinib arm showed no evidence of plateau during 1 yea

101 In the letrozole-lapatinib arm, the probability of achieving a clinical r

102 HER2-directed drugs such as trastuzumab and lapatinib as well as depletion of HER2 or HER3 stimulate

103 showing a trend of increasing sensitivity to lapatinib as YAP decreased.

104 osphorylation was reduced by ErbB2 inhibitor lapatinib, as well as by knockdown of PKC-delta but not

105 ells, both sensitive and resistant to TZ and lapatinib, as well as in a preclinical BC model resistan

106 blasts strongly protect carcinoma cells from lapatinib, attributable to its reduced accumulation in c

107 inib bound to Tb927.4.5180 (termed T. brucei lapatinib-binding protein kinase-1 (TbLBPK1)) while AEE7

108 Lapatinib binds to a unique conformation of protein kina

109 lapatinib exposure, despite highly variable lapatinib bioavailability.

110 on sensitizes HER2(+) breast cancer cells to lapatinib both in vitro and in vivo, including JAK2/STAT

111 Lapatinib bound to Tb927.4.5180 (termed T. brucei lapati

112 longer with trastuzumab-capecitabine versus lapatinib-capecitabine (hazard ratio [HR] for PFS, 1.30;

113 ases were randomly assigned (1:1) to receive lapatinib-capecitabine (lapatinib 1,250 mg per day; cape

114 f relapse was 3% (eight of 251 patients) for lapatinib-capecitabine and 5% (12 of 250 patients) for t

115 17% (45 of 267 patients) of patients in the lapatinib-capecitabine and trastuzumab-capecitabine arms

116 However, lapatinib-capecitabine efficacy may have been affected b

117 -positive metastatic breast cancer receiving lapatinib-capecitabine or trastuzumab-capecitabine.

118 rly with 540 enrolled patients (271 received lapatinib-capecitabine, and 269 received trastuzumab-cap

119 ieved with chemotherapy plus trastuzumab and lapatinib compared with chemotherapy plus either trastuz

120 edictive effect on risk for progression with lapatinib compared with trastuzumab among patients with

121 exes, which confirmed that TbLBPKs can adopt lapatinib-compatible conformations.

122 c responses were seen in three patients with lapatinib concentrations approaching 10,000 ng/mL.

123 e-daily dosing with no DLTs; however, plasma lapatinib concentrations plateaued in this dose range.

124 2 values (HR per 10-ng/mL increase in sHER2: lapatinib-containing therapies, 1.009 v nonlapatinib-con

125 benefit (HR per 10-ng/mL increase in sHER2: lapatinib-containing therapies, 1.017 v nonlapatinib-con

126 33 [48%] of 490) than with capecitabine plus lapatinib control treatment (291 [60%] of 488).

127 uzumab emtansine (n=495) or capecitabine and lapatinib (control; n=496).

128 atients, the HER2 inhibitors trastuzumab and lapatinib controlled tumor progression in the breast but

129 ted that resistance to the ERBB1/2 inhibitor lapatinib could be overcome by the B cell CLL/lymphoma-2

130 Similarly, inhibition of ErbB RTKs with lapatinib did not affect PI3K signaling in PIK3CA(H1047R

131 ule tyrosine kinase inhibitors erlotinib and lapatinib differentially enhance the dimerization of the

132 Lapatinib dose was escalated to 7,000 mg per day in twic

133 ERBB2 Mab), pertuzumab (anti-ERBB2 Mab), and lapatinib (dual ERBB1 and ERBB2 tyrosine kinase inhibito

134 Strikingly, the combinatorial treatment with lapatinib [dual kinase inhibitor of EGFR (ERBB1) and ERB

135 Trastuzumab and lapatinib each synergized with XL147 for inhibition of p

136 The co-administration of foretinib and lapatinib effectively inhibited both MET and HER2 phosph

137 In addition, both canertinib and lapatinib eluted Tb10.60.3140 (TbLBPK4), whereas only ca

138 ed from the protocol, AEE788, canertinib and lapatinib eluted TbLBPK1, TbLBPK2, and Tb927.3.1570 (TbL

139 ment with the HER2 inhibitors trastuzumab or lapatinib enhanced XL147-induced cell death and inhibiti

140 Lapatinib exhibited potent competitive inhibition agains

141 Lapatinib exposure can be safely and significantly incre

142 hese, only ketoconazole was able to increase lapatinib exposure, despite highly variable lapatinib bi

143 nal cohorts evaluated strategies to increase lapatinib exposure, including the food effect, CYP3A4 in

144 ; MK2206 for PIK3CA, AKT, or PTEN mutations; lapatinib for ERBB2 mutations or amplifications; and sun

145 stigated the efficacy and safety of adjuvant lapatinib for patients with trastuzumab-naive HER2-posit

146 Substitution of lapatinib for trastuzumab in combination with chemothera

147 o neoadjuvant therapy of the substitution of lapatinib for trastuzumab in combination with weekly pac

148 ively by the small-molecule kinase inhibitor lapatinib frequently acquire resistance to this drug.

149 as powered for a 50% improvement in PFS with lapatinib from 5 to 7.5 months.

150 91 (53.2%, 45.4-60.3) of 171 patients in the lapatinib group (p=0.9852); and 106 (62.0%, 54.3-68.8) o

151 ade 4 in five patients (3%), 28 [16%] in the lapatinib group [grade 4 in eight patients (5%)], and 29

152 ow-up of 47.4 months (range 0.4-60.0) in the lapatinib group and 48.3 (0.7-61.3) in the placebo group

153 1230 confirmed HER2-positive patients in the lapatinib group and in 208 (17%) of 1260 in the placebo

154 ase-free survival events had occurred in the lapatinib group versus 264 (17%) in the placebo group (h

155 ere enrolled: 154 (34%) were assigned to the lapatinib group, 149 (33%) to the trastuzumab group, and

156 -free survival was 78% (95% CI 70-84) in the lapatinib group, 76% (68-82) in the trastuzumab group, a

157 ts in the trastuzumab group, 35 [20%] in the lapatinib group, and 46 [27%] in the combination group;

158 in the trastuzumab group, seven (4%) in the lapatinib group, and one (<1%) in the combination group;

159 ated recently that the 4-anilinoquinazolines lapatinib (GW572016, 1) and canertinib (CI-1033) kill T.

160 Lapatinib had significant PFS benefit over control (haza

161 By using the DREAM-in-CDM approach, lapatinib has been identified as a promising mPGES-1 inh

162 rastuzumab and the tyrosine kinase inhibitor lapatinib have complementary mechanisms of action and sy

163 nd small molecule kinase inhibitors, such as lapatinib, have been developed, rapid identification and

164 inhibitions (IC(50): 5.4-12 nM) compared to lapatinib (IC(50): 95.5 nM).

165 pecific inhibitor BYL719 in combination with lapatinib impaired mammary tumor growth and PI3K signali

166 vent leading to permanent discontinuation of lapatinib in affected patients.

167 ith a HER2-enriched profile may benefit from lapatinib in combination with endocrine therapy.

168 Treatment with trastuzumab or lapatinib in combination with taxane chemotherapy (pacli

169 was dependent on ERBB2; targeting ERBB2 with lapatinib in combination with the RAF inhibitor PLX4720

170 The combination of letrozole-lapatinib in early breast cancer was feasible, with expe

171 layed potent synergy with the HER2 inhibitor lapatinib in HER2iR BC cells in vitro.

172 en PIK3CA mutation and response to letrozole-lapatinib in HR-positive/HER2-negative early breast canc

173 rge, randomized, placebo-controlled trial of lapatinib in human epidermal growth factor receptor 2-po

174 ) analysis in amorphous solid dispersions of lapatinib in hypromellose phthalate (HPMCP) and hypromel

175 mab, lapatinib, or combined trastuzumab plus lapatinib in patients with human epidermal growth factor

176 ation review suggested marginal benefit with lapatinib in terms of disease-free survival.

177 (n = 42) showed no significant benefit with lapatinib in terms of PFS and overall survival ( P > .05

178 ting a number of genes caused sensitivity to lapatinib in this context.

179 atic breast cancer to receive trastuzumab or lapatinib, in combination with a taxane, from January 17

180 gher sHER2 predicts greater PFS benefit with lapatinib independent of tHER2 status.

181 Mechanistically, the synergy was based on a lapatinib induced inhibition of the multidrug-resistance

182 Lapatinib-induced FOXO transcription factors, normally t

183 carriage as a predictor of increased risk of lapatinib-induced liver injury and implicate an immune p

184 itors of PI3K/AKT prevented trastuzumab- and lapatinib-induced stimulation of MLK3 activity.

185 o gain insight into the structural basis for lapatinib interaction with TbLBPKs, we constructed three

186 The strategy of extracting lapatinib intermolecular drug interactions from the tota

187 e of its modest efficacy, the HER2 inhibitor lapatinib is currently used predominantly in combination

188 ndomized to receive trastuzumab (T; N = 34), lapatinib (L; N = 36), or both (TL; N = 58) as HER2-targ

189 tment with the small-molecule ERBB inhibitor lapatinib led to prolonged clinical benefit and a lastin

190 eracted in an additive fashion to facilitate lapatinib lethality.

191 was conducted using a 3+3 design with plasma lapatinib level monitoring.

192 ngs shed new light on mechanisms involved in lapatinib-mediated autophagy in Her2-expressing breast c

193 Thus lapatinib might be an option for women with HER2-positiv

194 i-ERBB2 Mabs, suggesting that the effects of lapatinib might mainly be through ERBB1.

195 r the HPMC-E3 rich preparations showing that lapatinib molecules do not cluster in the same way as ob

196 h survival advantage following foretinib and lapatinib monotherapy and in combination in murine subcu

197 CTC-directed therapeutics and suggests that lapatinib monotherapy is not having any demonstrable cli

198 vival (PFS) and clinical benefit rate versus lapatinib monotherapy, offering a chemotherapy-free opti

199 omen were enrolled and 3147 were assigned to lapatinib (n=1571) or placebo (n=1576).

200 Lapatinib-naive (cohort 3A) and lapatinib-treated (cohor

201 HER2-targeted therapies (lapatinib, neratinib, tucatinib and trastuzumab emtansin

202 (84%) who were randomly assigned to receive lapatinib or control in the trials EGF30001, EGF30008, a

203 man primary DCIS was reduced further by DAPT/lapatinib or DAPT/gefitinib regardless of ErbB2 receptor

204 tch inhibitor, DAPT, and ErbB1/2 inhibitors, lapatinib or gefitinib.

205 risk indicated that the coadministration of lapatinib or imatinib at clinical doses could result in

206 is largely blocked in cells pretreated with lapatinib or pertuzumab.

207 to trastuzumab alone and in combination with lapatinib or pertuzumab.

208 cycles) were randomly assigned one to one to lapatinib or placebo after completion of first-line/init

209 nical and biologic effects of letrozole plus lapatinib or placebo as neoadjuvant therapy in hormone r

210 tive patients received either trastuzumab or lapatinib or the combination plus anthracycline-taxane c

211 PIM1 restored MAPK or PI3K activation after lapatinib or trastuzumab treatment, but rather inactivat

212 cy of pazopanib plus vorinostat, everolimus, lapatinib or trastuzumab, and MEK inhibitor in patients

213 during or after treatment with trastuzumab, lapatinib, or both, were eligible.

214 during or after treatment with trastuzumab, lapatinib, or both.

215 thracycline in combination with trastuzumab, lapatinib, or combined trastuzumab plus lapatinib in pat

216 f 3 neoadjuvant treatment arms: trastuzumab, lapatinib, or the combination for 6 weeks followed by th

217 ve early-stage breast cancer to trastuzumab, lapatinib, or the combination for 6 weeks followed by th

218 ve early-stage breast cancer to trastuzumab, lapatinib, or the combination for 6 weeks followed by th

219 lihood of pCR after neoadjuvant trastuzumab, lapatinib, or their combination when given with chemothe

220 ting agents have gained regulatory approval: lapatinib, pertuzumab, and trastuzumab-emtansine.

221 r sHER2 values still independently predicted lapatinib PFS benefit (HR per 10-ng/mL increase in sHER2

222 Lapatinib PFS benefit is independently predicted by high

223 9.6 months with T-DM1 versus 6.4 months with lapatinib plus capecitabine (hazard ratio for progressio

224 and overall survival with less toxicity than lapatinib plus capecitabine in patients with HER2-positi

225 grade 3 or 4 adverse events were higher with lapatinib plus capecitabine than with T-DM1 (57% vs. 41%

226 and overall survival with less toxicity than lapatinib plus capecitabine.

227 -plantar erythrodysesthesia were higher with lapatinib plus capecitabine.

228 d with trastuzumab and a taxane, to T-DM1 or lapatinib plus capecitabine.

229 was higher with T-DM1 (43.6%, vs. 30.8% with lapatinib plus capecitabine; P<0.001); results for all a

230 ore frequent with lapatinib (27 [17.5%]) and lapatinib plus trastuzumab (15 [9.9%]) than with trastuz

231 the trastuzumab group, and 152 (33%) to the lapatinib plus trastuzumab group.

232 Lapatinib plus trastuzumab improves outcomes relative to

233 Phase III EGF104900 data demonstrated that lapatinib plus trastuzumab significantly improved progre

234 In addition, the drug combination (i.e. lapatinib plus YM155) decreased neuroblastoma tumor size

235 In contrast, lapatinib radiosensitized RAD51KD and RT112 cells but no

236 Using a femtosecond pulsed laser, lapatinib release from a nanoshell-based human serum alb

237 oproteome changes in an established model of lapatinib resistance to systematically investigate initi

238 estigated and in the case of NIBP (TRAPPC9), lapatinib resistance was found to be mediated through NF

239 or verteporfin, eliminated modulus-dependent lapatinib resistance.

240 sts new biomarkers and treatment options for lapatinib-resistant cancers.

241 an innovative therapeutic agent for TZ- and lapatinib-resistant ErbB-2-positive BC and GC.

242 Lapatinib-resistant ERBB2-amplified breast cancer cell l

243 ta/PDGF and ErbB pathways with imatinib plus lapatinib, respectively, not only prevented myofibroblas

244 sulting in sustained MTOR signaling and poor lapatinib response.

245 Five candidates, including lapatinib, SB-202190, RO-316233, GW786460X and indirubin

246 Using the lapatinib-sensitive breast cancer cell lines BT474 and S

247 Lapatinib sensitivity was not altered by fibroblasts in

248 d capecitabine and 241 [49%] of 495 received lapatinib (separately or in combination) after study dru

249 that combination therapy with foretinib and lapatinib should be tested as a treatment option for HER

250 the receptor tyrosine kinase (RTK) inhibitor lapatinib significantly improves survival, yet tumor res

251 Upon lapatinib stimulation, activated FOXO3a displaces FOXM1

252 antly alter the Km for ATP or sensitivity to lapatinib, suggesting that, unlike EGFR lung cancer muta

253 , we constructed three-dimensional models of lapatinib*TbLBPK complexes, which confirmed that TbLBPKs

254 ER3 signaling can be inactivated by doses of lapatinib that fully inactivate the HER2 kinase.

255 egative/HER2-enriched disease benefited from lapatinib therapy (median PFS, 6.49 vs 2.60 months; prog

256 Neoadjuvant lapatinib therapy in HER2(+) breast tumors lead to a sig

257 reast carcinoma cells that do not succumb to lapatinib, this Her1/2 inhibitor disrupts the cell surfa

258 ly paclitaxel combined with trastuzumab plus lapatinib (THL), trastuzumab (TH), or lapatinib (TL).

259 An investigational arm of paclitaxel plus lapatinib (TL) was closed early.

260 b plus lapatinib (THL), trastuzumab (TH), or lapatinib (TL).

261 lls with obatoclax enhanced the lethality of lapatinib to a greater extent than concomitant treatment

262 Adding lapatinib to fulvestrant does not improve PFS or OS in a

263 ts in outcome by the addition of maintenance lapatinib to standard of care.

264 inhibitor suppressing c-Myc synergizes with lapatinib to suppress cancer growth in vivo, partly by r

265 he pCR rates were 16%, 24.3%, and 17.4% with lapatinib, trastuzumab, and the combination, respectivel

266 logic complete response (pCR) to neoadjuvant lapatinib, trastuzumab, and their combination.

267 cells with acquired or innate resistance to lapatinib, trastuzumab, neratinib, and afatinib, all of

268 of mice with BT474 xenografts compared with lapatinib/trastuzumab (P = 0.0012).

269 The combination of LJM716/lapatinib/trastuzumab significantly improved survival of

270 Lapatinib-naive (cohort 3A) and lapatinib-treated (cohort 3B) patients were enrolled.

271 apoptotic tumor cells in residual disease of lapatinib-treated HER2(+) mammary tumors in MMTV-Neu mic

272 In lapatinib-treated patients, the overall risk for Nationa

273 In lapatinib-treated patients, there was a significant diff

274 Lapatinib treatment of BT474 or SKBR3 cells resulted in

275 esses the induction of HER3 that accompanies lapatinib treatment of HER2-amplified cancers and synerg

276 Combined DAPT/lapatinib treatment was more effective at reducing acini

277 by PRKACA and PIM1, and sensitized cells to lapatinib treatment.

278 owed no evidence of plateau during 1 year of lapatinib treatment.

279 patients experiencing hepatotoxicity during lapatinib treatment.

280 bition against several UGTs (i.e., UGT1A7 by lapatinib; UGT1A1 by imatinib; UGT1A4, 1A7 and 1A9 by ax

281 ne, in 3-week cycles, stratified by previous lapatinib use.

282 nts with advanced breast cancer treated with lapatinib using data from three randomized trials.

283 eraction) < .001) and by positive tHER2 (HR [lapatinib v nonlapatinib]: tHER2 positive, 0.638 v tHER2

284 dian PFS was 4.7 months for fulvestrant plus lapatinib versus 3.8 months for fulvestrant plus placebo

285 ykerb Evaluation After Chemotherapy [TEACH]: Lapatinib Versus Placebo In Women With Early-Stage Breas

286 Lapatinib was administered on days 1 through 5 of repeat

287 For HER2-positive tumors, lapatinib was associated with longer median PFS (5.9 v 3

288 The antiproliferative effect of lapatinib was inversely proportional to the elastic modu

289 st cancer drugs, docetaxel and HER2-targeted lapatinib, were delivered to MDA-MB-231 and SKBR3 (overe

290 strated reduced sensitivity to foretinib and lapatinib when used as a single agent.

291 ll survival, including in cells resistant to lapatinib, where cytotoxicity could be restored.

292 We examined whether lapatinib which binds both HER2 and EGFR could induce de

293 nhibitor; the MAPK signal inhibitor PD98059; lapatinib, which inhibits both the epidermal growth fact

294 ation in combination with either imatinib or lapatinib, which inhibits NHEJ and cell survival assesse

295 reated with a combination of trastuzumab and lapatinib who had wild-type PIK3CA obtained a total path

296 ilities, we combined the EGFR/HER2 inhibitor lapatinib with a novel small molecule, CBL0137, which in

297 Coadministration of lapatinib with obatoclax caused synergistic cell killing

298 Coadministration of lapatinib with obatoclax elicited autophagic cell death

299 ctivity after combining both trastuzumab and lapatinib with the anti-VEGFR2 antibody.

300 were screened, in the presence or absence of lapatinib, with an RNA interference library targeting 36

301 CALGB 40302 sought to determine whether lapatinib would improve progression-free survival (PFS)