ライフサイエンスコーパス: metastatic

1 castration-resistant disease that is highly metastatic.

2 icated in multiple processes associated with metastatic aggressiveness including immune evasion, coll

3 rolled patients with locally advanced and/or metastatic anaplastic thyroid carcinoma in a phase II co

4 for MRI-guided radiotherapy with respect to metastatic and primary liver cancers.

5 two isogenic canine OS cell lines, POS (low metastatic) and HMPOS (highly metastatic), under normoxi

6 st palliative care to minimize the impact of metastatic bone disease on physical functioning.

7 Metastatic breast cancer (MBC) is an extremely recalcitr

8 ERBB2 levels spiked in metastatic breast cancer between 10.0 and 4.0 months pre

9 r the treatment of hormone-receptor-positive metastatic breast cancer following antiestrogen therapy.

10 ral tumor implantation technique in a murine metastatic breast cancer model (E0771) coupled with anti

11 andomly assigned patients with HER2-positive metastatic breast cancer previously treated with trastuz

12 mal growth factor receptor 2 (HER2)-negative metastatic breast cancer represents a major milestone in

13 mal growth factor receptor 2 (HER2)-negative metastatic breast cancer who had received <=2 chemothera

14 mal growth factor receptor 2 (HER2)-positive metastatic breast cancer who have disease progression af

15 mal growth factor receptor 2 (HER2)-negative metastatic breast cancer with prior clinical benefit fro

16 1) mutations occur frequently in ER-positive metastatic breast cancer, and confer clinical resistance

17 represents a potential therapeutic target in metastatic breast cancer, as its histone-binding capabil

18 avily pretreated patients with HER2-positive metastatic breast cancer, including those with brain met

19 ated efficacy in patients with BRCA-positive metastatic breast cancer.

20 than two previous lines of chemotherapy for metastatic breast cancer.

21 efore CT in most participants with bone-only metastatic breast cancer.

22 breast cancers from two patient cohorts (149 metastatic breast cancers, 63 untreated primary tumors,

23 ecruitment and activation were impaired, and metastatic burden was increased in E2 (-/-)mice.

24 as follows: septic shock, 7.27 (7.19-7.35); metastatic cancer and acute leukemia (Hierarchical Condi

25 CBFbeta can determine the plasticity of the metastatic cancer cell phenotype, suggesting that its re

26 the genes that control the transmigration of metastatic cancer cells across the BBB, offering new tar

27 S100A4 regulates the motility of metastatic cancer cells by binding to non-muscle (NM) my

28 In fact, the majority of patients with metastatic cancer develop a debilitating muscle-wasting

29 re becoming more pertinent, as patients with metastatic cancer have extended overall survival because

30 that promote metabolic adaptations to drive metastatic cancer remain unclear.

31 daptation of the multi-cellular ecosystem of metastatic cancer shapes clinical outcomes.

32 Nasopharyngeal carcinoma (NPC) is a highly metastatic cancer that is consistently associated with E

33 lasma-derived cell-free DNA and eight frozen metastatic cancer tissues collected during rapid autopsy

34 mic therapy may be used to treat advanced or metastatic cancer using the same indications and combina

35 In metastatic cancer, the degree of heterogeneity of the tu

36 Besides applications to wound healing and metastatic cancer, these studies are relevant for tissue

37 further reveals the disruptive reality that metastatic cancers are tremendously complex and individu

38 We identified 40 genes overexpressed in metastatic cancers from patients reporting high pain (n

39 tinctions suggest a strategy for eradicating metastatic cancers in which initial therapy, by reducing

40 ecently been implicated in accelerating bone metastatic cancers, such as acute myelogenous leukemia a

41 omising results for the treatment of certain metastatic cancers.

42 We posit that melanoma cells acquire metastatic capability by adopting an embryonic-like phen

43 cts on tumor growth, and strongly suppressed metastatic capacity in vivo.

44 erts preneoplastic lesions into invasive and metastatic carcinomas.

45 SERPINB5 and CSTB enhanced late steps in the metastatic cascade by elevating invadopodia formation an

46 out of IQGAP1 to investigate its role in the metastatic cascade of both melanoma and breast cancer ce

47 and arrest during the earliest phase of the metastatic cascade, the trafficking of immune cells duri

48 s, with a prevalence over 60% in a cohort of metastatic cases and 25% in a cohort comprising predomin

49 small primary PanNETs (<3 cm), including 32 metastatic cases and 55 nonmetastatic cases after a 5-ye

50 g, 67 for biochemical recurrence, and 23 for metastatic castration-resistant PCa.

51 primary prostate cancer differ from those of metastatic castration-resistant prostate cancer (mCRPC).

52 erica, and there are no curative options for metastatic castration-resistant prostate cancer (mCRPC).

53 ethods: Safety and survival of patients with metastatic castration-resistant prostate cancer and live

54 obtained from 294 patients with progressing metastatic castration-resistant prostate cancer taken pr

55 candidates for clinical translation to treat metastatic castration-resistant prostate cancer.

56 d with treatment failure and poor outcome in metastatic castration-resistant prostate cancer.

57 (TAT) is an emerging treatment modality for metastatic castration-resistant prostate cancer.

58 SMA-617 was administered to patients who had metastatic castration-resistant prostate carcinoma and w

59 ods: We studied 5 patients with localized or metastatic ccRCC in a microdosing regimen, after the adm

60 Twist1 is a known regulator of metastatic cell behaviors but not directly targetable.

61 retroviral element RNAs were upregulated in metastatic cells and detected extracellularly.

62 ion of global transcriptomic changes in rare metastatic cells during seeding using single-cell RNA se

63 ); Pdx-1 Cre (KPC) mice, and KPC- Liver/Lung metastatic cells were used to evaluate the CSC, EMT (epi

64 parental, circulating tumor cells, and lung metastatic cells.

65 s versus taxol or DDM; and 5) attenuation of metastatic characteristics in treated cancer cells.

66 hat systemic Akt1 deletion maintains the pro-metastatic cluster within primary tumors but ablates pro

67 ibitors significantly delay tumor growth and metastatic colonization and reverse neuroendocrine featu

68 generated by tumor cell clusters supporting metastatic colonization.

69 ningfully improves survival of patients with metastatic colorectal cancer compared with doublets + be

70 strated that highly activated fibroblasts in metastatic colorectal cancer increase tissue stiffness a

71 n an application to real data collected from metastatic colorectal cancer tumors, more associations b

72 rgical modalities of stage II/III rectal and metastatic colorectal cancer.

73 ain microenvironment, thereby inducing brain metastatic competence.

74 ctal cancer (CRC) cohort, among which 70 had metastatic CRC (mCRC).

75 undred six patients with BRAF(V600E)-mutated metastatic CRC previously treated with one or two regime

76 a-PSMA-11 PET/CT imaging of 10 patients with metastatic CRC to assess metastasis avidity.

77 at genomic and transcriptional features from metastatic CRPC biopsies prior to treatment would be pre

78 ngs, treatment, and outcome of patients with metastatic cutaneous melanoma to the vitreous.

79 57-year-old kidney transplant recipient with metastatic cutaneous squamous cell carcinoma (CSCC).

80 result in differential impacts on the ccRCC metastatic destinations of VHL-wt ccRCC cells under diff

81 rd systemic therapy (69% M1a; 43% M1b/c) for metastatic disease (153/382, 40%).

82 was alive with metastases, and 6 had died of metastatic disease (including 2 patients who declined ad

83 ocalization (n = 225/388, 58%), or restaging metastatic disease (M1) before or during systemic therap

84 lso been implicated in tumor progression and metastatic disease and have thus become an attractive th

85 ease at diagnosis; 38 of 103 (37%) developed metastatic disease at a median of 5.9 months (interquart

86 Seventeen of 103 (16%) patients had metastatic disease at diagnosis; 38 of 103 (37%) develop

87 f circulating melanoma cells and reduced the metastatic disease burden in patient-derived xenografts

88 ts who experience relapse after treatment of metastatic disease but worse compared with those who hav

89 Among the patients who developed metastatic disease during neoadjuvant treatment, median

90 Patients with metastatic disease had OS rates of 77.8% and 22.2% at 1-

91 drive the progression of primary melanoma to metastatic disease have been studied extensively, the ea

92 ogrammed regulatory elements commissioned in metastatic disease hijack latent developmental programs,

93 Six patients showed metastatic disease in the central nervous system.

94 e suggesting that the effect of P-AscH(-) on metastatic disease is mediated by hydrogen peroxide.

95 Further, studies on resection for metastatic disease to the lung were systematically revie

96 USBR for SB-NETs in the presence of metastatic disease was associated with better patient-or

97 with LGT tumors, including 15 patients with metastatic disease, 1 patient with suspected local relap

98 For patients with advanced-stage or metastatic disease, comprehensive genomic profiling has

99 chondrosarcoma; for locally advanced and/or metastatic disease, no known effective systemic therapy

100 isoforms is a promising approach to address metastatic disease, one that may be readily combined wit

101 atients after diagnosis of colorectal cancer metastatic disease, yet how RAS-ERK signaling regulates

102 t worse compared with those who have de-novo metastatic disease.

103 on of primary tumors and are ineffective for metastatic disease.

104 to identify a distant primary malignancy or metastatic disease.

105 lular transformation, disease progression to metastatic disease.

106 is sculpted differentially by primary versus metastatic disease.

107 dow associates with high risk for subsequent metastatic disease.

108 up to two previous lines of chemotherapy for metastatic disease.

109 rimary tumours, ~50% of patients progress to metastatic disease.

110 ltaNp63 in established tumors is crucial for metastatic dissemination in breast cancer.

111 oskeleton reorganization, cell motility, and metastatic dissemination.

112 activity, emergence of chemoresistance, and metastatic dissemination.

113 R1 elicited a robust anti-tumour and/or anti-metastatic effect.

114 EMT), VAL exerts potent pro-invasive and pro-metastatic effects through directly binding to Vimentin

115 HIF-1alpha expression levels are elevated in metastatic estrogen receptor-positive (ER+) and TNBC cli

116 PSMA SUV(max) and metastatic findings were compared with prostate-specific

117 context, we also determine that IQGAP1's pro-metastatic functions are dependent on multiple domains a

118 monotherapy as 2 L chemotherapy for advanced/metastatic gastric cancer and a third received doublets.

119 nd-line (2 L) chemotherapies for advanced or metastatic gastric cancer have shown improved survival b

120 rall survival in patients with HER2-positive metastatic gastric cancer.

121 g progression-free survival in patients with metastatic gastroenteropancreatic neuroendocrine tumors.

122 le mRNA construct to vaccinate patients with metastatic gastrointestinal cancer.RESULTSThe vaccine wa

123 that BCL11A sustains TNBC cell invasion and metastatic growth by repressing MBNL1-directed splicing

124 ry mediators of mammary engraftment and lung metastatic growth in triple-negative breast cancer (TNBC

125 red as a novel therapeutic approach to treat metastatic hormone-naive and castration-resistant prosta

126 een shown to play a detrimental role in many metastatic human cancers, including melanoma and other n

127 for detection of metastases in patients with metastatic ILC.

128 scientifically, as the stochastic nature of metastatic lesion formation introduces complexity for bo

129 eiter et al. assess genetic diversity across metastatic lesions and identify a tight selective bottle

130 topic thyroid tumors compared with pulmonary metastatic lesions by 79% +/- 23 (standard deviation; P

131 ed on the longitudinal measurements of liver metastatic lesions from 599 mCRC patients.

132 ptors and tumor-infiltrating immune cells in metastatic lesions with or without ER mutations.

133 nts showed high tracer uptake in primary and metastatic lesions with T/M, T/B, and T/I ranging from 5

134 with a controlled primary malignancy and 1-5 metastatic lesions, with all metastases amenable to ster

135 n objective response with regression of bone metastatic lesions.

136 as used to compare atypical haemangiomas and metastatic lesions.

137 n (SRFA) for very large (>=8 cm) primary and metastatic liver tumors with curative treatment intent.

138 viously showed that PLG was able to identify metastatic LNs in animal models.

139 A 43-year-old female patient with metastatic lung adenocarcinoma, who harbored KIF5B-RET f

140 es in mouse models of mammary tumours and of metastatic lung cancer, as well as during fluorescence-g

141 nt; one patient assigned amiloride died from metastatic lung cancer, one patient assigned riluzole di

142 find that E-cadherin expression persists in metastatic lung nodules and circulating tumor cells (CTC

143 of MTA2 in IKK2/NF-kappaB-driven primary-to-metastatic lung tumor progression.

144 ssues were compared with primary INS and INS-metastatic lymph nodes, revealing more than 3,000 genes

145 e treatments are available for patients with metastatic MCC.

146 /2, which has been approved for treatment of metastatic melanoma and anaplastic thyroid cancer in pat

147 e, and that a lineage approach would uncover metastatic melanoma biology.

148 Metastatic melanoma carries a poor prognosis despite mod

149 Metastatic melanoma is challenging to manage.

150 rotein and mRNA expression in paired primary/metastatic melanoma or colorectal cancer cells than thos

151 th inflammation-attenuating glycoprotein non-metastatic melanoma protein B (GPNMB) signaling in human

152 Despite the advent of immunotherapy, metastatic melanoma represents an aggressive tumor type

153 s in the systemic treatment of patients with metastatic melanoma using immune checkpoint and tyrosine

154 may represent a novel therapeutic target in metastatic melanoma, the most lethal form of skin cancer

155 e checkpoint inhibitors for the treatment of metastatic melanoma.

156 CI, ipilimumab, in 2011 for the treatment of metastatic melanoma.

157 apy in 10 patients with anti-PD-1-refractory metastatic melanoma.

158 in BRAF(V600) mutation-positive advanced or metastatic melanoma.

159 r patients with advanced-ie, unresectable or metastatic-melanoma.

160 s (aged >=18 years) with locally advanced or metastatic, MET-amplified, EGFR mutation-positive non-sm

161 f IL33 instigated type 2 inflammation in the metastatic microenvironment and mediated recruitment of

162 ge-independent growth and highlights how the metastatic microenvironment restores this malignant prop

163 ces a substantial survival benefit in highly metastatic murine TNBC models poorly responsive to PD-1

164 luster within primary tumors but ablates pro-metastatic neutrophils.

165 their role in the formation of a permissive metastatic niche is unresolved.

166 upon cancer initiation is transformed into a metastatic niche that captures aggressive circulating tu

167 llular matrix (ECM), a critical component of metastatic niches, in metastases to the brain, lungs, li

168 olumes greater than or equal to the smallest metastatic node while 4 normal nodes had SUV > 4.5.

169 69 y; median serum PSA, 3.69 mug/L) with 232 metastatic nodes less than 12 mm in diameter (mean lesio

170 The platform has been applied to advanced metastatic non-small cell lung cancer (NSCLC).

171 Patients with metastatic nonseminomatous GCT (NSGCT) who were evaluate

172 its of toxicity, for palliative treatment of metastatic NSCLC.

173 and chemotherapy in first-line HER2-positive metastatic oesophagogastric cancer is underway.

174 fficacy and safety analysis of patients with metastatic or locally advanced solid tumours harbouring

175 dhood soft-tissue sarcoma, yet patients with metastatic or recurrent disease continue to do poorly, i

176 nti-PD-1) therapy is modest in patients with metastatic or recurrent head and neck squamous cell carc

177 ells from 7 primary, 2 recurrent, and 2 lung metastatic osteosarcoma lesions, 11 major cell clusters

178 Epigen knockdown profoundly reduces metastatic outgrowth and switches clusters from a prolif

179 to lose their cytotoxic ability and promote metastatic outgrowth.

180 In a mouse model of metastatic ovarian cancer, fluorescently labeled silica,

181 These lesions progress to metastatic pancreatic cancer with high frequency.

182 We previously reported that metastatic pancreatic cancers were dependent on the gluc

183 monitoring patients with locally advanced or metastatic pancreatic ductal adenocarcinoma (PDAC) treat

184 borderline resectable, locally advanced, and metastatic; patient condition is also an important consi

185 Our study sheds light on the complicated metastatic pattern in CRC and has great clinical implica

186 Mutational status and metastatic pattern were correlated with MFS and OS using

187 ssociation of mutational status of MIUC with metastatic pattern, metastasis-free survival (MFS), and

188 vasive urothelial cancer has implications on metastatic pattern, metastasis-free survival, and overal

189 ility profiles and positive outcomes for non-metastatic PC with androgen receptor antagonists, respec

190 , with three or more siblings diagnosed with metastatic PCa, we identified mutations in 31 genes invo

191 els and somatic testing were recommended for metastatic PCA.

192 etermining precisely what differentiates the metastatic phenotype has proven to be more elusive.

193 d transcriptomic changes characteristic of a metastatic phenotype, and inhibition of TRIM37 substanti

194 and animal models confers a less aggressive/metastatic phenotype.

195 ted proteins is responsible for inducing the metastatic phenotype.

196 s), which are necessary for the invasive and metastatic phenotype.

197 ptosis, hence developing more aggressive and metastatic phenotypes.

198 he activity of cabozantinib in patients with metastatic platinum-refractory urothelial carcinoma.

199 miR-431 may be targeted to manage metastatic PNETs.

200 mong cancer cells thus confer differences in metastatic potential as metastasizing cells depend on MC

201 re, the applicability for discriminating the metastatic potential of cancer cells by directly analyzi

202 strategy that is capable of determining the metastatic potential of human cancer cell lines in mouse

203 ancer that has a worse prognosis and greater metastatic potential than the more common pancreatic duc

204 on (based on an in vitro assessment of their metastatic potential) in PANC-1, a PDAC cell line.

205 ations might have gained growth advantage or metastatic potential, as a result of viral integration e

206 ing an U2OS osteosarcoma cell line with high metastatic potential, proven by a xenotransplant in zebr

207 B-231 breast cancer cells that vary in their metastatic potential, we show that 3D refractive index t

208 alter their antioxidant capacity for maximal metastatic potential.

209 GIT or anti-KLRG1 antibodies further reduced metastatic potential.

210 for disease progression, especially for the metastatic process in GC.

211 Ovarian cancer metastatic progression can be restricted by targeting a

212 s antitumor immune responses and enhance the metastatic progression of cancer.

213 lying mechanisms that drive MCC invasion and metastatic progression.

214 ation, migration, and in the case of cancer, metastatic progression.

215 These cell lines offer a model for CRC metastatic progression; SW480 derived from primary adeno

216 To link metastatic propensity to a hypoxia-induced proteotype, w

217 metastatic tumor biopsies from patients with metastatic prostate adenocarcinoma and CRPC-NE, we ident

218 D-CC in a test-retest trial in subjects with metastatic prostate adenocarcinoma.

219 tase activity in the development of advanced metastatic prostate cancer and suggests that blocking SR

220 Lethal metastatic prostate cancer seems to arise from a single

221 , such as (177)Lu-PSMA-617, is used to treat metastatic prostate cancer.

222 ts FASN as a potential therapeutic target in metastatic prostate cancer.

223 g pathways has been observed in advanced and metastatic prostate cancers.

224 Metastatic prostate carcinoma overexpresses prostate-spe

225 e prognosis of patients with bulky nodal and metastatic PSCC is dismal and new management approaches

226 man breast cancers and independently predict metastatic rather than loco-regional recurrence.

227 th tumor response and disease progression in metastatic RCC treated with vascular endothelial growth

228 Forty-five patients with metastatic RCC were included.

229 We enrolled patients with metastatic RCC with no prior checkpoint inhibitor exposu

230 d surrogate endpoints used in trials for non-metastatic rectal cancer.

231 Despite this, the genomic events that drive metastatic recurrence are poorly understood.

232 TWIST1 and PRKD1 expression correlated with metastatic recurrence, particularly in basal breast canc

233 a key function of IL33 in facilitating lung metastatic relapse by modulating the immune microenviron

234 Eligible patients had metastatic renal cell carcinoma (RCC), endometrial cance

235 nt inhibitors (ICIs) are standard therapy in metastatic renal cell carcinoma (RCC).

236 acy of atezolizumab in patients with mUC and metastatic renal cell carcinoma, even in tumors that wer

237 ts highlight the novel context-specific, pro-metastatic role of SIRT3 in ovarian cancer.

238 that increase fitness along glucose-replete metastatic routes.

239 chromosome 6, and had the highest number of metastatic samples.

240 of upfront small bowel resection (USBR) for metastatic SB-NET compared to non-operative management (

241 molecular targets for a subset of recurrent/metastatic SDC.

242 an unexpected advantage at initial steps of metastatic seeding, suggesting that Rab27a may alter cel

243 In the unresectable/metastatic setting, ipilimumab plus nivolumab, nivolumab

244 o had received <=2 chemotherapy lines in the metastatic setting.

245 ransferase 3B (DNMT3B) is induced at distant metastatic sites and mediates epigenetic reprogramming o

246 inal tissue biopsies from the bone and other metastatic sites have been challenging to collect.

247 stage, tumor grade, ER, PR, HER2, number of metastatic sites, and presence of bone-only metastases.

248 In soft microenvironments reminiscent of metastatic sites, breast cancer cells were more resistan

249 d by cancer to promote growth at primary and metastatic sites.

250 ppressor, a class of proteins which inhibits metastatic spread of cancer cells without impact on grow

251 tumor-promoting phenotype that supports the metastatic spread of cancer cells.

252 e tumor-derived pioneers responsible for the metastatic spread of cancer.

253 rostate cancer patients can be attributed to metastatic spread of disease or tumor recurrence after i

254 elated deaths, yet the mechanisms underlying metastatic spread remain poorly understood.

255 aracterized by its aggressive biology, early metastatic spread, and poor survival outcomes.

256 us to interrogate the pattern and timing of metastatic spread.

257 s and explore studies investigating modes of metastatic spread.

258 often presenting with signs and symptoms of metastatic spread.

259 tion (EMT) in lung cancer cells and promoted metastatic spreading.

260 f cellular identity and progression toward a metastatic state.

261 effect, adjusting for age, cancer type, and metastatic status.

262 stemic treatment for progressive advanced or metastatic STS who had Eastern Cooperative Oncology Grou

263 Metastatic subclones at autopsy were present in tissue a

264 RNA-Seq results suggested that the metastatic subclones had greater activation of EMT-relat

265 ces between model parameters for primary and metastatic subgroups and that correlation coefficients w

266 The metastatic suppressing ability of Zic1 was mediated by r

267 5A, a non-canonical Wnt ligand that drives a metastatic, therapy-resistant phenotype, stabilizes the

268 beta(PV/PV) knock-in (PV) mice that develop metastatic thyroid cancer that most closely resembles FT

269 erogeneous stromal components in primary and metastatic TMEs and discuss emerging strategies to targe

270 Three decades ago, high-risk NB metastatic to bone and bone marrow in children was not c

271 ing outcomes in patients with uveal melanoma metastatic to the liver.

272 th untreated locally recurrent inoperable or metastatic triple-negative breast cancer using a block m

273 ur activity of chemotherapy in patients with metastatic triple-negative breast cancer.

274 display invasive features and alterations in metastatic tropism when xenografted into mice.

275 cing of cell free DNA (cfDNA) and of matched metastatic tumor biopsies from patients with metastatic

276 host WNT5A significantly reduced peritoneal metastatic tumor burden.

277 entifying and sorting highly tumorigenic and metastatic tumor cells from a heterogeneous cell populat

278 tored in lung neutrophils are transported to metastatic tumor cells through a macropinocytosis-lysoso

279 tes and mediates epigenetic reprogramming of metastatic tumor cells.

280 senting cells (APC), and abrogates local and metastatic tumor growth by a T-cell-related effect.

281 Analysis of matched primary and metastatic tumor samples supports a unidirectional, line

282 Here, we compared primary with metastatic tumors and found that the nuclei of tumor cel

283 Many primary and metastatic tumors express high levels of DeltaNp63, whil

284 Integration of BKPyV in both primary and metastatic tumors followed the mechanism of microhomolog

285 Metastatic tumors that have become resistant to androgen

286 and non-irradiated distant tumors, including metastatic tumors, when adrenergic stress or signaling t

287 tumors, including drug-resistant tumors and metastatic tumors.

288 However, metastatic tumour cells are exposed to highly perfused a

289 may play a key role in the establishment of metastatic tumours.

290 Therapeutic options for metastatic UM are limited, with clinical trials having l

291 ines, POS (low metastatic) and HMPOS (highly metastatic), under normoxia and hypoxia.

292 us ipilimumab (CaboNivoIpi) in patients with metastatic urothelial carcinoma (mUC) and other genitour

293 ntify the patients with previously untreated metastatic urothelial carcinoma who benefit from treatme

294 with heavily pretreated, platinum-refractory metastatic urothelial carcinoma with measurable disease

295 d 18 years or older with locally advanced or metastatic urothelial carcinoma, from 221 sites in 35 co

296 d progression-free survival in patients with metastatic urothelial carcinoma.

297 ineligible patients with locally advanced or metastatic urothelial carcinoma.

298 Metastatic uveal melanoma has poor overall survival (OS)

299 mab plus ipilimumab demonstrates activity in metastatic uveal melanoma, with deep and sustained confi

300 line: HR, 1.66; 95% CI, 1.10-2.51, P = .016; metastatic vs resectable or borderline: HR, 2.50; 95% CI