1 SCLC cells normally express neuroendocrine and neuronal
2 SCLC is notable for dense clustering of high-level methy
3 Data from
26 SCLC human patients showed negligible immune cell infilt
4 T alterations (7%-24%), EGFR C797X (0%-
29%),
SCLC transformation (2%-15%), and oncogene fusions (1%-1
5 Of 1,574 patients who had pT1-
2N0M0 SCLC during the study period, 954 patients (61%) underwe
6 Patients with pT1-
2N0M0 SCLC treated with surgical resection alone have worse ou
7 urvival of patients with pathologic T1-
2N0M0 SCLC who underwent complete resection in the National Ca
8 ve to no adjuvant therapy for stage T1-
2N0M0 SCLC.
9 Three correspond to known subtypes (SCLC-
A,
SCLC-N, and SCLC-Y), while the fourth is a previously un
10 ration of cytotoxic T cells, and
accelerated SCLC.
11 mation in cells and dramatically
accelerates SCLC progression in an Rb1/Trp53-deleted mouse model.
12 the immune cell contexture of lung ADCA
and SCLC and suggest that molecular and histological traits
13 higher expression in atypical carcinoid
and SCLC, and could be a new therapeutic target for SCLC.
14 SCLC has remained stagnant for decades,
and SCLC is expected to persist as a threat to human health.
15 ently high to image established melanoma
and SCLC xenografts using PSMA-based nuclear and optical ima
16 nonprostatic cancers including melanoma
and SCLC.
17 spond to known subtypes (SCLC-A, SCLC-N,
and SCLC-Y), while the fourth is a previously undescribed AS
18 Although NSCLC
and SCLC are commonly thought to be different diseases owing
19 have described the coexistence of NSCLC
and SCLC, further challenging the commonly accepted view of
20 , exemplified by prostate cancer, NSCLC,
and SCLC.
21 w that KDM5A promotes SCLC proliferation
and SCLC's neuroendocrine differentiation phenotype in part
22 r more EGFR tyrosine kinase inhibitor
before SCLC transformation.
23 The biological relationships
between SCLC and LCNEC are still largely unknown and a current m
24 ent of patients with small-cell lung
cancer (
SCLC) after failure of first-line therapy.
25 Treatments for small-cell lung
cancer (
SCLC) after failure of platinum-based chemotherapy are l
26 target expressed in small cell lung
cancer (
SCLC) and high-grade neuroendocrine carcinomas.
27 cancer, we show that small cell lung
cancer (
SCLC) and lung adenocarcinoma (ADCA) exhibit unique immu
28 een proposed in both small-cell lung
cancer (
SCLC) and non-small-cell lung cancer (NSCLC) to try to i
29 omplete resection of small-cell lung
cancer (
SCLC) are limited, and in particular, there have been no
30 Using small cell lung
cancer (
SCLC) as a model, we demonstrated the presence of differ
31 quently activated in small cell lung
cancer (
SCLC) but represent poor drug targets.
32 d leukemia (AML) and small cell lung
cancer (
SCLC) cell lines, and antitumor efficacy in patient-deri
33 Most patients with small-cell lung
cancer (
SCLC) have extensive-stage disease at presentation, and
34 r the development of small-cell lung
cancer (
SCLC) in LEMS patients in multivariable analysis.
35 chemotherapy against small-cell lung
cancer (
SCLC) in preclinical studies.
36 Small cell lung
cancer (
SCLC) is a common, aggressive malignancy with universall
37 Small cell lung
cancer (
SCLC) is a devastating disease due to its propensity for
38 Small cell lung
cancer (
SCLC) is a devastating neuroendocrine carcinoma.
39 Small cell lung
cancer (
SCLC) is a difficult to treat subtype of lung cancer.
40 Small cell lung
cancer (
SCLC) is a highly aggressive and lethal neoplasm.
41 Small cell lung
cancer (
SCLC) is a highly aggressive malignancy with poor outcom
42 Small cell lung
cancer (
SCLC) is a highly aggressive subtype of lung cancer that
43 Small-cell lung
cancer (
SCLC) is a highly aggressive subtype of lung cancer with
44 Small cell lung
cancer (
SCLC) is a neuroendocrine tumor treated clinically as a
45 Small cell lung
cancer (
SCLC) is a recalcitrant, aggressive neuroendocrine-type
46 Small cell lung
cancer (
SCLC) is an aggressive form of lung cancer for which the
47 Small-cell lung
cancer (
SCLC) is an aggressive form of lung cancer with dismal s
48 Small cell lung
cancer (
SCLC) is an aggressive neuroendocrine cancer characteriz
49 Small cell lung
cancer (
SCLC) is an exceptionally lethal malignancy for which mo
50 Small cell lung
cancer (
SCLC) is an understudied cancer type for which effective
51 Small cell lung
cancer (
SCLC) is characterized by prevalent circulating tumour c
52 Small cell lung
cancer (
SCLC) is one of the most lethal and most metastatic canc
53 ated in Lu-iPSCs and small cell lung
cancer (
SCLC) lines and clinical specimens.
54 afts of melanoma and small cell lung
cancer (
SCLC) origin.
55 to initial therapy, small-cell lung
cancer (
SCLC) relapse occurs within a year and exhibits resistan
56 Purpose Treating small-cell lung
cancer (
SCLC) remains a therapeutic challenge.
57 mouse model of human small cell lung
cancer (
SCLC) to investigate the mechanisms that drive the metas
58 Small cell lung
cancer (
SCLC) tumor suppressors regulate the stem cells: Rb and
59 enome instability in small cell lung
cancer (
SCLC) while simultaneously triggering immune-response si
60 ific cytotoxicity in small-cell lung
cancer (
SCLC), a neuroendocrine carcinoma with high mortality an
61 atypical carcinoid, small cell lung
cancer (
SCLC), and large cell NE cancer.
62 Small cell lung
cancer (
SCLC), as a proportion, makes up only 15-17% of lung can
63 go transformation to small-cell lung
cancer (
SCLC), but their clinical course is poorly characterized
64 ss this question for small cell lung
cancer (
SCLC), finding that changes in genomic accessibility med
65 E) cancer, including small cell lung
cancer (
SCLC), is a particularly aggressive malignancy.
66 olid tumors, such as small-cell lung
cancer (
SCLC), is unknown.
67 In small cell lung
cancer (
SCLC), plasticity from NE to nonNE phenotypes is driven
68 ve-stage or relapsed small-cell lung
cancer (
SCLC), respectively.
69 rgeted therapies for small-cell lung
cancer (
SCLC), the most aggressive form of lung cancer, remain u
70 Applied to small cell lung
cancer (
SCLC), the workflow identifies four subtypes based on gl
71 ive tumors including small-cell lung
cancer (
SCLC), where its loss, along with TP53, is required and
72 n most patients with small-cell lung
cancer (
SCLC)-a metastatic, aggressive disease-the condition is
73 clinical activity in small cell lung
cancer (
SCLC).
74 ignancies, including small cell lung
cancer (
SCLC).
75 an active kinase in small cell lung
cancer (
SCLC).
76 oncogenic events in small cell lung
cancer (
SCLC).
77 tensive-disease (ED) small-cell lung
cancer (
SCLC).
78 extensive stage (ES) small-cell lung
cancer (
SCLC).
79 g cancer (NSCLC) and small-cell lung
cancer (
SCLC).
80 More than 90% of small cell lung
cancers (
SCLCs) harbor loss-of-function mutations in the tumor su
81 ative precursors to small cell lung
cancers (
SCLCs), and we can increase PNECs by reducing levels of
82 Cancer (majority small-cell lung
carcinoma [
SCLC]) was detected in 66 of 84 evaluated patients (79%)
83 inoma, LCNEC, and small-cell lung
carcinoma,
SCLC) are among the most deadly lung cancer conditions w
84 cell genomic analysis reveals
characteristic SCLC genomic changes in both VE-cadherin-positive and -n
85 regulated surface receptor in
chemoresistant SCLC cell lines and in chemoresistant PDX compared with
86 ochondrial dysfunction in the
chemoresistant SCLC cell line H69AR.
87 Patients and Methods Patients with
confirmed SCLC (limited or extensive disease) and performance stat
88 ionable therapeutic strategies that
consider SCLC intratumoral heterogeneity.
89 Coinclusion of a KDM5A sgRNA
decreased SCLC tumorigenesis and metastasis, and the SCLCs that fo
90 origin, and tumor cell plasticity
determine SCLC subtype.
91 Distinct SCLC molecular subtypes have been defined based on expre
92 ongs the survival of mice bearing MYC-
driven SCLC beyond that of combination chemotherapy.
93 l targeted treatment approach for MYC-
driven SCLC.
94 indings show that MYCN overexpression
drives SCLC chemoresistance and provide a therapeutic strategy
95 ation of widespread chromatin changes
during SCLC progression reveals an unexpected global reprogramm
96 etoposide in the first-line treatment of
ED-
SCLC had an acceptable toxicity profile and led to a sta
97 and Methods Treatment-naive patients with
ED-
SCLC were randomly assigned to receive either cisplatin
98 amide to CE failed to improve survival in
ES SCLC.
99 Previously untreated patients with
ES SCLC were randomly assigned in a 1:1 fashion to receive
100 In a group of 270
ES-
SCLC cases retrospective study, 78 patients (28.9%) had
101 h extensive-stage small-cell lung cancer (
ES-
SCLC) in the CASPIAN study.
102 c extensive stage small-cell lung cancer (
ES-
SCLC) to the overall survival (OS).
103 istologically or cytologically documented
ES-
SCLC, with a WHO performance status of 0 or 1.
104 d of care for the first-line treatment of
ES-
SCLC.
105 ublet in untreated, extensive-stage SCLC (
ES-
SCLC).
106 linical activity in extensive-stage SCLC (
ES-
SCLC).
107 le addition of chemotherapy when treating
ES-
SCLC patients with oligometastases and polymetastases.
108 gible patients were adults with untreated
ES-
SCLC, with WHO performance status 0 or 1 and measurable
109 howed signal of efficacy in patients with
ES-
SCLC and the study met its prespecified end point.
110 mproved overall survival in patients with
ES-
SCLC versus a clinically relevant control group.
111 Patients with
ES-
SCLC, stratified by sex and serum lactate dehydrogenase
112 oposide) in treatment-naive patients with
ES-
SCLC.
113 with Skp2 loss or inhibition in
established SCLC primary lung tumors, in liver metastases, and in ch
114 rrelates with limited treatment advances
for SCLC in the time frame we examined.
115 immunotherapies as a potential approach
for SCLC treatment.
116 noPET, can serve as an imaging biomarker
for SCLC.
117 dence and propose a working nomenclature
for SCLC subtypes defined by relative expression of these fo
118 rovided effective therapeutic strategies
for SCLC.
119 s a potential immunotherapeutic strategy
for SCLC.
120 The median survival
for SCLC remained 7 months, and the 12-month relative surviv
121 hlight ASXL3 as a novel candidate target
for SCLC therapy.
122 C, and could be a new therapeutic target
for SCLC.
123 may help to develop effective therapies
for SCLC patients.
124 There are no effective therapies
for SCLC.
125 ctedin was active as second-line therapy
for SCLC in terms of overall response and had an acceptable
126 potential as a new and targeted therapy
for SCLC.
127 The development of treatments
for SCLC has remained stagnant for decades, and SCLC is expe
128 ibitors should be explored as treatments
for SCLC.
129 disorders and has high predictive value
for SCLC.
130 rystals such as rubrene with high, trap-
free SCLC mobilities up to 0.2 cm(2)/Vs and a width of the re
131 Several lines of evidence,
from SCLC primary human tumours, patient-derived xenografts,
132 mutations in candidate genes identified
from SCLC sequencing studies.
133 In contrast, mortality
from SCLC declined almost entirely as a result of declining i
134 VE-cadherin is required for VM in NCI-
H446 SCLC xenografts, where VM decreases tumour latency and,
135 mics underlie the emergence of
heterogeneous SCLC phenotypes.
136 markedly synergistic effects in ASCL1(
High)
SCLC in vitro and in mouse models.
137 IGFBP5 as a secreted marker for ASCL1(
High)
SCLC.
138 Human SCLC exhibits intratumoral subtype heterogeneity, sugges
139 Here we show that mouse and
human SCLC cells in culture and in vivo can grow cellular prot
140 ecule (NCAM), promoted phagocytosis in
human SCLC cell lines that was enhanced when combined with CD4
141 fied many recurrently mutated genes in
human SCLC tumors.
142 YCL (L-Myc) is frequently amplified in
human SCLC, but its roles in SCLC progression are poorly under
143 MYC family proteins that is mutated in
human SCLC.
144 is highly expressed on the surface of
human SCLC cells; therefore, we investigated CD47-blocking imm
145 ed macrophage-mediated phagocytosis of
human SCLC patient cells in culture.
146 tically activated in a small subset of
human SCLC, promotes SCLC development.
147 ponding to transcriptional profiles of
human SCLC.
148 ations in NOTCH family genes in 25% of
human SCLC.
149 Freshly collected primary
human SCLC tumor cells were permissive to MYXV and intratumora
150 herapy followed by relapse, similar to
human SCLC.
151 Using an
immunocompetent SCLC mouse model, we demonstrated the safety of intrapul
152 In SCLC models in vitro and in vivo, LY2606368 exhibited st
153 -L1 expression is typically low or absent
in SCLC, which has precluded its use as a predictive biomar
154 eviously shown to have selective activity
in SCLC models, but the underlying mechanism was elusive.
155 nsive study of somatic genome alterations
in SCLC uncovers several key biological processes and ident
156 To study roles for MYCN amplification
in SCLC progression and chemoresistance, we developed a gen
157 networks, such as the GNAS/PKA/PP2A axis
in SCLC.
158 peutic target to overcome chemoresistance
in SCLC.
159 pressed cell-cycle checkpoint kinase CHK1
in SCLC.
160 ncreases Fas-induced apoptotic cell death
in SCLC cells.
161 Max deletion
in SCLC resulted in derepression of metabolic genes involve
162 K1 inhibition may be especially effective
in SCLC with MYC amplification or MYC protein overexpressio
163 is the first to investigate MEK5 and ERK5
in SCLC, linking the activity of these two kinases to the c
164 loss of candidate tumor suppressor genes
in SCLC, and we anticipate that this approach will facilita
165 DELTA-P scores were significantly higher
in SCLC-LEMS patients (3.5, 95% CI 3 to 4) compared to non-
166 ble target downstream of RB1, inactivated
in SCLC and other advanced tumors, could have a broad impac
167 In vivo, sensitivity to LSD1 inhibition
in SCLC patient-derived xenograft (PDX) models correlated w
168 ght to identify novel mechanisms involved
in SCLC chemoresistance.
169 This work establishes a role for KDM5A
in SCLC tumorigenesis and suggests that KDM5 inhibitors sho
170 To test the role of KDM5A
in SCLC tumorigenesis in vivo, we developed a CRISPR/Cas9-b
171 expressed at significantly higher levels
in SCLC, compared to lung adenocarcinoma.
172 elated with increased genomic copy number
in SCLC lines.
173 ur suppressors TP53 and RB1 is obligatory
in SCLC.
174 , we show here that DDX5 is overexpressed
in SCLC cell lines and that its down-regulation results in
175 s pathway, is significantly overexpressed
in SCLC compared to non-small cell lung cancer.
176 nase CHK1, is significantly overexpressed
in SCLC, compared to lung adenocarcinoma.
177 ging initial safety and efficacy profiles
in SCLC in the clinic.
178 with uncontrolled cell cycle progression
in SCLC, we find that CDC25A, B and C mRNAs are expressed a
179 al leukocyte content was markedly reduced
in SCLC compared with lung ADCA, which was validated in hum
180 ortant regulators of cisplatin resistance
in SCLC cells, including EZH2.
181 air (NER) and govern cisplatin resistance
in SCLC.
182 ivity for overcoming cisplatin resistance
in SCLC.
183 ly amplified in human SCLC, but its roles
in SCLC progression are poorly understood.
184 e tumor cells, promoting a temporal shift
in SCLC from ASCL1(+) to NEUROD1(+) to YAP1(+) states.
185 pression activates canonical Hh signaling
in SCLC cells, and markedly accelerates tumor progression.
186 autocrine, ligand-dependent Hh signaling
in SCLC has been disputed.
187 e, ligand-dependent model of Hh signaling
in SCLC pathogenesis, and reveal a novel role for non-canon
188 in the DNA damage response, specifically
in SCLC.
189 -based selection of targeted therapeutics
in SCLC patients.
190 elation for response to SC16LD6.5 therapy
in SCLC patient-derived xenograft models.
191 b in phase 3 randomised controlled trials
in SCLC.
192 The functional significance of VM
in SCLC suggests VM regulation may provide new targets for
193 We observed
increased SCLC survival following intrapulmonary MYXV that was enh
194 tivation of the Cd47 gene markedly
inhibited SCLC tumor growth.
195 igher NOTCH activity compared to
KDM5A (+/+)
SCLCs.
196 and non-neuroendocrine/mesenchymal-like (
ML)
SCLC phenotypes.
197 sis in an autochthonous Rb/p53-deleted
mouse SCLC model and found significant tumor inhibition.
198 When compared to
mouse SCLC tumors expressing an activating, ligand-independent
199 xic damage and apoptosis in human and
murine SCLC cell lines, but not in lung adenocarcinoma cells.
200 We further demonstrate that
murine SCLC tumors were highly sensitive to ATR- and CHK1 inhib
201 ctively identified patients with EGFR-
mutant SCLC and other high-grade neuroendocrine carcinomas seen
202 , 58 patients had NSCLC and nine had de
novo SCLC or mixed histology.
203 Unlike nonsmall cell lung cancer (
NSCLC),
SCLC harbors few actionable mutations for therapeutic in
204 and optic neuritis in a patient with
occult SCLC.
205 rograms and drives the metastatic ability
of SCLC cells.
206 ontributes to the high metastatic ability
of SCLC.
207 These data offer insight into the biology
of SCLC and LCNEC, providing a useful framework for develop
208 nhibitors block the self-renewal capacity
of SCLC cells, the lack of activating pathway mutations hav
209 This is the first reported case
of SCLC-associated CAR to present with chorioretinitis.
210 e in basal cells leads to the development
of SCLC, thus differentially influencing the lung cancer ty
211 kinases known to promote the development
of SCLC.
212 s) with a pathologically proven diagnosis
of SCLC, Eastern Cooperative Oncology Group performance sta
213 s had tissue genotyping at first evidence
of SCLC.
214 reveal that MYC drives dynamic evolution
of SCLC subtypes.
215 quired for optimal survival and expansion
of SCLC cell lines in vitro and in vivo.
216 CAR can be a herald feature
of SCLC, and early recognition of the disease should prompt
217 Trp53 and Rb1, a defining genetic feature
of SCLC, leads to hypersensitivity to Hh ligand in vitro, a
218 of Skp2 completely blocked the formation
of SCLC in Rb1/Trp53-knockout mice (RP mice).
219 nished clonogenicity and malignant growth
of SCLC cells in vivo Collectively, our studies validate th
220 metabolism axis that promotes the growth
of SCLC.
221 pathway, potently suppressing the growth
of SCLC.
222 One of the hallmarks
of SCLC is its almost uniform chemotherapy sensitivity.
223 Although the incidence
of SCLC decreased during each decade, the overall survival
224 for the MEK5-ERK5 axis in the metabolism
of SCLC cells, including lipid metabolism.
225 c neuroendocrine cells from a mouse model
of SCLC and found that ectopic expression of L-Myc, c-Myc,
226 developed a CRISPR/Cas9-based mouse model
of SCLC by delivering an adenovirus (or an adeno-associated
227 mation of primary cilia, in a mouse model
of SCLC induced by conditional deletion of both Trp53 and R
228 s, appear to be converging on a new model
of SCLC subtypes defined by differential expression of four
229 system to a well-established murine model
of SCLC to rapidly model loss-of-function mutations in cand
230 letion genetically engineered mouse model
of SCLC, the combination of ABT-263 and AZD8055 significant
231 a conditional Tp53;Rb1 mutant mouse model
of SCLC, we now demonstrate a requirement for the Hh ligand
232 Mycl in two genetically engineered models
of SCLC resulted in strong suppression of SCLC.
233 multiple highly aggressive murine models
of SCLC, providing a rationale for new combination regimens
234 nd human patient-derived xenograft models
of SCLC.
235 ve patient-derived xenograft (PDX) models
of SCLC.
236 Sonic Hedgehog (Shh) for the progression
of SCLC.
237 activity is required for the propagation
of SCLC stem cells in transplantation studies.
238 scription factor ASCL1 and the repression
of SCLC tumorigenesis.
239 Higher DELTA-P scores increased the risk
of SCLC stepwise (score 0 = 0%, 1 = 18.8%, 2 = 45%, 3 = 55.
240 The subset
of SCLC lines and primary samples that undergo growth inhib
241 ves a neuroendocrine-low "variant" subset
of SCLC with high NEUROD1 expression corresponding to trans
242 e a therapeutic target for a broad subset
of SCLC.
243 apeutic vulnerabilities of these subtypes
of SCLC should help to focus and accelerate therapeutic res
244 ls of SCLC resulted in strong suppression
of SCLC.
245 ssible therapeutic targets on the surface
of SCLC cells.
246 ), whereas median survival since the time
of SCLC transformation was 10.9 months (95% CI, 8.0 to 13.7
247 ibed ASCL1+ neuroendocrine variant (NEv2,
or SCLC-A2).
248 d delineation of subcutaneous and
orthotopic SCLC tumor xenografts as well as distant organ metastase
249 rogates tumorigenesis in MYCL-
overexpressing SCLC.
250 erapeutic strategies for MYCN-
overexpressing SCLC, we performed a genome-scale CRISPR-Cas9 sgRNA scre
251 ngineered mouse model of MYCN-
overexpressing SCLC.
252 efficacy in patient-derived xenograft (
PDX)
SCLC models.
253 ulating tumor cells (CTCs) from
pretreatment SCLC blood samples.
254 We show that KDM5A
promotes SCLC proliferation and SCLC's neuroendocrine differentia
255 ed in a small subset of human SCLC,
promotes SCLC development.
256 ty of patient tissues for research
purposes,
SCLC patient-derived xenografts (PDX) have provided the
257 num-sensitive or platinum-resistant
relapsed SCLC.
258 However, a subset of relatively
resistant SCLC cell lines has concomitant high expression of the a
259 Notably, depletion of MEK5/ERK5
sensitized SCLC cells to pharmacologic inhibition of the mevalonate
260 for depletion with DZNep strongly
sensitizes SCLC cells and tumors to cisplatin.
261 ts (testing set, 112 CTC samples) and in
six SCLC patient-derived CTC explant tumors.
262 -care for patients with cancer,
specifically SCLC.
263 and PNECs, but tumors resembling early-
stage SCLC grew in immunodeficient mice after subcutaneous inj
264 n screens to a cellular model of early-
stage SCLC.
265 the profiles resemble those from early-
stage SCLC; and when both RB and TP53 levels are reduced, the
266 CE+V) doublet in untreated, extensive-
stage SCLC (ES-SCLC).
267 strated clinical activity in extensive-
stage SCLC (ES-SCLC).
268 older, had limited-stage or extensive-
stage SCLC, and had disease progression after at least one pre
269 ion Pravastatin 40 mg combined with
standard SCLC therapy, although safe, does not benefit patients.
270 Three correspond to known
subtypes (
SCLC-A, SCLC-N, and SCLC-Y), while the fourth is a previ
271 tivation of the PP2A phosphatase,
suppresses SCLC expansion in culture and in vivo.
272 Altogether, our data indicate
that SCLC displays an actionable dependence on ATR/CHK1-media
273 Our findings indicate
that SCLC phenotypic heterogeneity can be specified dynamical
274 Targeted drug screening reveals
that SCLC with high MYC expression is vulnerable to Aurora ki
275 We show
that SCLC patients (37/38) have rare CTC subpopulations co-ex
276 Here, we show
that SCLC tumor samples feature co-expression of Shh and BBS-
277 The SCLC cohort of this phase 1/2 multicentre, multi-arm, op
278 ; here, we report an interim analysis of
the SCLC cohort.
279 d SCLC tumorigenesis and metastasis, and
the SCLCs that formed despite the absence of KDM5A had highe
280 The topology of
this SCLC TF network was derived from prior knowledge and was
281 Thus,
SCLC heterogeneity may be best understood as states with
282 contribution of the MAPK module MEK5-ERK5
to SCLC growth.
283 We propose that NE stem cells give rise
to SCLC, and transformation results from constitutive activ
284 transient and patients frequently succumb
to SCLC within a year following diagnosis.
285 eciation that EGFR-mutant NSCLCs can
undergo SCLC transformation.
286 rge photogeneration, and recombination
using SCLC, GIXRD, AFM, XPS, NEXAFS, R-SoXS, TEM, STEM, fs/ns
287 med MYXV cytotoxicity in classic and
variant SCLC subtypes as well as cisplatin-resistant cells.
288 s modest but significant reduction of
viable SCLC cells.
289 and safety of lurbinectedin in patients
with SCLC after failure of platinum-based chemotherapy.
290 immunotherapeutic regimens in patients
with SCLC and other cancers.
291 cidence of brain metastases in patients
with SCLC and with non-metastatic NSCLC, but also improves ov
292 calculated survival changes in patients
with SCLC during each decade between 1983 and 2012 to determi
293 In total, 106,296 patients
with SCLC were identified, with the overall incidence per 100
294 d nivolumab plus ipilimumab in patients
with SCLC who progressed after one or more previous regimens.
295 o improves overall survival in patients
with SCLC who respond to first-line treatment.
296 a potential new treatment for patients
with SCLC, who have few options especially in the event of a
297 s and other immunotherapies in patients
with SCLC.
298 profiles in previously treated patients
with SCLC.
299 could guide the use of ICIs in patients
with SCLC.
300 abled an improvement in OS for patients
with SCLC; however, a substantial amount of research remains