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2 nal and micropapillary urothelial carcinoma, small cell, and squamous cell carcinoma subtypes of inva
3 ort: A 57-year-old male, with a diagnosis of small-cell cancer of the right lung (microcellular anapl
4 4,036), squamous cell carcinoma (n = 1,998), small cell carcinoma (n = 1,524), undifferentiated carci
7 or understanding the origin and treatment of small cell carcinoma of the urinary bladder has become e
10 by additional neural autoantibody markers of small-cell carcinoma, including collapsin response-media
19 the most common malignancy distributed into small cell lung cancer (n = 57) and non-small cell lung
21 ted with these workflows, we analyzed 32 non-small cell lung cancer (NSCLC) and 22 breast cancer pati
22 qCC) are the two predominant subtypes of non-small cell lung cancer (NSCLC) and are distinct in their
23 Dose-dependent synergy was observed in Non-Small Cell Lung Cancer (NSCLC) and Head and Neck Squamou
24 of the most frequently mutated genes in non-small cell lung cancer (NSCLC) and is commonly comutated
25 f Notch signaling is a common feature of non-small cell lung cancer (NSCLC) and is correlated with po
26 YEATS2 gene is highly amplified in human non-small cell lung cancer (NSCLC) and is required for cance
28 aspiration (EBUS-TBNA) in patients with non-small cell lung cancer (NSCLC) can facilitate the select
29 molecule inhibitor (HL001) that induces non-small cell lung cancer (NSCLC) cell cycle arrest and apo
30 er siRNA to cytoplasm of KRAS mutant H23 Non-Small Cell Lung Cancer (NSCLC) cells for oncogene knockd
33 whether radiomics features measured from non-small cell lung cancer (NSCLC) change during therapy and
35 ion within the tumor microenvironment in non-small cell lung cancer (NSCLC) has not yet been adequate
38 udinal blood samples from advanced stage non-small cell lung cancer (NSCLC) patients (n = 29) receivi
39 onse are unpredictable in ALK-rearranged non-small cell lung cancer (NSCLC) patients treated with cri
40 sis to study resistance mechanisms in 43 non-small cell lung cancer (NSCLC) patients treated with the
46 c (18)F-FDG PET for tumor delineation in non-small cell lung cancer (NSCLC) radiation therapy plannin
47 s used on the plasma of 48 patients with non-small cell lung cancer (NSCLC) to detect EGFR mutations.
48 inical outcome of patients with advanced non-small cell lung cancer (NSCLC) treated with platinum-bas
49 ntification of patients with early stage non-small cell lung cancer (NSCLC) with high risk of recurre
50 efinitive management of locally advanced non-small cell lung cancer (NSCLC), but long-term prospectiv
51 the HDI-based anticancer therapeutics in non-small cell lung cancer (NSCLC), in the present study, we
52 ost common genomically defined subset of non-small cell lung cancer (NSCLC), KRAS-mutant lung cancer.
54 of subtype-specific prognostic genes for non-small cell lung cancer (NSCLC), we had previously propos
71 d as a novel therapeutic target expressed in small cell lung cancer (SCLC) and high-grade neuroendocr
72 ng mouse models of lung cancer, we show that small cell lung cancer (SCLC) and lung adenocarcinoma (A
79 ich was markedly upregulated in Lu-iPSCs and small cell lung cancer (SCLC) lines and clinical specime
81 genetically engineered mouse model of human small cell lung cancer (SCLC) to investigate the mechani
84 st signal was detected in a patient with non-small cell lung cancer (SUVmax, 10.9; T/B ratio, 8.4) an
88 etables" pattern, and stronger for other non-small cell lung cancer and never smokers for the "Americ
89 ibitor resistance mechanisms.EGFR-mutant non-small cell lung cancer are often resistant to EGFR tyros
90 of forty-seven patients with early-stage non-small cell lung cancer before and after three weeks of t
91 targeting reduced mitogenic signaling in non-small cell lung cancer cell lines, suggesting that targe
93 tro system to delineate their effects on non-small cell lung cancer cell proliferation and apoptosis.
94 nanosomes was assessed in H1299 and A549 non-small cell lung cancer cells, normal MRC9 lung fibroblas
97 comes of patients diagnosed with stage 1 non-small cell lung cancer in the NLST to a nationally repre
98 t downregulation of LZTFL1 expression in non-small cell lung cancer is associated with recurrence and
99 y that resistance to targeted therapy in non-small cell lung cancer is highly dynamic, and also one w
101 evolved resistance in an ALK rearranged non-small cell lung cancer line (H3122) to a panel of 4 ALK
104 chemotherapy combined with radiation in Non-Small Cell Lung Cancer patients for use in clinical tria
106 prompt a beneficial clinical response in non-small cell lung cancer patients who harbor activating mu
111 cation of double-positive human NCI-H358 non-small cell lung cancer target tumors over single-positiv
115 cally proven or radiologically suspected non-small cell lung cancer were prospectively enrolled in th
116 cly available gene expression dataset of non-small cell lung cancer when combined with the existing p
119 previously treated advanced KRAS-mutant non-small cell lung cancer, addition of selumetinib to docet
120 lected cancer patients, most especially with small cell lung cancer, although the long-term survival
121 urvival rates of small cell lung cancer, non-small cell lung cancer, and non-lung cancer patients all
124 antiprogrammed cell death-1 therapy for non-small cell lung cancer, from May 2012 to September 2014.
125 ly identified as a prognostic marker for non-small cell lung cancer, in cerebrovascular pathogenesis
126 sustained since the 1-year survival rates of small cell lung cancer, non-small cell lung cancer, and
127 LST group undergoing surgery for stage 1 non-small cell lung cancer, those in the SEER-Medicare NLST
128 f this phenomenon occurs in ALK-positive non-small cell lung cancer, where targeted therapies are use
141 ntial treatment strategy for KRAS mutant non-small cell lung cancers (NSCLC) and colorectal carcinoma
142 ective study, 36 patients with stage III non-small cell lung cancers (NSCLC), who underwent dynamic c
143 utation of LKB1, frequently occurring in non-small cell lung cancers (NSCLCs), is a predominant cauti
144 ial histologic sections from 90 archival non-small cell lung cancers from January 1, 2008, to Decembe
146 e mutational "hotspots" in nonsmall cell and small cell lung cancers, supporting a possible role of o
148 rative genomic and proteomic analysis of non-small cell lung carcinoma (NSCLC) cell lines revealed si
150 death worldwide, and among this cancer, non-small cell lung carcinoma (NSCLC) comprises the majority
151 midine ((18)F-FLT) PET in advanced-stage non-small cell lung carcinoma (NSCLC) patients with an activ
152 -driving genes in patients with advanced non-small cell lung carcinoma (NSCLC), especially in those w
155 ntly in clinical trials for the treatment of small cell lung carcinoma, was synthesized using this st
156 olymerase chain reaction analyses of 102 non-small cell lung tumors, 61 ovarian tumors, 70 liver tumo
157 lioblastoma multiforme, prostate tumors, non-small cell lung tumors, and ovarian tumors, but not nont
158 ic (IRR, 2.07; 95% CI, 1.95 to 2.20) and non-small-cell lung (IRR, 1.69; 95% CI, 1.54 to 1.86) cancer
160 metastatic or polymetastatic extensive stage small-cell lung cancer (ES-SCLC) to the overall survival
161 based detection of early- and late-stage non-small-cell lung cancer (n = 518 late-stage validation co
162 ic Assessment (DS-GPA) for patients with non-small-cell lung cancer (NSCLC) and brain metastases.
163 abolism, thereby selectively sensitizing non-small-cell lung cancer (NSCLC) and glioblastoma (GBM) ce
164 mal growth factor receptor (EGFR)-mutant non-small-cell lung cancer (NSCLC) are associated with poor
165 patients with unresectable IIIA and IIIB non-small-cell lung cancer (NSCLC) are carboplatin-paclitaxe
167 r ROS proto-oncogene 1 (ROS1)-rearranged non-small-cell lung cancer (NSCLC) are sensitive to tyrosine
168 who previously received radiotherapy for non-small-cell lung cancer (NSCLC) before receiving pembroli
169 that CLCb is specifically upregulated in non-small-cell lung cancer (NSCLC) cells and is associated w
172 Purpose Multiple agents for advanced non-small-cell lung cancer (NSCLC) have been approved in the
176 -associated cardiac injury for stage III non-small-cell lung cancer (NSCLC) is unclear, but higher he
177 r first-line chemotherapy for metastatic non-small-cell lung cancer (NSCLC) occurs most often at site
178 ession profiling of individual CTCs from non-small-cell lung cancer (NSCLC) patients with remarkable
180 ving anti-PD-1 or anti-PD-L1 therapy for non-small-cell lung cancer (NSCLC) presented hair repigmenta
181 ed survival in the treatment of advanced non-small-cell lung cancer (NSCLC) previously treated with c
182 nt chemotherapy for resected early-stage non-small-cell lung cancer (NSCLC) provides a modest surviva
183 inhibitors has changed the landscape of non-small-cell lung cancer (NSCLC) therapy, with 2 approvals
184 n both small-cell lung cancer (SCLC) and non-small-cell lung cancer (NSCLC) to try to improve inciden
186 patients with treatment-naive, advanced non-small-cell lung cancer (NSCLC) with a programmed cell de
188 reasingly used to treat locally advanced non-small-cell lung cancer (NSCLC), IMRT and three-dimension
189 ocally advanced or incompletely resected non-small-cell lung cancer (NSCLC), it remains uncertain whe
190 shown promise in patients with advanced non-small-cell lung cancer (NSCLC), particularly with squamo
191 blockade, have improved the treatment of non-small-cell lung cancer (NSCLC), supporting the premise t
192 l component in the care of patients with non-small-cell lung cancer (NSCLC), yet cardiac injury after
216 ranial irradiation has been proposed in both small-cell lung cancer (SCLC) and non-small-cell lung ca
218 pite favorable responses to initial therapy, small-cell lung cancer (SCLC) relapse occurs within a ye
224 ients with FGFR1-amplified squamous cell non-small-cell lung cancer (sqNSCLC; arm 1) or other solid t
225 ars with ALK-rearranged stage IIIB or IV non-small-cell lung cancer (with at least one measurable les
226 ts were enrolled, including 74 patients with small-cell lung cancer and eight with large-cell neuroen
229 of relapse following primary surgery for non-small-cell lung cancer and the characterization of emerg
230 We assessed outcomes in patients with non-small-cell lung cancer and the EGFR Thr790Met mutation w
231 recapitulated in mutant KRAS homozygous non-small-cell lung cancer cells and in vivo, in spontaneous
233 ctDNA of the first 100 TRACERx (Tracking Non-Small-Cell Lung Cancer Evolution Through Therapy (Rx)) s
234 ertinib is approved for the treatment of non-small-cell lung cancer in patients who develop the EGFR
236 ad histologically or cytologically confirmed small-cell lung cancer or large-cell neuroendocrine tumo
237 ical specimens obtained from EGFR-mutant non-small-cell lung cancer patients with acquired EGFR tyros
239 thod to quantify radiosensitivity in 134 non-small-cell lung cancer patients, by using K-Means cluste
240 carboplatin-paclitaxel in patients with non-small-cell lung cancer receiving thoracic radiation.
241 l according to the time interval between non-small-cell lung cancer resection and the initiation of p
245 tactic Body Radiotherapy for Early-Stage Non-Small-Cell Lung Cancer was reviewed for developmental ri
246 t-related adverse events in 74 patients with small-cell lung cancer were thrombocytopenia (eight [11%
247 to treat multiple brain metastases from non-small-cell lung cancer when highly active targeted thera
248 in patients with advanced ALK-rearranged non-small-cell lung cancer who had previously progressed fol
249 -naive patients with completely resected non-small-cell lung cancer who received postoperative multia
250 atients with EGFR-mutant or ALK-positive non-small-cell lung cancer with brain metastases now have th
251 were eligible for inclusion, 42 (39%) in non-small-cell lung cancer, 36 (33%) in breast cancer, 25 (2
254 b is used in advanced melanoma, advanced non-small-cell lung cancer, and in head and neck cancer.
256 oradiotherapy in patients with limited-stage small-cell lung cancer, and toxicity was similar and low
257 high-grade serous ovarian, oesophageal, and small-cell lung cancer, are driven by somatic structural
258 ntrolled trials of systemic therapies in non-small-cell lung cancer, breast cancer, colorectal cancer
259 apy is the standard of care in limited-stage small-cell lung cancer, but the optimal radiotherapy sch
260 ly or histologically confirmed limited-stage small-cell lung cancer, Eastern Cooperative Oncology Gro
261 ed treatments for patients with advanced non-small-cell lung cancer, especially focusing on data from
262 l versus docetaxel in previously treated non-small-cell lung cancer, regardless of PD-L1 expression o
263 atients who had squamous or non-squamous non-small-cell lung cancer, were 18 years or older, had meas
264 s particularly active in platinum-refractory small-cell lung cancer, which tends not to respond to to
277 A, we find that HLA LOH occurs in 40% of non-small-cell lung cancers (NSCLCs) and is associated with
278 and it is often genetically activated in non-small-cell lung cancers (NSCLCs) by, for instance, mutat
285 s the outcomes of patients with advanced non-small-cell lung carcinoma (NSCLC) harbouring epidermal g
286 er 2013, solid tumour samples (including non-small-cell lung carcinoma [NSCLC], colorectal carcinoma,
290 nosed with cancer (prostate, colorectal, non-small-cell lung, non-Hodgkin lymphoma, breast, uterine,
291 gnosed with advanced breast, colorectal, non-small-cell lung, or pancreatic cancer from 2009 to 2012
292 P chimeras, we observed fluorescence also in small cells neighboring the motor neurons, identified as
294 , excluding those with pancreatic tumours or small-cell or large-cell lung cancer, as well as those w
295 viously reported a general method to improve small, cell-permeable fluorophores which resulted in the
298 ifferentiated embryonal and undifferentiated small cells (SCU) progressively lose EGFR and ASAP1 expr
299 R maintained typical immaturity traits (e.g. small cell size, high amino acid contents and reduced su
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