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1 ay arise from a minority of cells within the primary tumour.
2  metastasis and a xenograft derived from the primary tumour.
3  because cells have already escaped from the primary tumour.
4 eminated cells after surgical removal of the primary tumour.
5 , depending upon the ER concentration in the primary tumour.
6 ded from different clones present within the primary tumour.
7  the adjuvant setting after resection of the primary tumour.
8  (ECM) and increased local invasion from the primary tumour.
9 multiple competing subclones within a single primary tumour.
10 fter apparently curative surgery removed the primary tumour.
11 nome-wide DNA copy number alterations in 701 primary tumours.
12 tions of histopathologically well-classified primary tumours.
13 pattern reminiscent of that reported in some primary tumours.
14 with colorectal cancer had surgery to remove primary tumours.
15 7%) neuroblastoma cell lines and 10/50 (20%) primary tumours.
16 majority of events were classified as second primary tumours.
17 ng late ipsilateral and contralateral second primary tumours.
18  which very rarely has p53 gene mutations in primary tumours.
19 sent in five lines and at least three of ten primary tumours.
20 tastases in 55% of the animals that produced primary tumours.
21 ours and metastases, as well as the injected primary tumours.
22 rcinoma (HCC) following surgical ablation of primary tumours.
23 36%] of 9169 patients; p=0.0003), have colon primary tumours (1116 [84%] of 1334 patients vs 5603 [66
24 umour cells from 19 women with ER(+)/HER2(-) primary tumours, 84% of whom had acquired circulating tu
25          Of these six mutations, two were in primary tumours (a colorectal cancer and a breast cancer
26 al-like breast cancer: peripheral blood, the primary tumour, a brain metastasis and a xenograft deriv
27  show that within a predominantly epithelial primary tumour, a small proportion of tumour cells under
28          Here, we build a compendium of 2218 primary tumours across 12 human cancer types and systema
29 illed and conservative surgery to remove the primary tumour; adjuvant therapies are also given before
30                  Gliomas are the most common primary tumours affecting the adult central nervous syst
31 egulated in approximately 90% and 86% of all primary tumours analysed, respectively.
32                        Identification of the primary tumour and development of a tailored site-specif
33 d-derived suppressor cells infiltrate in the primary tumour and distant organs with different time ki
34 hat after metastatic cancer cells escape the primary tumour and enter the circulation, their interact
35        They also carry information about the primary tumour and have the potential to be valuable bio
36 ons, providing growth advantages both in the primary tumour and in the lung microenvironment.
37 lysis of 100 single cells from a monogenomic primary tumour and its liver metastasis indicated that a
38 aimed to evaluate initial PET/CT features of primary tumour and locoregional metastatic lymph nodes (
39  reduced neutrophil infiltration to both the primary tumour and metastatic sites.
40                  These cells detach from the primary tumour and move from the bloodstream to a new si
41    Radiotherapy directly interferes with the primary tumour and possibly reverses some immunosuppress
42 um associated with relapse, we sequenced the primary tumour and relapse genomes from eight AML patien
43 ed that a single clonal expansion formed the primary tumour and seeded the metastasis.
44               At 20 mg/kg growth of both the primary tumour and the number of metastatic deposits in
45 orrelations between PET/CT parameters of the primary tumour and those of metastatic axillary LNs.
46 SF1A methylation status in a large series of primary tumour and tumour lines; (b) chromosome 3p allel
47                                   We studied primary tumours and 156 lymph nodes from 32 patients wit
48   Notably, PARP14 is highly expressed in HCC primary tumours and associated with poor patient prognos
49  myc-induced apoptosis by Cbfa1 as explanted primary tumours and cell lines from CD2-Cbfa1-G1/CD2-myc
50 that are unique to breast cancer cell lines, primary tumours and colon cancer cells.
51  and assessed transcriptional profiles in 43 primary tumours and copy number profiles in 38 primary t
52 nts with LN metastases had relatively larger primary tumours and higher SUVmax values.
53                                          All primary tumours and histologically involved lymph nodes
54           Loss of FBXL4 was also detected in primary tumours and it was highly associated with progno
55 collected at autopsy together with available primary tumours and longitudinal metastatic biopsies tak
56 tant p53 resulted in the rapid appearance of primary tumours and metastases.
57 mediates regression of both light-irradiated primary tumours and non-irradiated distant tumours by in
58 nd SNAIL in the metastases compared with the primary tumours and renal vein tumour thrombi.
59 ous degrees of genetic heterogeneity between primary tumours and their distant metastases.
60 ter region CpG island was hypermethylated in primary tumours and tumour cell lines.
61 d expression of the human CAVEOLIN-1 gene in primary tumours and tumour-derived cell lines.
62 ases, N2 disease, or poor differentiation of primary tumour), and previous adjuvant treatment with ox
63  to AJCC staging criteria, ulceration of the primary tumour, and patient sex.
64 ions and a large deletion not present in the primary tumour, and was significantly enriched for 20 sh
65 LMO1 expression (P = 0.028) in neuroblastoma primary tumours, and ablates GATA3 binding (P < 0.0001).
66 hway was significantly higher in BMs than in primary tumours, and SERPINI1 was the most frequently mu
67 e driver mutations beyond those required for primary tumours, and that phylogenetic trees across meta
68                                          The primary tumours arising from the S100A4-expressing cells
69 ironment-ideally, recovering the role of the primary tumour as an immunogenic hub.
70  methylation occurs frequently (> or =20% of primary tumours) at CASP8, SLIT2 and RASSF1A in Wilms' t
71 ivity, and that fusion-positive ES cells and primary tumours both express low or undetectable levels
72 the increasing use of primary cell cultures, primary tumour cell explants, early passage cell lines,
73 wing uncontrolled proliferation, a subset of primary tumour cells acquires additional traits/mutation
74              Cancer metastasis requires that primary tumour cells evolve the capacity to intravasate
75   Strong nuclear expression of maspin within primary tumour cells is correlated with increased surviv
76 lls from high-burden tissues were similar to primary tumour cells, which were more heterogeneous and
77 -) mice that phenotypically resemble nascent primary tumour cells.
78 tion, but promotes proliferation in advanced primary tumour cells.
79 d-stage blood, we detect both metastatic and primary tumour clones, even years after removal of the p
80 1 expression in neuroblastoma cell lines and primary tumours, consistent with a gain-of-function role
81  specialization, for example, dominating the primary tumour, contributing to metastatic populations,
82 e in-frame deletion of 30 base pairs) in six primary tumours, corresponding to an overall mutation fr
83 lysis of human disseminated cancer cells and primary tumours corroborated the relevance of these find
84 ication (a biomarker for bone metastasis) in primary tumours could predict the treatment outcomes of
85                             Similarly, 10/15 primary tumour cultures (including three matched to norm
86 ressed induction of GADD45alpha was found in primary tumour cultures compared and to matched peripher
87 s), an algorithm that mines pan-cancer human primary tumour data to identify mutation-specific SL par
88  and growth rate in mice implanted with both primary tumour-derived GBMNS and GBMDC.
89 henotypically distinct clones derived from a primary tumour-derived human prostate cancer cell line (
90 was largely abandoned when no differences in primary tumour development were found between athymic nu
91  that protects immunocompetent hosts against primary tumour development, but this idea was largely ab
92                 Symptoms, time frame between primary tumour diagnosis and the finding of metastases,
93  colorectal cancer who had surgery to remove primary tumours done by colorectal surgeons or non-color
94 ognosis, we examined seven cell lines and 87 primary tumours for co-amplification of candidate genes
95 somatic, and those evaluated occurred in the primary tumour from which the cell line was derived.
96  Care (TCC) protocol, we calculated GARD for primary tumours from 20 disease sites treated using stan
97 lassify lung cancer histologies, distinguish primary tumours from metastases to the lung from other s
98             Studies on GTICs have focused on primary tumours from which GTICs could be isolated and t
99 lastic stroma, ultimately recapitulating the primary tumours from which they arose.
100 g AML relapse: (1) the founding clone in the primary tumour gained mutations and evolved into the rel
101  models of vascular permeability, emphysema, primary tumour growth and metastasis.
102  of CD8 T-cell proliferation, thus promoting primary tumour growth and metastatic progression.
103 ) phenotype has been implicated in promoting primary tumour growth and progression to metastatic dise
104  enhanced tumorigenicity in murine models of primary tumour growth and pulmonary metastases.
105 lation of haematopoietic FAK does not affect primary tumour growth but enhances the incidence of meta
106 at selective Lgr5(+) cell ablation restricts primary tumour growth, but does not result in tumour reg
107  CTC-derived cultures has minimal effects on primary tumour growth, but it greatly increases apoptosi
108      Caspase-8 status was not a predictor of primary tumour growth; rather, caspase-8 selectively pot
109 motherapy, and is helpful in identifying the primary tumour in patients who present with axillary ade
110 risk of developing local recurrence or a new primary tumour in previously irradiated areas.
111 n metastasis and xenograft compared with the primary tumour indicate that secondary tumours may arise
112                                     When the primary tumour is located in the pancreas, it is associa
113 reful monitoring for development of a second primary tumour is necessary, with further investigation
114                  In young male patients, the primary tumour is usually in the testis, in other patien
115 d metastases, and HOTAIR expression level in primary tumours is a powerful predictor of eventual meta
116 n of vascular endothelial growth factor C in primary tumours is associated with increased disseminati
117 ajor clinical problem as serial re-biopsy of primary tumours is often not a clinical option.
118 1269a expression in their surgically removed primary tumours is strongly associated with risk of CRC
119                                              Primary tumours liberate circulating tumour cells (CTCs)
120 es differentiates metastatic cell lines from primary tumour lines.
121 ive Oncology Group (ECOG) performance score, primary tumour location [colon vs rectum], previous trea
122                                       Of the primary tumours, malignant lesions are more frequent tha
123 arly lesions in mice and before any apparent primary tumour masses are detected, there is a sub-popul
124 establishing transcription-factor mapping in primary tumour material, we show that there is plasticit
125 Patients were stratified by histology of the primary tumour, metastatic tumour size, and number of me
126                           In common with the primary tumours, methylation-associated gene silencing o
127                   The xenograft retained all primary tumour mutations and displayed a mutation enrich
128    The comparison of relapse-specific versus primary tumour mutations in all eight cases revealed an
129 n was stratified by Breslow thickness of the primary tumour, N stage according to AJCC staging criter
130 were stratified according to the site of the primary tumour, nodal status (N0 or N1 vs N2 or N3), and
131 ree independent observers, who segmented the primary tumour of 20 NSCLC patients twice, to manual sli
132 ized fibrous tumour of the pleura) is a rare primary tumour of the pleura of mesenchymal origin.
133                                              Primary tumours of the bony spine and adjacent soft tiss
134                  Gliomas are the most common primary tumours of the central nervous system, with near
135 CpG island, this is not methylated in either primary tumours or in tumour-derived cell lines in which
136                  Intestinal melanomas can be primary tumours or metastases of cutaneous, ocular, or a
137 sis contain fewer genetic abnormalities than primary tumours or than DCCs from patients with metastas
138                 Detachment of cells from the primary tumour precedes metastatic progression by facili
139                       NQO1 expression in the primary tumour predicts response to neoadjuvant chemothe
140  differential protein expression between the primary tumours, renal vein tumour thrombi and metastase
141 iated with poor clinical outcome observed in primary tumours reveal gene signatures that predict clin
142 hism in colon and lung cancer cell lines and primary tumours revealed a small number of mutations, su
143 comprehensive genomic characterization of 22 primary tumours sampled before and after 4 months of neo
144 is of enhancer elements in a large series of primary tumour samples reveals insights into cis-regulat
145                                Additionally, primary tumour samples were enriched for FBW7 inactivati
146              1739 AZURE patients contributed primary tumour samples, of whom 865 (50%) had two assess
147 cancer and who gave consent for use of their primary tumour samples.
148 We developed an automated system for scoring primary tumour sections of 91 late-stage ovarian cancer
149 sis of IMP3 status (positive vs negative) in primary tumours showed hazard ratios of 5.84 (95% CI 3.6
150 therapy drug, cisplatin, enables significant primary tumour shrinkage and metastasis prevention.
151  (p<0.0001), as was tumour grade, stage, and primary tumour site (all p<0.0001).
152 caused by cancer cells that migrate from the primary tumour site (the mammary duct) through the blood
153 eceived subsequent local radiotherapy to the primary tumour site followed by maintenance therapy.
154 ustained expression of CXCL12 by MSCs in the primary tumour site inhibits metastasis through reductio
155  be a useful approach to unmask the original primary tumour site of cancer of unknown primary cases a
156  consolidation, and radiation therapy to the primary tumour site plus meta-iodobenzylguanidine avid m
157 invade and, hence, guide cells away from the primary tumour site to an extracortical location.
158 tly associated with tumour grade, stage, and primary tumour site, and leads to shorter survival compa
159 equencing of matching peripheral and central primary tumour specimens reveals various region-specific
160  and kidney cancer cell lines and in several primary tumours such as endometrial carcinomas, malignan
161 duced mouse models of cancer have shown that primary tumour susceptibility is thereby enhanced in imm
162 ilateral axillary LNs (SUVmax-LN), SUVmax of primary tumour (SUVmax-T) and NT ratios (SUVmax-LN/SUVma
163 eomic analysis to identify biomarkers in the primary tumour that predict response to neoadjuvant chem
164 n metastatic tumours but also in a subset of primary tumours that were likely to subsequently develop
165            In the human cases, compared with primary tumours, the metastatic deposits had a significa
166 n the area of breast immediately next to the primary tumour; this is despite the finding that two-thi
167              The NPM-ALK kinase is active in primary tumour tissue and forms a multimeric complex wit
168 ) to predict the pathological node status in primary tumour tissue from three independent cohorts of
169 om brain metastases compared to same-patient primary tumour tissue.
170 possibility in some cases of downstaging the primary tumour to avoid mastectomy, and to allow breast-
171 ltaneously satisfying a critical need of the primary tumour to be fed by the vasculature.
172 imary tumours and copy number profiles in 38 primary tumours to discover molecular subgroups of atypi
173  and did immunohistochemical analyses on 125 primary tumours to evaluate clinicopathological signific
174 n technique, stratified by hospital, site of primary tumour, tumour size, planned radiotherapy, and i
175 in at least a 4:1 ratio on the basis of sex, primary tumour type, age at diagnosis, smoking status, c
176 though The Cancer Genome Atlas has sequenced primary tumour types obtained from surgical resections,
177      In responders, surgical excision of the primary tumour was attempted, followed by myeloablation
178                                      In both primary tumours, we also identified an unexpectedly abun
179 f translocation in 21 myeloma cell lines and primary tumours, we show that the novel, karyotypically
180 n two others PIK3CA mutations present in the primary tumour were no longer detected at the time of pr
181 ding to the oestrogen-receptor status of the primary tumour were not statistically significant (pinte
182           In a subgroup of 41 subjects whose primary tumours were allelotyped, the fractional allelic
183                  371 patients with localised primary tumours were further investigated by use of surv
184                                  Twenty-five primary tumours were judged to carry only wild type p53
185 mic profiles, suggesting all are independent primary tumours, which are consistent with comprehensive
186  20%, minimisation by hospital site, site of primary tumour, WHO performance status, 16-week CT scan
187                                              Primary tumours will give us the statistical power to dr
188                            Two lines and one primary tumour with this translocation selectively expre
189                                              Primary tumours with aberrant TSC1 pre-mRNA splicing wer
190 cell lines correlate with distinct groups of primary tumours with different outcomes.
191 in addition colorectal tumour cell lines and primary tumours with low RASSF2 levels show decreased MS
192  pathway analysis has been from study of the primary tumour, with little attention to the metastatic

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