戻る
「早戻しボタン」を押すと検索画面に戻ります。 [閉じる]

コーパス検索結果 (1語後でソート)

通し番号をクリックするとPubMedの該当ページを表示します
1 ary model with two distinct trajectories for malignant progression.
2  for amplification of the MAPK signal during malignant progression.
3 matin landscape and unveil its importance in malignant progression.
4 (mTOR) functions, which is important for the malignant progression.
5      There is a strong link between TANs and malignant progression.
6 y selected, present in most cells, and drive malignant progression.
7 s and their microenvironment is critical for malignant progression.
8 otypes, suggesting inhibition of early-stage malignant progression.
9 vestigations into the role of the glycome in malignant progression.
10 d are coupled with the angiogenic switch and malignant progression.
11 ivator to drive podoplanin expression in the malignant progression.
12 promotes tumor initiation and contributes to malignant progression.
13 ultifocal benign neoplasms followed by their malignant progression.
14  gained functions that help to contribute to malignant progression.
15 ts a strong barrier against tumor growth and malignant progression.
16 e tumour-cell differentiation and antagonize malignant progression.
17 ression and signaling paradoxically promotes malignant progression.
18 tiating a feed-forward loop that can sustain malignant progression.
19 in vivo, defining a new function for DDB2 in malignant progression.
20 f-stimulation of tumor growth and presumably malignant progression.
21 ir association with epigenetic silencing and malignant progression.
22 ing CSCs may be a useful strategy to inhibit malignant progression.
23 tervention and likely also the mechanisms of malignant progression.
24  eliminates exosome-dependent differences in malignant progression.
25 cial during wound healing, inflammation, and malignant progression.
26 ing that stimulates their in vivo growth and malignant progression.
27 gs or contrast-enhanced MR imaging suggested malignant progression.
28 berrations leading to disease relapse and/or malignant progression.
29 ngly exacerbates pancreatic inflammation and malignant progression.
30 anisms involved in both tumor initiation and malignant progression.
31 t likely contribute to viral persistence and malignant progression.
32 e between hepatocyte loss, regeneration, and malignant progression.
33 cer where it contributes to inflammation and malignant progression.
34  whose mutational attenuation contributes to malignant progression.
35 anced stages significantly delays aggressive malignant progression.
36 related inflammation, immunosuppression, and malignant progression.
37 nd invasion (D) are not always necessary for malignant progression.
38 ed fibroblasts (CAF) play a critical role in malignant progression.
39 ssociated macrophages (TAM) that can promote malignant progression.
40 butions from the microenvironment to undergo malignant progression.
41 udy suggests that these are not required for malignant progression.
42 Ttf-1 or Titf1) as a candidate suppressor of malignant progression.
43 , mammary tumors, and lung metastases during malignant progression.
44 resents an opportunity to intervene prior to malignant progression.
45 scularization to facilitate tumor growth and malignant progression.
46 ccompanying activation and a strong drive to malignant progression.
47  necessary and sufficient for EMT during PDA malignant progression.
48 omatic alterations at this locus, leading to malignant progression.
49 ing an axis for either tissue homeostasis or malignant progression.
50 g tumors cleverly find alternative routes to malignant progression.
51 trates how deregulated ROS may contribute to malignant progression.
52 cells and the tumor microenvironment and for malignant progression.
53 types is the single greatest risk factor for malignant progression.
54 at macrophages promote cancer initiation and malignant progression.
55 ting tumor-associated myeloid cells to drive malignant progression.
56 been implicated in tumor cell metastasis and malignant progression.
57 commonly occurs in solid tumors and promotes malignant progression.
58  and its loss of function is associated with malignant progression.
59 tance of tissue architecture and polarity in malignant progression.
60 ar association of the "T-pro phenotype" with malignant progression.
61  tumor-associated macrophages (TAMs) promote malignant progression.
62 ion, thus sustaining a feed-forward loop for malignant progression.
63 ents may directly link Tax to early steps in malignant progression.
64  facilitates either inflammatory diseases or malignant progression.
65 important in cancer-related inflammation and malignant progression.
66 prostate cancer, SIN3B provides a barrier to malignant progression.
67 , multiplicity, growth rate, and the rate of malignant progression.
68 ng how phenotypic shifting can contribute to malignant progression.
69 ial link between inflammatory activation and malignant progression.
70 uman tumors, suggesting its participation in malignant progression.
71 tumors showing shortened incubation time and malignant progression.
72  in three stages: initiation, promotion, and malignant progression.
73 genic roles at different stages of mammalian malignant progression.
74  expression in human glioma decreases during malignant progression.
75  revealed a novel aspect of SnoN function in malignant progression.
76 ining 22% (n = 26) had little or no risk for malignant progression.
77 evelopment by secreting factors that promote malignant progression.
78 f (p16(Ink4a)/p19(Arf)) or p53 enables their malignant progression.
79 sitive proliferative cell compartment during malignant progression.
80 , characteristics frequently associated with malignant progression.
81  the tumor suppressor activity of p53 during malignant progression.
82 lts in an increased number of papillomas and malignant progression.
83 or immunity genes and may therefore restrain malignant progression.
84  enhances transport kinetics, which promotes malignant progression.
85 tophagy in HNSCC stromal cells that promotes malignant progression.
86 nction, a Krtap can serve as a switch toward malignant progression.
87 2f7/8 enhanced tumorigenesis and accelerated malignant progression.
88 is important in breast cancer initiation and malignant progression.
89 ical HSC numbers in check and interfere with malignant progression.
90 ing model with two distinct trajectories for malignant progression.
91  very high levels in tumors, contributing to malignant progression.
92 nce of metabolic rewiring during lung cancer malignant progression.
93 alignant growth rather than a consequence of malignant progression.
94 e potentially serve as genomic biomarkers of malignant progression.
95 utic strategy for targeting c-MYC-associated malignant progression.
96 -small cell lung cancer (NSCLC) cells during malignant progression.
97 ate tumor-associated macrophages that enable malignant progression.
98 e gastric epithelial differentiation but not malignant progression.
99 y against BTN3A1(+) cancer cells, abrogating malignant progression.
100 e ligand guanylin contributes universally to malignant progression.
101 d other immunosuppressive cells that promote malignant progression.
102 ment of the B-cell receptor is important for malignant progression.
103 toglutarate-driven demethylation facilitates malignant progression.
104 mpeded early-stage tumor growth and retarded malignant progression.
105 n human prostate cancers and associated with malignant progression.
106 RAF(V600E)-induced lung adenomas, leading to malignant progression.
107 elial-to-mesenchymal transition (EMT) during malignant progression.
108 ted to a proinflammatory state that supports malignant progression.
109 t cancer stem-like cells (CSC) that promotes malignant progression.
110 ampening antitumor immunity and accelerating malignant progression.
111 transformation (11/20) than in those without malignant progression (3.2 +/- 0.9 vs. 1.9 +/- 0.5; P =
112 cancer, but it is unclear whether it affects malignant progression after diagnosis.
113 arcinomas where it appears to be involved in malignant progression, although the biology of this inte
114 MAPK signalling as a critical determinant of malignant progression and also a stimulator of Arf tumou
115 ance of the ATR pathway both as a barrier to malignant progression and as a potential target for canc
116  transition program becomes activated during malignant progression and can enrich for cancer stem cel
117 ress the question whether ITH increases with malignant progression and can hence be exploited as a pr
118 already established tumors markedly impaired malignant progression and caused regression of individua
119 ncer cell stemness is essential for enabling malignant progression and clonal evolution.
120  may diminish tumor cell invasiveness during malignant progression and following antivascular therapi
121  because it is frequently inactivated during malignant progression and has recently been shown to fun
122 poral, dynamic control of ROS underpins full malignant progression and helps to rationalize conflicti
123  specific changes and processes required for malignant progression and identification of prognostic i
124 ow result in positive roles for autophagy in malignant progression and in subsequent tumor maintenanc
125                    The c-Myc oncogene drives malignant progression and induces robust anabolic and pr
126  RAS expression provides an early barrier to malignant progression and is mediated by TGF-beta recept
127 clinical severity, play an important role in malignant progression and metastatic dissemination of PC
128 rf or p53 tumor suppressor genes accelerates malignant progression and metastatic spread of 7,12-dime
129 olic phenotype has long been correlated with malignant progression and poor clinical outcome.
130  expression and activity are associated with malignant progression and poor patient prognosis in a nu
131 2 in breast cancer specimens correlated with malignant progression and poor patient survival.
132 ium cooperates with PTEN deletion to augment malignant progression and produce an aggressive metastas
133 periencing telomere dysfunction enables full malignant progression and provides a mechanism for acqui
134 er, our findings indicated that AK4 promotes malignant progression and recurrence by promoting metast
135 ciated macrophages are major contributors to malignant progression and resistance to immunotherapy, b
136 vates multiple signaling cascades to promote malignant progression and resistance to PLX4720 treatmen
137 ased beta1 integrin signaling is involved in malignant progression and that inhibitory antibody to be
138 er, p21-associated inhibition of early-stage malignant progression and the intense expression in papi
139 elp identify cellular processes critical for malignant progression and therapeutic intervention.
140 nk4a) epimutation drives tumor formation and malignant progression and validate a targeted methylatio
141  intervention with respect to inhibiting the malignant progression and/or reducing the treatment resi
142  molecular mechanism of p62/Sqstm1-dependent malignant progression, and suggest that molecular target
143  in neuroblastoma, we serially characterized malignant progression, angiogenesis, and sensitivity to
144              However, cancer development and malignant progression are also associated with accumulat
145 nitrosamine-induced hepatocarcinogenesis and malignant progression are suppressed.
146       Unresected tumor causes recurrence and malignant progression, as observed within a year in one
147 g the most neovascularised neoplasms and its malignant progression associates with striking neovascul
148 that TLR5-dependent commensal bacteria drive malignant progression at extramucosal locations by incre
149           Commensal microorganisms influence malignant progression by altering systemic inflammation.
150 sms that block or reverse stromal support of malignant progression by isolating the HER family from a
151 transition (EMT) in carcinoma cells enhances malignant progression by promoting invasion and survival
152 myeloid cells to oncogenic transformation or malignant progression by promoting whole chromosome inst
153 d the role of constitutive EGFR signaling in malignant progression by stably transfecting colon cance
154          We propose that p53 not only limits malignant progression by suppressing the acquisition of
155 nses, but these responses are limited during malignant progression by the development of immunosuppre
156 , however, information on tumor activity and malignant progression cannot be obtained on the basis of
157           These cancers exhibit a relentless malignant progression characterized by widespread invasi
158 horylation (OXPHOS) toward glycolysis during malignant progression, even when aerobic metabolism is a
159 .007; 95% CI, 1.001 to 1.014; P = .035), and malignant progression-free survival was predicted by EOR
160 ation will also be useful in deciphering the malignant progression from leiomyoma to leiomyosarcoma.
161 c balance of the mammary epithelium to drive malignant progression; however, complexities of Wnt path
162 associated macrophages (TAM) correlates with malignant progression, immune suppression, and poor prog
163  relevance in the context of premalignant to malignant progression in Barrett's esophagus.
164                                              Malignant progression in cancer requires populations of
165 ssociated macrophages (TAMs) associates with malignant progression in cancer.
166  endogenous wild-type Ras and predisposes to malignant progression in cooperation with Ras oncogenic
167 h deregulated kinase pathways are drivers of malignant progression in glioblastoma multiforme, glioma
168 paB), a transcription factor, which promotes malignant progression in HNSCC.
169 ivated oncogenes are the dominant drivers of malignant progression in human cancer, yet little is kno
170 sive tumor-bearing mice but only accelerates malignant progression in IL-6-unresponsive tumors.
171 at the hMENA splicing program is relevant to malignant progression in invasive disease.
172 is study, TANs were strongly associated with malignant progression in IPMNs.
173    We conclude that fibulin-2 is a driver of malignant progression in lung adenocarcinoma and plays a
174 l adhesion molecule that may impact risks of malignant progression in many cancers.
175    Persistent STAT3 signaling contributes to malignant progression in many diverse types of human can
176 sponses may underlie genetic instability and malignant progression in melanoma.
177 t as a lesion driving MDS or contributing to malignant progression in MPN.
178 ent a model in which SPR drives ODC-mediated malignant progression in NB.
179                               Hypoxia drives malignant progression in part by promoting accumulation
180 sine ((18)F-FET) PET to noninvasively detect malignant progression in patients with LGG.
181 on, activation of CDK2 alone does not induce malignant progression in Ras-mediated tumorigenesis.
182 vide new insight into the mechanisms driving malignant progression in squamous cancer.
183 ses tumor incidence, tumor multiplicity, and malignant progression in the chemically induced mouse mo
184  epigenetic modifications that contribute to malignant progression in the GC remain poorly defined.
185               Myeloid cells that orchestrate malignant progression in the tumor microenvironment offe
186 meres also may cause genomic instability and malignant progression in these marrow failure syndromes.
187 t occur in the tumor microenvironment during malignant progression in this disease.
188 is persistently activated and contributes to malignant progression in various cancers.
189 quisition of many phenotypes associated with malignant progression, including accelerated growth rate
190  completely prevented matriptase-induced pre-malignant progression, including inflammatory cytokine p
191  cells did not prevent matriptase-driven pre-malignant progression, indicating that matriptase activa
192 tion in colonic inflammation and its related malignant progression, indicating that targeting ubiquit
193 nic gain-of-function activities that promote malignant progression, invasion, metastasis and chemores
194 esponses to p53 contributes to inhibition of malignant progression is beginning to be clarified, with
195 y of targeting CDK2 in tumor development and malignant progression is dependent on the oncogenic path
196 d suggest that subgroups of patients in whom malignant progression is driven by EMT activators may re
197                       An important aspect of malignant progression is the acquired ability of tumor c
198 g because this tissue may have potential for malignant progression, is not visible by conventional en
199 wever, study of stromal or immune drivers of malignant progression may be limited.
200 s of multiscale intratumour heterogeneity to malignant progression, metastasis, and poor survival are
201 ly reserved for patients that have undergone malignant progression (MP) to an anaplastic glioma or se
202 cient to overcome a p53-regulated barrier to malignant progression, nor establish the prometastatic c
203 small, nonfunctioning tumors can predict the malignant progression observed in a minority of them.
204 hed that ECM stiffness, per se, promotes the malignant progression of a mammary epithelium by activat
205 tudy, we investigated the role of CYP24A1 on malignant progression of a murine model of Braf(V600E) -
206 of the ER stress response is associated with malignant progression of B cell chronic lymphocytic leuk
207       The treatment of choice to prevent the malignant progression of BE remains controversial.
208 a recently discovered oncogene implicated in malignant progression of both endocrine and nonendocrine
209 ment, highlighting the mechanisms that limit malignant progression of BRAF(V600E)-initiated tumors.
210 ing SnoN decreases TAZ expression as well as malignant progression of breast cancer cells.
211 ance of histone-binding activity of Pygo2 in malignant progression of breast cancer, we generated a k
212 ding to breast cancer development, promoting malignant progression of cancer cells and unfavorable cl
213     The myriad changes that occur during the malignant progression of cancer cells present challenges
214  growth factor (HGF), has been implicated in malignant progression of cancer involving stimulation of
215 mplicated in the survival, proliferation and malignant progression of cancers.
216 xtracellular matrix plays a decisive role in malignant progression of carcinomas.
217 deletion exhibited accelerated formation and malignant progression of chemically induced skin tumors
218  and found that XBP-1 deficiency decelerates malignant progression of CLL-associated disease.
219 vating the ER stress response in support for malignant progression of CLL.
220 could be targeted to prevent the relapse and malignant progression of CML.
221  a pro-inflammatory cytokine linked to rapid malignant progression of colorectal cancer (CRC) and the
222 rvous system and have been implicated in the malignant progression of different tumor types.
223 alloproteinase (TIMP)-4, are associated with malignant progression of ductal carcinoma in situ, a pre
224 xpression of Prdx6 led to an acceleration of malignant progression of existing tumors, revealing a du
225 en shown to promote mesenchymal features and malignant progression of glioblastoma.
226 n a myeloid cell sublineage is necessary for malignant progression of gliomas in transgenic murine mo
227 tes in vivo contributes to the formation and malignant progression of gliomas.
228 onally, we found that ZEB1 causally promotes malignant progression of HBECs and tumorigenicity, invas
229 FR3 variants exhibit specific effects in the malignant progression of HCC cells.
230 nce of the epithelial-stromal compartment in malignant progression of HCC in cirrhosis.
231 of viral persistence, which is requisite for malignant progression of HPV-infected lesions.
232 and is a critical contributing factor to the malignant progression of human prostate tumors.
233 ed our understanding of the pathogenesis and malignant progression of intestinal metaplasia.
234 in the intestine, deletion of Cnnm4 promoted malignant progression of intestinal polyps to adenocarci
235 at p27 is a potent barrier to the growth and malignant progression of Kras-initiated lung tumors.
236 information for the noninvasive detection of malignant progression of LGG.
237 tand the molecular mechanisms underlying the malignant progression of low-grade gliomas with mutation
238 nhibited the angiogenic switch necessary for malignant progression of low-grade to high-grade tumors.
239 lification of PHF19 is found associated with malignant progression of MM and plasma cell leukemia, co
240  of MYC is implicated in the development and malignant progression of most (~70%) human tumors.
241 sine kinase c-Met promotes the formation and malignant progression of multiple cancers.
242                                              Malignant progression of normal alveolar epithelial cell
243 and pattern of FGF-BP1 expression during the malignant progression of pancreas and colorectal carcino
244 ome epithelial tumors, but their role in the malignant progression of pancreatic ductal adenocarcinom
245                                          The malignant progression of pancreatic ductal adenocarcinom
246  microRNAs (miRNAs) during tumorigenesis and malignant progression of pancreatic neuroendocrine tumor
247          Furthermore, tumor multiplicity and malignant progression of papillomas after chemical skin
248 gly implicate Aurora-A overexpression in the malignant progression of skin tumors and suggest that Au
249 dy reveals a novel role for Stat3 in driving malignant progression of skin tumors in vivo.
250 embrane glycoprotein closely associated with malignant progression of squamous cell carcinomas (SCCs)
251 -tumor cells and their surrounding stroma in malignant progression of the cerebellar tumor medullobla
252 ventually causing resistance to imatinib and malignant progression of the disease.
253  to inhibitors such as imatinib mesylate and malignant progression of the disease.
254 ion of hepatic neoplasias yet constrain full malignant progression of these neoplasms possibly due to
255 uate their involvement in transformation and malignant progression of these tumor types.
256 into the mechanism by which p53 prevents the malignant progression of transformed cells.
257 , is an important mechanism to constrain the malignant progression of tumour cells.
258 7 deficiency accelerated both the growth and malignant progression of urethane-induced lung tumors, a
259                                              Malignant progression phenotypes were also affected at t
260 precise roles in cancer stem cells (CSC) and malignant progression remain uncertain.
261 ins and relative functional contributions to malignant progression remain uncertain.
262 to promote lung tumour formation in mice but malignant progression requires additional genetic altera
263                                              Malignant progression requires these genes, whose knockd
264                                              Malignant progression results from a dynamic cross-talk
265 sis leads to inappropriate cell survival and malignant progression, selective induction of apoptosis
266 of miRNAs during multistep tumorigenesis and malignant progression serves to down-regulate distinctiv
267 via reexpression of HoxD10, which is lost in malignant progression, significantly attenuated VEGF exp
268 tanding of the contributions of microRNAs to malignant progression, specifically their functions in m
269 lvement of Lck in different levels of glioma malignant progression, such as migration, tumor growth,
270  of this mutation in tumors at all stages of malignant progression suggests that it is an early event
271 her diagnostic accuracy for the detection of malignant progression than changes of contrast enhanceme
272 nd the mechanisms of cell transformation and malignant progression that are reinforced by mouse model
273 ve broad activity in tissue inflammation and malignant progression that depends on the expression of
274 erexpressed in EOC and play key roles in its malignant progression though their contribution in devel
275 cessively by many solid tumors and can drive malignant progression through multiple effects on the tu
276 stability, leading to disease relapse and/or malignant progression to a fatal blast phase.
277 acytidine (5-AzaC), have been shown to lower malignant progression to acute myeloid leukemia and to p
278 ated through promoter hypomethylation during malignant progression to high-grade glioblastoma were en
279 s and multiplicity of skin tumors as well as malignant progression to SCC.
280 y expressed, particularly at early stages of malignant progression to squamous cell carcinoma (SCC),
281 pment of epidermal hyperplasia and increased malignant progression to squamous cell carcinoma.
282  D3 results in reduced tumor development and malignant progression to squamous cell carcinomas (SCC).
283 l vascular invasion is a crucial step in the malignant progression toward metastasis.
284       In patients with histologically proven malignant progression toward WHO grade III or IV (n = 18
285  its dependence on IGF-II and by accelerated malignant progression upon IGF-1R overexpression.
286 n possessed the potency to limit early-stage malignant progression via cyclin D1/E2 inhibition.
287 sential role in mediating hypoxic effects on malignant progression via genetic alterations, resulting
288 ll and -wild-type littermates, implying that malignant progression was dependent specifically upon tu
289 y of imaging parameters for the detection of malignant progression was evaluated by receiver-operatin
290             To better understand its role in malignant progression, we deleted Shh in a well-defined
291              Dissecting TGF-beta's impact on malignant progression, we demonstrate that TGF-beta conc
292 rominent role for p16(Ink4a) in constraining malignant progression, we sought to assess the pathologi
293                              Progression and malignant progression were identified in 95 (44%) and 44
294 quirement of the HIF-alpha-c-Myc pathway for malignant progression, whereas the canonical transcripti
295 The common CSC signature was associated with malignant progression, which is enriched in poorly diffe
296 erexpressing mice increased tumor burden and malignant progression, while Loxl2-deficient mice exhibi
297 setting of telomere dysfunction enabled full malignant progression with alleviation of telomere dysfu
298 ng an adaptive immune response that promotes malignant progression, with implications for cancer prev
299  systemic inflammatory pathways that promote malignant progression, with implications for how to prev
300  proliferation and invasion are critical for malignant progression, yet how these processes relate to

 
Page Top