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1 ype colorectal cancers but down-regulated in colorectal adenocarcinoma.
2  novel target for anti-angiogenic therapy in colorectal adenocarcinoma.
3 erum hypergastrinemia promotes the growth of colorectal adenocarcinoma.
4  identified 4,879 incident cases of invasive colorectal adenocarcinoma.
5  to treat patients with pelvic recurrence of colorectal adenocarcinoma.
6 o chemoradiotherapy in preclinical models of colorectal adenocarcinoma.
7 g in a genetically defined organoid model of colorectal adenocarcinoma.
8 dence rates were obtained for pancreatic and colorectal adenocarcinoma.
9  (MSI-H) is frequently observed in localized colorectal adenocarcinoma.
10 ioembolization for liver-dominant metastatic colorectal adenocarcinoma.
11 eceptors (TCRs) expressed on TILs from human colorectal adenocarcinoma.
12 ed from whole-genome sequencing of a primary colorectal adenocarcinoma.
13 ible to experimental triggers of colitis and colorectal adenocarcinoma.
14  epithelial cell line, SKCO-15, derived from colorectal adenocarcinoma.
15 carcinoma, C33a cervix carcinoma, and LS174T colorectal adenocarcinoma.
16 tatus in patients with Dukes' stage B2 and C colorectal adenocarcinomas.
17  K-ras, and/or p53, occur in the majority of colorectal adenocarcinomas.
18 quencies of allelic losses in pancreatic and colorectal adenocarcinomas.
19 , the Smad3 mutant mice become moribund with colorectal adenocarcinomas.
20  in p27 expression in primary and metastatic colorectal adenocarcinomas.
21            Ras mutations are found in 50% of colorectal adenocarcinomas.
22 ontrols in breast, endometrial, pancreas, or colorectal adenocarcinomas.
23 sufficient to induce formation of metastatic colorectal adenocarcinomas.
24 clusivity with inactivating APC mutations in colorectal adenocarcinomas.
25 showed frequent overexpression of OATP1B3 in colorectal adenocarcinomas.
26  with a significant risk of gastric, but not colorectal, adenocarcinoma.
27                                        Among colorectal adenocarcinomas, 10%-15% are mucinous and hav
28 ata for 139 457 adult patients with invasive colorectal adenocarcinoma: 12 958 patients in Denmark, 9
29 h transmural lesions and a high incidence of colorectal adenocarcinomas (60%) was observed in 6-mo-ol
30 ed mucosa of human IBD patients and in human colorectal adenocarcinoma, accounting for the epithelial
31 cted with PDGF-BB-bearing tumor cells and in colorectal adenocarcinoma, activated PDGF beta-receptors
32 dies simultaneously compared the patterns in colorectal adenocarcinoma (ADC) and neuroendocrine neopl
33 g transcriptomic differences between primary colorectal adenocarcinoma and distant metastases, which
34 Caco-2 cells, which are derived from a human colorectal adenocarcinoma and have similar functions to
35  identified recurrent oncogenic mutations in colorectal adenocarcinoma and have surveyed exons of pro
36 tively compare the transcriptomes of primary colorectal adenocarcinoma and metastatic lesions at both
37 by immunohistochemical methods in 30 primary colorectal adenocarcinomas and 24 adenomatous polyps.
38 mmunohistochemical analysis was performed on colorectal adenocarcinomas and adjacent normal mucosa fo
39 rt somatic mutations of RNF43 in over 18% of colorectal adenocarcinomas and endometrial carcinomas.
40 re increased dramatically in 85-90% of human colorectal adenocarcinomas and in 40-50% of colonic aden
41 ation at the EVL/hsa-miR-342 locus in 86% of colorectal adenocarcinomas and in 67% of adenomas, indic
42 em cell features of cells to be increased in colorectal adenocarcinomas and inversely correlated with
43 2 (colorectal adenocarcinoma), HT29-MTX-E12 (colorectal adenocarcinoma) and HepG2 (hepatocellular car
44 pended on the cancer cell lines of melanoma, colorectal adenocarcinoma, and breast carcinoma.
45 tate cancer, 80% of B-cell lymphomas, 90% of colorectal adenocarcinomas, and many other forms of canc
46 partment, that its expression is elevated in colorectal adenocarcinomas, and that MSI2 loss-of-functi
47 s with locally advanced pelvic recurrence of colorectal adenocarcinoma are described.
48  previously that the pulmonary metastases of colorectal adenocarcinoma are less responsive to therapy
49                         Skin metastases from colorectal adenocarcinoma are rare conditions that are m
50                          Ten to 20% of human colorectal adenocarcinomas are of this histological type
51             Patients with a new diagnosis of colorectal adenocarcinoma at the major hospitals in metr
52 ded people aged 52 to 85 years who died from colorectal adenocarcinoma between 2011 and 2017 (cases);
53 oembolization to treat liver metastases from colorectal adenocarcinoma between July 2002 and December
54              Overall, upon transformation to colorectal adenocarcinoma, broad radiation sensitivity o
55  intestinal cells and primary and metastatic colorectal adenocarcinomas but not by extraintestinal ti
56 erved in approximately 25% of stage I/II/III colorectal adenocarcinomas but rarely found in advanced
57 s; e.g., EPA induced a ferroptotic effect on colorectal adenocarcinoma, but LA or alphaLA did not.
58 i-ras protooncogene frequently is mutated in colorectal adenocarcinomas, but the etiology of this mol
59 drome (MetS) are differently associated with colorectal adenocarcinoma (CA) by anatomical location is
60                                          The colorectal adenocarcinoma Caco-2 cell line forms polariz
61 icity of so-obtained BRJ to human epithelial colorectal adenocarcinoma (Caco-2) and human non-maligna
62 ssay, pecan phenolics were taken up by human colorectal adenocarcinoma (Caco-2) cells and bestowed CA
63 n vitro cell culture model (human epithelial colorectal adenocarcinoma, Caco-2).
64 ctal adenoma cases and 544 controls, and 535 colorectal adenocarcinoma cases and 656 controls) among
65 f follow-up (through February 20, 2004), 220 colorectal adenocarcinoma cases were documented.
66  levels, and patient survival times from 456 colorectal adenocarcinoma cases, and a separate set of 5
67 essed by studying the survival of four human colorectal adenocarcinoma cell cultures after 1 hour of
68 reening phage libraries derived from a human colorectal adenocarcinoma cell line and from noncancerou
69  gallate (ECG, IC50 = 76 microM) against the colorectal adenocarcinoma cell line HCT116.
70             Our studies involving the murine colorectal adenocarcinoma cell line MC38 confirm that IF
71 rt, placenta, skeletal muscle, kidney, and a colorectal adenocarcinoma cell line.
72 32H mutation on the metabolism of the HCT116 colorectal adenocarcinoma cell line.
73                    Tumors derived from human colorectal adenocarcinoma cell lines HT29 and HCT-8 rang
74                                     In human colorectal adenocarcinoma cell lines, we found two major
75 itions, and cytotoxic activity against human colorectal adenocarcinoma cells (Caco-2 and HT-29 cell l
76 GF and TGFalpha were investigated with human colorectal adenocarcinoma cells (Caco-2).
77 mbled to deliver CO to a suspension of human colorectal adenocarcinoma cells (HT-29) under the contro
78 ributor to heightened sensitization of human colorectal adenocarcinoma cells (SW620/Ad300) to paclita
79 cancer activity of 4-EPS using HCT-116 human colorectal adenocarcinoma cells and CCD 841 normal colon
80 lysis was, here, compared using Caco-2 human colorectal adenocarcinoma cells and HaCaT human keratino
81 C3 is expressed in human intestine and LS180 colorectal adenocarcinoma cells and is upregulated by ag
82                   In contrast, PD-L1 on MC38 colorectal adenocarcinoma cells is sufficient to suppres
83 n of cell cytotoxicity was observed in human colorectal adenocarcinoma cells line after FLC-dc-APGD-t
84 ke, and inhibited the proliferation of DLD-1 colorectal adenocarcinoma cells to a greater extent than
85 of lung carcinoma and xenotransplanted human colorectal adenocarcinoma cells was observed after admin
86                  Transfection of LS180 human colorectal adenocarcinoma cells with an miR-18a-5p mimic
87 these mutants in HAI-2-knockout Caco-2 human colorectal adenocarcinoma cells.
88 release compounds in Caco-2 human epithelial colorectal adenocarcinoma cells.
89                               In the case of colorectal adenocarcinoma (CRA), grading is partly deter
90 ie transformation of colonic epithelium into colorectal adenocarcinoma (CRC) are well described.
91 ase (IBD) and the incidence and mortality of colorectal adenocarcinoma (CRC) has not been evaluated r
92  patients with previously treated metastatic colorectal adenocarcinoma, demonstrating higher response
93 cids (LNA30bcd) in both human IECs and human colorectal adenocarcinoma-derived Caco-2 cells resulted
94 Sinai Hospital between 1960 and 1989 in whom colorectal adenocarcinoma developed.
95 lorectal cancer) was tumor registry-verified colorectal adenocarcinoma diagnosed at least 6 months af
96 26 813 patients with a diagnosis of incident colorectal adenocarcinoma diagnosed between January 1, 1
97  county-level proportion of patients who had colorectal adenocarcinoma diagnosed between January 1, 2
98                                        Human colorectal adenocarcinomas exhibited reductions in Rab25
99 Routine molecular screening of patients with colorectal adenocarcinoma for the Lynch syndrome identif
100 8-99 years diagnosed with primary, invasive, colorectal adenocarcinoma from Jan 1, 2010, to Dec 31, 2
101         Finally, bioinformatic analysis of a colorectal adenocarcinoma from The Cancer Genome Atlas d
102 -malignant colon tumor sample and late-stage colorectal adenocarcinoma from the same individual.
103 reased among all age groups, whereas that of colorectal adenocarcinoma has increased among younger ag
104  potent cytotoxicity (GI(50) < 1 nM vs human colorectal adenocarcinoma (HCT-116) cells) but did not e
105 17 with a colorectal adenoma (S/RG/C2) and a colorectal adenocarcinoma (HCT116) derived cell line.
106                                           In colorectal adenocarcinomas, high expression levels of ge
107 MB was associated with decreased survival in colorectal adenocarcinoma: HR = 1.32 [1.00-1.74], p < 0.
108                               Tapcin reduced colorectal adenocarcinoma HT-29 cell proliferation and t
109      As the model system, spheroids of human colorectal adenocarcinoma HT-29 cells are generated by c
110  lines [human breast adenocarcinoma (MCF-7), colorectal adenocarcinoma (HT-29), non-small cell lung c
111 n this study three human cell lines, Caco-2 (colorectal adenocarcinoma), HT29-MTX-E12 (colorectal ade
112 ologic condition of the tumor was metastatic colorectal adenocarcinoma in 18 lesions, primary hepatoc
113 s were found in one-half of the patients and colorectal adenocarcinomas in 14%.
114  cases, and a separate set of 594 samples of colorectal adenocarcinomas, in The Cancer Genome Atlas.
115                        This study found that colorectal adenocarcinoma incidence rates in people aged
116 Among White individuals aged 40 to 49 years, colorectal adenocarcinoma incidence rates increased from
117 Among Black individuals aged 40 to 49 years, colorectal adenocarcinoma incidence rates were not signi
118 follow-up period, we identified 712 interval colorectal adenocarcinomas, including 255 advanced-stage
119 ave analysed specimens from 50 patients with colorectal adenocarcinomas, including cases in which an
120                                              Colorectal adenocarcinoma is a leading cause of death wo
121 ss The Cancer Genome Atlas and identify that colorectal adenocarcinoma is an outlier relative to all
122 ylation defects have also been observed in a colorectal adenocarcinoma line that harbors one of these
123 lded long-lasting growth arrest of the human colorectal adenocarcinoma LS174T grown as s.c. xenograft
124          Athymic mice xenografted with human colorectal adenocarcinoma LS174T were treated intravenou
125                           Aneuploid mucinous colorectal adenocarcinoma (MAC) is an aggressive subtype
126 obar distribution of hepatic metastases from colorectal adenocarcinoma may not be associated with the
127 tomic differences between primary tumors and colorectal adenocarcinoma metastases and delineates path
128                          The two subtypes of colorectal adenocarcinoma metastases that were identifie
129                    These findings identify a colorectal adenocarcinoma metastasis-specific gene-expre
130               Of these, the histologies were colorectal adenocarcinoma (N = 1) and breast adenocarcin
131 ascl2 as a gene significantly upregulated in colorectal adenocarcinomas (n=36 cancers, n=16 normals;
132 tigate the impact of the primary location of colorectal adenocarcinoma on the lobar distribution of i
133 ts the model's generalizability in detecting colorectal adenocarcinoma on whole slide images across d
134 es with at least two siblings diagnosed with colorectal adenocarcinoma or high-grade dysplasia were e
135 years or older with a confirmed diagnosis of colorectal adenocarcinoma or mucinous adenocarcinoma.
136                                              Colorectal adenocarcinoma patients as control group with
137 ated in metastases that could be targeted in colorectal adenocarcinoma patients with metastatic disea
138                                              Colorectal adenocarcinoma patients with pre-operative ir
139 n-small cell lung cancer patients and 25,064 colorectal adenocarcinoma patients, TET2-mutant CH is as
140 ately 20% of colorectal cancer patients with colorectal adenocarcinomas present with metastases at th
141                   To study the regulation of colorectal adenocarcinoma progression by O-GlcNAc, we ha
142                         Here, we report that colorectal adenocarcinoma represents one important excep
143                      Human tumors, including colorectal adenocarcinoma, secrete angiogenic factors, i
144 g multivariate statistical tools, nine human colorectal adenocarcinoma sections are analyzed with thr
145 ll lines, with the highest levels in Caco-2 (colorectal adenocarcinoma), SKOV3 (ovarian), and HepG2 (
146 DNA methyltransferase genes in 25 individual colorectal adenocarcinoma specimens and matched normal m
147 d A643T in the B3 domain of human CEACAM5 in colorectal adenocarcinomas; structural studies indicated
148 r growth in mice bearing xenografts of human colorectal adenocarcinoma, suggesting a novel way to tar
149 patients with metastatic breast, ovarian, or colorectal adenocarcinomas that overexpressed HER-2/neu
150 potentially resectable hepatic metastases of colorectal adenocarcinoma, the use of PET-CT compared wi
151         The 30 patients in the series had 33 colorectal adenocarcinomas; three patients (10%) present
152                                     We found colorectal adenocarcinomas to express mutant forms of CE
153 pound 6 potently inhibits the growth of LoVo colorectal adenocarcinoma tumor cells in vitro and has h
154 ATR mediated phosphorylation of Chk1 in HT29 colorectal adenocarcinoma tumor cells with an IC50 of 50
155 xpression) and Caco2 (low NTSR-1 expression) colorectal adenocarcinoma tumor models.
156 we have found that RREB1 is overexpressed in colorectal adenocarcinoma tumors and cell lines, and the
157 e bearing syngeneic B16F10 melanoma and MC38 colorectal adenocarcinoma tumors.
158 e patients with a diagnosis of nonmetastatic colorectal adenocarcinoma undergoing surgical resection
159                                  The APC for colorectal adenocarcinoma was -3.31 (95% CI, -3.54 to -3
160 , prospective, cohort study of patients with colorectal adenocarcinoma was performed from August 1, 1
161                                           In colorectal adenocarcinomas, we also found an inverse cor
162 alysis of APC, K-ras, and p53 to evaluate 50 colorectal adenocarcinomas, we have shown that mutation
163 in is associated with aggressive behavior in colorectal adenocarcinomas, we used immunohistochemistry
164 h histologically proven pelvic recurrence of colorectal adenocarcinoma were enrolled on a multimodali
165              Individuals with pancreatic and colorectal adenocarcinoma were included.
166            Mouse xenografts of human primary colorectal adenocarcinomas were found to retain viable F
167 umor microenvironment (B16 melanoma and MC38 colorectal adenocarcinoma), where they contributed to th
168 id bilayer membrane from Caco-2 cells (human colorectal adenocarcinoma), which we examined for use as
169 resence of loss-of-function APC mutations in colorectal adenocarcinoma, which are strongly associated
170 oma (SRCC) is a rare histological subtype of colorectal adenocarcinoma, which has been associated wit
171 cally or cytologically documented metastatic colorectal adenocarcinoma who had received all current s
172           Eighty-six patients diagnosed with colorectal adenocarcinoma, who had hepatic metastases on
173 led a poorly differentiated signet ring cell colorectal adenocarcinoma with metastases in seven peric
174 luded one partial response in a patient with colorectal adenocarcinoma with neuroendocrine features,
175 erate antitumor activity against HT-29 human colorectal adenocarcinoma xenograft in mice without over
176 ng the relative change in elastic modulus in colorectal adenocarcinoma xenograft models in vivo and i

 
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