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1 ion (synchronous) or after a period of time (metachronous).
2 ording to disease timing (synchronous versus metachronous).
3       Lesion development was synchronous and metachronous.
4              Five patients (15.2%) developed metachronous adenocarcinoma at a median of 6 years (rang
5 reduction in the odds of any and nonadvanced metachronous adenoma after adjustment for baseline adeno
6 nor was any single SNP in VDR related to any metachronous adenoma after correction for multiple compa
7                                     Rates of metachronous adenoma and advanced adenoma at follow-up w
8 elation coefficients <0.2) between unrelated metachronous adenoma-cancer pairs.
9 was found for any single SNP and the odds of metachronous adenoma.
10 ively) having an 89% lower odds for advanced metachronous adenomas (OR, 0.11; 95% CI, 0.01-0.80) when
11 elated to most histologic characteristics of metachronous adenomas among men but not among women.
12 uence in the APC gene and individual risk of metachronous adenomatous polyps.
13 and 100 histologically proven synchronous or metachronous adenomatous polyps.
14                                    Risk of a metachronous advanced adenoma was higher among patients
15 rom the proportion of low-risk patients with metachronous advanced neoplasia (14.6%) (relative risk f
16 d histologic features who were found to have metachronous advanced neoplasia (17.6%) did not differ s
17 plasia was not associated independently with metachronous advanced neoplasia after adjustment for oth
18                    Patients at high risk for metachronous advanced neoplasia were defined as patients
19 ted significantly with an increased risk for metachronous advanced neoplasia, as were the number and
20 n a patient being considered at low risk for metachronous advanced neoplasia, resulting in an inappro
21 anced histologic features and their risk for metachronous advanced neoplasia.
22 features; and the risk of these patients for metachronous advanced neoplasia.
23 histologic features do not increase risk for metachronous advanced neoplasia.
24 s, have an increased risk of synchronous and metachronous advanced neoplasia.
25                     We evaluated 13 cases of metachronous and 23 cases of synchronous primary and met
26 noma, 1 with sebaceous carcinoma, and 1 with metachronous bilateral lymphomas were treated.
27 edures and may have utility in patients with metachronous bladder cancer and in low-resource settings
28                                  The risk of metachronous breast cancer is low in patients with known
29 e patients who presented with synchronous or metachronous breast plus colorectal cancer.
30 ed 126 cases of SCR (14.8%) and 118 cases of metachronous cancer (13.8%).
31                          One patient died of metachronous cancer after STC.
32 olorectal cancer risk approaching 80%, and a metachronous cancer rate of approximately 25%.
33 , given the mentioned increased frequency of metachronous cancer.
34 uent high-risk adenomas and 3 (8%) developed metachronous cancer.
35 ciated with a genetic defect, synchronous or metachronous cancers in the same individual, growth abno
36                                Stages of the metachronous cancers were I-16, II-18, III-12, and IV-2.
37 ave increased risk of developing synchronous/metachronous cancers, including nonhematologic and hemat
38 ncludes a history of multiple synchronous or metachronous cancers.
39 5)] but saw no absolute reduction in risk of metachronous CBC (MCBC).
40                                              Metachronous CBC risk (N = 1,027) according to the distr
41 d 341 patients who underwent hepatectomy for metachronous CLM (disease-free interval >/=12 months, 19
42 er patients treated with liver resection for metachronous CLM after adjuvant FOLFOX for CRC have wors
43  and inferior outcomes after hepatectomy for metachronous CLM.
44                        The array contained a metachronous cohort of samples from individuals who eith
45 nomas in situ, pseudomelanosis coli, and two metachronous colon cancers.
46                                              Metachronous colorectal adenoma and carcinoma developmen
47 ) in the APC gene and the odds of developing metachronous colorectal adenomas as a surrogate measure
48 213 participants in 7 prospective studies of metachronous colorectal adenomas were pooled to assess w
49  support for the association between BMI and metachronous colorectal adenomas, particularly among men
50                                  The risk of metachronous colorectal cancer (CRC) among patients with
51 al cell carcinoma, a duodenal carcinoma, two metachronous colorectal carcinomas, and multi-regional s
52                         We hypothesized that metachronous colorectal liver metastases (CLM) have diff
53 202 small (0.8-4.0 cm; mean: 2.2 cm +/- 1.1) metachronous colorectal liver metastases underwent ultra
54 chieved local control in a large majority of metachronous colorectal liver metastases.
55 icate that allelic variation in RXRA affects metachronous colorectal neoplasia, perhaps of particular
56 ar signature was observed in the primary and metachronous colorectal tumors from all 3 patients.
57 mpared molecular profiles of the primary and metachronous colorectal tumors using next-generation seq
58 tions in RXRA and VDR and odds of recurrent (metachronous) colorectal neoplasia in a pooled populatio
59 nt anti-CD4 therapy; and (2) simultaneous or metachronous combined liver-heart and kidney-heart trans
60 hemotherapy (CBCT) reduces the occurrence of metachronous contralateral (second) germ cell testicular
61        HL survivors had an increased risk of metachronous contralateral breast cancer (adjusted hazar
62                             The incidence of metachronous contralateral RCC is stable on long-term fo
63 ease, either at diagnosis (nine of 53) or as metachronous contralateral recurrence (two of 53).
64 etermine the observed and expected number of metachronous contralateral renal tumors developing after
65                                          The metachronous contralateral tonsil second primary tumor r
66 mary outcome measure was the synchronous and metachronous contralateral tonsil second primary tumor r
67  in tonsillar SCCa is safe with markedly low metachronous contralateral tonsillar second primary tumo
68 was 89.2%, and the 2-year cumulative risk of metachronous contralateral WT was 3.1%.
69         The 2-year disease-free (relapse and metachronous contralateral WT) survival rate was 86.5%.
70 2-year disease-free survival rate (excluding metachronous contralateral WT) was 89.2%, and the 2-year
71 isk of relapse, including the development of metachronous contralateral WT, of 13.5% 2 years after di
72                     Three patients developed metachronous, contralateral WT 1.1, 1.4, and 2.3 years a
73 eviewed pathology reports to identify likely metachronous CRC (histologically proven adenocarcinoma l
74 ubclassified into synchronous CRC (SCRC) and metachronous CRC (MCRC).
75 50SerfsTer23), a 39-year old individual with metachronous CRC (p.Leu61GlufsTer11 mutation), and a 41-
76  meta-analysis to compare incidence rates of metachronous CRC and CRC-related mortality after a basel
77              The primary outcome was odds of metachronous CRC and CRC-related mortality per 10,000 pe
78 d meta-analysis demonstrate that the risk of metachronous CRC and mortality is significantly higher f
79                                 The rates of metachronous CRC and of rectal cancer were evaluated, to
80 was suspected as the most likely etiology of metachronous CRC in 5 patients.
81 s of hepatic metastasectomy in patients with metachronous CRC liver metastases.
82 -effective option for selected patients with metachronous CRC metastases limited to the liver.
83           The risk of death in patients with metachronous CRC was 6-fold increased.
84 l survival between patients with and without metachronous CRC were evaluated using a time-dependent C
85 clearing and for postoperative prevention of metachronous CRC, specific considerations for the detect
86 5 control cases with a different etiology of metachronous CRC, the molecular signature of the primary
87 mary and secondary tumors from patients with metachronous CRC, we found that primary tumor cells migh
88  cells in damaged mucosa) increases risk for metachronous CRC.
89 ess on this potentially preventable cause of metachronous CRC.
90               Seventeen patients (26.2%) had metachronous CRC.
91 ia carry a high risk of rectal cancer and of metachronous CRC.
92 s associated with a significant reduction in metachronous CRC.
93 orectal cancer (CRC), 3% have recurrence of (metachronous) CRC.
94                              Synchronous and metachronous CRCs are extremely common.
95                     The risk of developing a metachronous CTGCT was evaluated in a nationwide cohort
96 cts at 5 years for patients with low-volume, metachronous disease (-1%, 95% CI -15 to 12, for progres
97  differences were observed between groups in metachronous disease rate (MRI group: 21 of 470 patients
98 ine level, and the risk for hemodialysis and metachronous disease were calculated.
99 renal function, and to determine the risk of metachronous disease.
100 5% will eventually develop potentially fatal metachronous distant metastases.
101             The results were correlated with metachronous distant metastasis risk (n = 22 patients).
102 ICD insertion is indicated in CABG patients, metachronous endocardial implantation should be consider
103                        Five H/DC tumors were metachronous, following FL by 2 months to 12 years; tumo
104 hronous group were younger than those in the metachronous group (median age 54 v 68 years).
105 patent processus vaginalis and contralateral metachronous hernia development in children justify the
106 rgoing partial colectomy have a high rate of metachronous high-risk adenomas and carcinomas.
107 ferent prognostic subgroups (synchronous and metachronous high-volume or low-volume disease) and in t
108 not present at the initial diagnosis, termed metachronous hormonal syndromes (MHSs).
109                                              Metachronous hormonal syndromes developed after a median
110                                              Metachronous hormonal syndromes were identified more oft
111  = 0.47, 95% CI 0.30-0.72; P < 0.01) but not metachronous (HR = 1.37, 95% CI 0.50-3.92; P = 0.56) dis
112 er OS for patients with synchronous mCRC (vs metachronous: HR, 1.90 [95% CI, 1.24-2.89]; P = .003).
113 onoscopy significantly increased the risk of metachronous HRA compared to the reference group (no ind
114 eased risk of metachronous large SPs but not metachronous HRA.
115  colonoscopy significantly increased risk of metachronous HRA.
116  71 (relative increase = 70%), contralateral metachronous IHR decreased from 29 to 11 (RR = 62%), and
117  adenocarcinoma are rare conditions that are metachronous in most of cases and may represent the firs
118             The egg cytoplasm, therefore, is metachronous in terms of cell-cycle progression; multipl
119  cancer was 77% (several deaths secondary to metachronous invasive cancer), compared with 43% in thos
120 eas 5 (15%) developed clinically significant metachronous IPMNs.
121 dex STSA with no index HRA increased risk of metachronous large SPs but not metachronous HRA.
122 ignificantly associated with the odds of any metachronous lesion among men (odds ratio = 1.36, 95% co
123 try to evaluate risk of clinically important metachronous lesions associated with SPs detected during
124                               For those with metachronous lesions liver lesions, the median time inte
125                                              Metachronous lesions or recurrence of cancer developed d
126 rge SPs (>1 cm) on surveillance colonoscopy (metachronous lesions).
127  history, colorectal subsite, or features of metachronous lesions.
128  reduction in odds was observed for advanced metachronous lesions.
129 py should be performed in 1 year to look for metachronous lesions.
130 L) develop metastatic disease, most often as metachronous lesions.
131           The 5-year cumulative incidence of metachronous liver metastases decreased from 18.6% (95%
132  epidemiological features of synchronous and metachronous liver metastases from colorectal cancer may
133 gnosis between patients with synchronous and metachronous liver metastases is controversial.
134 al features, and outcomes of synchronous and metachronous liver metastases is lacking.
135 val improved substantially for patients with metachronous liver metastases, whereas improvement was m
136 ld decrease in the probability of developing metachronous liver metastases.
137 signed multiple prediction models for 5-year metachronous liver metastasis (5YLM) using combinations
138 characteristics that could be predictive for metachronous liver metastasis.
139 patients with low-volume disease, those with metachronous low-volume disease have a more hormone-depe
140 ence of meaningful benefit for patients with metachronous, low-volume disease who should therefore be
141 tic literature review identified 79 cases of metachronous lung metastasis with a survival of 120.0 +/
142       We identified 73 patients including 28 metachronous lung oligometastasis and 45 synchronous liv
143 creatic cancer patients with synchronous and metachronous lung only metastasis might confer a surviva
144 an gastric mucosa in either a synchronous or metachronous manner.
145 er odds of receiving ICIs than patients with metachronous mCRC (OR, 0.57 [95% CI, 0.45-0.73]; P < .00
146 riptomic differences between synchronous and metachronous mCSPC and identify any differential respons
147 ynchronous (LS-group)], and (3) resection of metachronous metastases >14 months after resection of th
148 nt reduction in the expression of p27 in the metachronous metastases (mean positive cells: 14.5%) whe
149 ed or metastatic disease with synchronous or metachronous metastases and performed a comprehensive mo
150 ma, we observed that cell lines derived from metachronous metastases arising over a decade retained a
151 ors from patients with either synchronous or metachronous metastases than those who were disease-free
152 djusted ratio of death after synchronous and metachronous metastases was divided by 2.5 for patients
153 paration of outcomes between synchronous and metachronous metastases were excluded.
154 ic disease (EHD), larger CRLM, more frequent metachronous metastases, and lower pathologic response a
155 r synchronous liver metastases and 49.9% for metachronous metastases, and net survival at 5 years was
156 ients had synchronous metastases and 58% had metachronous metastases.
157 ere from patients with either synchronous or metachronous metastases.
158 r synchronous liver metastases and 13.2% for metachronous metastases.
159 on-metastatic-appearing PPGLs that developed metachronous metastases.
160      This effect was absent in resection for metachronous metastases.
161  with synchronous metastasis than those with metachronous metastasis (12 months v 31 months, generali
162 apse (p = 0.02), and increased likelihood of metachronous metastasis (p = 0.001), including after sta
163 nd metastasis-initiating cells, could reduce metachronous metastasis and enhance the response to stan
164                               Development of metachronous metastasis is assumed to be governed largel
165 er median overall survival than those with a metachronous metastasis.
166 ld be considered for synchronous cancers and metachronous MPCs of the LS tumor spectrum, particularly
167 characterized by early-onset synchronous and metachronous multiorgan tumors.
168 actor receptor (EGFR) somatic aberrations in metachronous multiple lung cancers to differentiate mult
169                                 Ninety-seven metachronous multiple lung cancers were identified to in
170 on rate of tumor clonality (77.3%; 75/97) in metachronous multiple lung cancers.
171 nts need to be aware of substantial risk for metachronous neoplasia after proctectomy.
172 rt an approximately 30% reduction in odds of metachronous neoplasia arising in the proximal colon amo
173 sess whether the association between BMI and metachronous neoplasia varied by these factors.
174 tion between RXRA SNP rs7861779 and proximal metachronous neoplasia was of borderline statistical sig
175 RA and any (P = 0.04) or proximal (P = 0.03) metachronous neoplasia.
176  cancer are at risk for recurrent cancer and metachronous neoplasms in the colon.
177 ity state of TAC (relative to SEG), rates of metachronous occurrence, and stage of cancer at the time
178 e, we differentiated between synchronous and metachronous oligometastatic disease.
179 represents the first randomised trial in the metachronous oligometastatic hormone-sensitive prostate
180 inical progression-free survival in men with metachronous oligorecurrent hormone-sensitive prostate c
181 ynchronous metastases and >=58% for solitary metachronous ones (if <=30 mm, >=54% and >=67%, respecti
182 y synchronous metastases; >=36% for solitary metachronous ones; >=21% for 2 to 3 metastases; >=15% fo
183 patients with NSCLC with those identified in metachronous or synchronous metastases.
184 ntify distinct mechanisms for development of metachronous or synchronous neoplasms in patients with I
185                For 11 patients who developed metachronous OS 24 months or more from initial diagnosis
186 iagnosis of primary OS to the development of metachronous OS was 1.4 years (range, 0.2 to 11.3 years)
187  small subset of patients who developed late metachronous OS, combined-modality therapy with surgery
188             Only 2 patients (0.5%) developed metachronous PDAC.
189 syndrome was referred to our institution for metachronous peritoneal recurrence of ascending colon ad
190 , a solitary site of first metastasis, and a metachronous presentation with recurrence.
191 mor in the contralateral tonsil, including 2 metachronous primary tumors in the unilateral group (1.8
192                  Inclusion criteria required metachronous pulmonary or synchronous liver metastasecto
193                                      Risk of metachronous RCC was 6%.
194 ients undergoing total colectomy developed a metachronous rectal cancer (18.2%).
195  (range 3-146) months, 41 patients developed metachronous recurrence.
196 ellent long-term outcomes but a high risk of metachronous recurrence.
197 ucosa could offer the risk stratification of metachronous recurrence.
198 with synchronous metastasis (PRIM + MET), or metachronous recurrence/metastases (MET), and also imati
199 entified in synchronous nodal metastases and metachronous recurrent tumors, respectively, were transm
200 ar to their paired index primary tumors than metachronous recurrent tumors.
201 s lymph node metastases and 10 patients with metachronous recurrent tumors.
202 tic disease and 116 (6%) were diagnosed with metachronous relapsing disease.
203 on reports of a high incidence of apparently metachronous second cancers in the first 2 years after r
204 We investigated the incidence and outcome of metachronous skeletal OS after initial treatment of the
205 mary OS may be applied to patients with late metachronous skeletal OS.
206       The prognosis for patients who develop metachronous skeletal osteosarcoma (OS) has been conside
207  significantly increased the risk of a large metachronous SP.
208 imary cancer diagnosis), and subsequent (ie, metachronous) stage-specific CBC occurrences in women wh
209 s results in heterogeneous loss of Nanog and metachronous state transition.
210 synchronous status and 3.7 for patients with metachronous status.
211 All the primary and metastatic tumors in the metachronous subgroup showed high levels of p27 mRNA exp
212                                       In the metachronous subgroup, 54% of the primary tumors were lo
213 r bed (n = 4), and abdomen (n = 2), with one metachronous tumor in the contralateral kidney (n = 1) a
214 ypectomy, occurred at the location where the metachronous tumor was subsequently detected, after endo
215 , the molecular signature of the primary and metachronous tumor were completely different.
216 erations at GC-rich regions of the genome in metachronous tumors and their derived cell lines from tw
217 umors were present in 33 patients (22%), and metachronous tumors developed in an additional 14 patien
218 ranscriptome, and deep-focused sequencing of metachronous tumors from 29 patients initially diagnosed
219                                 Because most metachronous tumors of the same histologic type have dif
220 tic analysis revealed a common origin of the metachronous tumors, with a higher proportion of clonal
221 ancer or adenoma because of the high rate of metachronous tumors.
222 y of multifocal IPMNs (86% synchronous, 100% metachronous) were composed of branch duct lesions, and

 
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