Numerical abnormalities of chromosomes 17 and 18 in sporadic colorectal cancer: Incidence and correlation with clinical and biological findings and the prognosis of the disease
Background In recent years important information has accumulated on the genetic alterations present in colorectal tumors. However, thus far few studies have analyzed the impact of numerical abnormalities of chromosomes 17 and 18, which carry the p53 and DCC plus SHAD4/DPC4 genes involved in colorect...
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Published in | Cytometry. Part B, Clinical cytometry Vol. 51B; no. 1; pp. 14 - 20 |
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Main Authors | , , , , , , , |
Format | Journal Article |
Language | English |
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New York
Wiley Subscription Services, Inc., A Wiley Company
01.01.2003
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Abstract | Background
In recent years important information has accumulated on the genetic alterations present in colorectal tumors. However, thus far few studies have analyzed the impact of numerical abnormalities of chromosomes 17 and 18, which carry the p53 and DCC plus SHAD4/DPC4 genes involved in colorectal cancer, on the clinical and biological behaviors of the disease.
Methods
With the use of interphase fluorescence in situ hybridization (FISH), we analyzed the incidence of numerical abnormalities of chromosomes 17 and 18 in a series of malignant colorectal tumors and explored its potential association with clinicobiological behavior and the prognosis of the disease. For this purpose, 94 consecutive patients newly diagnosed with colorectal cancer were analyzed. In all cases, FISH analyses of the number of copies and nuclei of chromosomes 17 and 18 were performed in interphase nuclei with the use of double stainings. For all patients, information on age, sex, tumor size, Dukes' stage, tumor localization, DNA ploidy status, and the proportion of S‐phase tumor cells was recorded. Median follow‐up was 38 months.
Results
Numerical abnormalities of chromosomes 17 and 18 were present in most patients with colorectal cancer (57% and 52%, respectively). Gains of chromosome 17 and monosomy 18 were found in 51% and 29% of cases, respectively, and they were the most frequent individual abnormalities for each chromosome. The simultaneous analysis of the number of copies of both chromosomes in the same cell showed that, in most cases displaying numerical abnormalities for these chromosomes, two or more different tumor cell clones were present. From a clinical point of view, numerical abnormalities of chromosome 17, especially monosomy 17, were associated with a significantly higher incidence of rectal tumors (P = 0.001) and Dukes' stage D (P = 0.02) and a lower median of disease‐free survival among patients who underwent curative surgery (P = 0.05), as compared with diploid cases. In addition, cases with an altered number of copies of chromosome 17 showed a higher incidence of DNA aneuploidy (P = 0.0001) and a greater proportion of S‐phase cells (P = 0.001) by flow cytometry. In contrast, no clear association was found between the presence of numerical abnormalities of chromosome 18 and clinicobiological disease characteristics, except for a higher incidence of DNA aneuploidy by flow cytometry (P = 0.001) and a lower median of disease‐free survival (P = 0.06). Multivariate analysis showed that numerical abnormalities of chromosome 17, but not of chromosome 18, are an independent prognostic factor for predicting disease‐free survival in patients with colorectal cancer.
Conclusions
Numerical abnormalities of chromosomes 17 and 18 were relatively common findings in patients with colorectal cancer, with chromosome 17 being associated with a higher incidence of tumors localized to the rectum and a worse clinical outcome. Cytometry Part B (Clin. Cytometry) 51B:14–20, 2003. © 2002 Wiley‐Liss, Inc. |
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AbstractList | Background In recent years important information has accumulated on the genetic alterations present in colorectal tumors. However, thus far few studies have analyzed the impact of numerical abnormalities of chromosomes 17 and 18, which carry the p53 and DCC plus SHAD4/DPC4 genes involved in colorectal cancer, on the clinical and biological behaviors of the disease. Methods With the use of interphase fluorescence in situ hybridization (FISH), we analyzed the incidence of numerical abnormalities of chromosomes 17 and 18 in a series of malignant colorectal tumors and explored its potential association with clinicobiological behavior and the prognosis of the disease. For this purpose, 94 consecutive patients newly diagnosed with colorectal cancer were analyzed. In all cases, FISH analyses of the number of copies and nuclei of chromosomes 17 and 18 were performed in interphase nuclei with the use of double stainings. For all patients, information on age, sex, tumor size, Dukes' stage, tumor localization, DNA ploidy status, and the proportion of S-phase tumor cells was recorded. Median follow-up was 38 months. Results Numerical abnormalities of chromosomes 17 and 18 were present in most patients with colorectal cancer (57% and 52%, respectively). Gains of chromosome 17 and monosomy 18 were found in 51% and 29% of cases, respectively, and they were the most frequent individual abnormalities for each chromosome. The simultaneous analysis of the number of copies of both chromosomes in the same cell showed that, in most cases displaying numerical abnormalities for these chromosomes, two or more different tumor cell clones were present. From a clinical point of view, numerical abnormalities of chromosome 17, especially monosomy 17, were associated with a significantly higher incidence of rectal tumors (P = 0.001) and Dukes'stage D (P = 0.02) and a lower median of disease-free survival among patients who underwent curative surgery (P = 0.05), as compared with diploid cases. In addition, cases with an altered number of copies of chromosome 17 showed a higher incidence of DNA aneuploidy (P = 0.0001) and a greater proportion of S-phase cells (P = 0.001) by flow cytometry. In contrast, no clear association was found between the presence of numerical abnormalities of chromosome 18 and clinicobiological disease characteristics, except for a higher incidence of DNA aneuploidy by flow cytometry (P = 0.001) and a lower median of disease-free survival (P = 0.06). Multivariate analysis showed that numerical abnormalities of chromosome 17, but not of chromosome 18, are an independent prognostic factor for predicting disease-free survival in patients with colorectal cancer. Conclusions Numerical abnormalities of chromosomes 17 and 18 were relatively common findings in patients with colorectal cancer, with chromosome 17 being associated with a higher incidence of tumors localized to the rectum and a worse clinical outcome. In recent years important information has accumulated on the genetic alterations present in colorectal tumors. However, thus far few studies have analyzed the impact of numerical abnormalities of chromosomes 17 and 18, which carry the p53 and DCC plus SHAD4/DPC4 genes involved in colorectal cancer, on the clinical and biological behaviors of the disease. With the use of interphase fluorescence in situ hybridization (FISH), we analyzed the incidence of numerical abnormalities of chromosomes 17 and 18 in a series of malignant colorectal tumors and explored its potential association with clinicobiological behavior and the prognosis of the disease. For this purpose, 94 consecutive patients newly diagnosed with colorectal cancer were analyzed. In all cases, FISH analyses of the number of copies and nuclei of chromosomes 17 and 18 were performed in interphase nuclei with the use of double stainings. For all patients, information on age, sex, tumor size, Dukes' stage, tumor localization, DNA ploidy status, and the proportion of S-phase tumor cells was recorded. Median follow-up was 38 months. Numerical abnormalities of chromosomes 17 and 18 were present in most patients with colorectal cancer (57% and 52%, respectively). Gains of chromosome 17 and monosomy 18 were found in 51% and 29% of cases, respectively, and they were the most frequent individual abnormalities for each chromosome. The simultaneous analysis of the number of copies of both chromosomes in the same cell showed that, in most cases displaying numerical abnormalities for these chromosomes, two or more different tumor cell clones were present. From a clinical point of view, numerical abnormalities of chromosome 17, especially monosomy 17, were associated with a significantly higher incidence of rectal tumors (P = 0.001) and Dukes' stage D (P = 0.02) and a lower median of disease-free survival among patients who underwent curative surgery (P = 0.05), as compared with diploid cases. In addition, cases with an altered number of copies of chromosome 17 showed a higher incidence of DNA aneuploidy (P = 0.0001) and a greater proportion of S-phase cells (P = 0.001) by flow cytometry. In contrast, no clear association was found between the presence of numerical abnormalities of chromosome 18 and clinicobiological disease characteristics, except for a higher incidence of DNA aneuploidy by flow cytometry (P = 0.001) and a lower median of disease-free survival (P = 0.06). Multivariate analysis showed that numerical abnormalities of chromosome 17, but not of chromosome 18, are an independent prognostic factor for predicting disease-free survival in patients with colorectal cancer. Numerical abnormalities of chromosomes 17 and 18 were relatively common findings in patients with colorectal cancer, with chromosome 17 being associated with a higher incidence of tumors localized to the rectum and a worse clinical outcome. Cytometry Part B (Clin. Cytometry) 51B:14-20, 2003. BACKGROUNDIn recent years important information has accumulated on the genetic alterations present in colorectal tumors. However, thus far few studies have analyzed the impact of numerical abnormalities of chromosomes 17 and 18, which carry the p53 and DCC plus SHAD4/DPC4 genes involved in colorectal cancer, on the clinical and biological behaviors of the disease.METHODSWith the use of interphase fluorescence in situ hybridization (FISH), we analyzed the incidence of numerical abnormalities of chromosomes 17 and 18 in a series of malignant colorectal tumors and explored its potential association with clinicobiological behavior and the prognosis of the disease. For this purpose, 94 consecutive patients newly diagnosed with colorectal cancer were analyzed. In all cases, FISH analyses of the number of copies and nuclei of chromosomes 17 and 18 were performed in interphase nuclei with the use of double stainings. For all patients, information on age, sex, tumor size, Dukes' stage, tumor localization, DNA ploidy status, and the proportion of S-phase tumor cells was recorded. Median follow-up was 38 months.RESULTSNumerical abnormalities of chromosomes 17 and 18 were present in most patients with colorectal cancer (57% and 52%, respectively). Gains of chromosome 17 and monosomy 18 were found in 51% and 29% of cases, respectively, and they were the most frequent individual abnormalities for each chromosome. The simultaneous analysis of the number of copies of both chromosomes in the same cell showed that, in most cases displaying numerical abnormalities for these chromosomes, two or more different tumor cell clones were present. From a clinical point of view, numerical abnormalities of chromosome 17, especially monosomy 17, were associated with a significantly higher incidence of rectal tumors (P = 0.001) and Dukes' stage D (P = 0.02) and a lower median of disease-free survival among patients who underwent curative surgery (P = 0.05), as compared with diploid cases. In addition, cases with an altered number of copies of chromosome 17 showed a higher incidence of DNA aneuploidy (P = 0.0001) and a greater proportion of S-phase cells (P = 0.001) by flow cytometry. In contrast, no clear association was found between the presence of numerical abnormalities of chromosome 18 and clinicobiological disease characteristics, except for a higher incidence of DNA aneuploidy by flow cytometry (P = 0.001) and a lower median of disease-free survival (P = 0.06). Multivariate analysis showed that numerical abnormalities of chromosome 17, but not of chromosome 18, are an independent prognostic factor for predicting disease-free survival in patients with colorectal cancer.CONCLUSIONSNumerical abnormalities of chromosomes 17 and 18 were relatively common findings in patients with colorectal cancer, with chromosome 17 being associated with a higher incidence of tumors localized to the rectum and a worse clinical outcome. Cytometry Part B (Clin. Cytometry) 51B:14-20, 2003. Background In recent years important information has accumulated on the genetic alterations present in colorectal tumors. However, thus far few studies have analyzed the impact of numerical abnormalities of chromosomes 17 and 18, which carry the p53 and DCC plus SHAD4/DPC4 genes involved in colorectal cancer, on the clinical and biological behaviors of the disease. Methods With the use of interphase fluorescence in situ hybridization (FISH), we analyzed the incidence of numerical abnormalities of chromosomes 17 and 18 in a series of malignant colorectal tumors and explored its potential association with clinicobiological behavior and the prognosis of the disease. For this purpose, 94 consecutive patients newly diagnosed with colorectal cancer were analyzed. In all cases, FISH analyses of the number of copies and nuclei of chromosomes 17 and 18 were performed in interphase nuclei with the use of double stainings. For all patients, information on age, sex, tumor size, Dukes' stage, tumor localization, DNA ploidy status, and the proportion of S‐phase tumor cells was recorded. Median follow‐up was 38 months. Results Numerical abnormalities of chromosomes 17 and 18 were present in most patients with colorectal cancer (57% and 52%, respectively). Gains of chromosome 17 and monosomy 18 were found in 51% and 29% of cases, respectively, and they were the most frequent individual abnormalities for each chromosome. The simultaneous analysis of the number of copies of both chromosomes in the same cell showed that, in most cases displaying numerical abnormalities for these chromosomes, two or more different tumor cell clones were present. From a clinical point of view, numerical abnormalities of chromosome 17, especially monosomy 17, were associated with a significantly higher incidence of rectal tumors (P = 0.001) and Dukes' stage D (P = 0.02) and a lower median of disease‐free survival among patients who underwent curative surgery (P = 0.05), as compared with diploid cases. In addition, cases with an altered number of copies of chromosome 17 showed a higher incidence of DNA aneuploidy (P = 0.0001) and a greater proportion of S‐phase cells (P = 0.001) by flow cytometry. In contrast, no clear association was found between the presence of numerical abnormalities of chromosome 18 and clinicobiological disease characteristics, except for a higher incidence of DNA aneuploidy by flow cytometry (P = 0.001) and a lower median of disease‐free survival (P = 0.06). Multivariate analysis showed that numerical abnormalities of chromosome 17, but not of chromosome 18, are an independent prognostic factor for predicting disease‐free survival in patients with colorectal cancer. Conclusions Numerical abnormalities of chromosomes 17 and 18 were relatively common findings in patients with colorectal cancer, with chromosome 17 being associated with a higher incidence of tumors localized to the rectum and a worse clinical outcome. Cytometry Part B (Clin. Cytometry) 51B:14–20, 2003. © 2002 Wiley‐Liss, Inc. Abstract Background In recent years important information has accumulated on the genetic alterations present in colorectal tumors. However, thus far few studies have analyzed the impact of numerical abnormalities of chromosomes 17 and 18, which carry the p53 and DCC plus SHAD4/DPC4 genes involved in colorectal cancer, on the clinical and biological behaviors of the disease. Methods With the use of interphase fluorescence in situ hybridization (FISH), we analyzed the incidence of numerical abnormalities of chromosomes 17 and 18 in a series of malignant colorectal tumors and explored its potential association with clinicobiological behavior and the prognosis of the disease. For this purpose, 94 consecutive patients newly diagnosed with colorectal cancer were analyzed. In all cases, FISH analyses of the number of copies and nuclei of chromosomes 17 and 18 were performed in interphase nuclei with the use of double stainings. For all patients, information on age, sex, tumor size, Dukes' stage, tumor localization, DNA ploidy status, and the proportion of S‐phase tumor cells was recorded. Median follow‐up was 38 months. Results Numerical abnormalities of chromosomes 17 and 18 were present in most patients with colorectal cancer (57% and 52%, respectively). Gains of chromosome 17 and monosomy 18 were found in 51% and 29% of cases, respectively, and they were the most frequent individual abnormalities for each chromosome. The simultaneous analysis of the number of copies of both chromosomes in the same cell showed that, in most cases displaying numerical abnormalities for these chromosomes, two or more different tumor cell clones were present. From a clinical point of view, numerical abnormalities of chromosome 17, especially monosomy 17, were associated with a significantly higher incidence of rectal tumors ( P = 0.001) and Dukes' stage D ( P = 0.02) and a lower median of disease‐free survival among patients who underwent curative surgery ( P = 0.05), as compared with diploid cases. In addition, cases with an altered number of copies of chromosome 17 showed a higher incidence of DNA aneuploidy ( P = 0.0001) and a greater proportion of S‐phase cells ( P = 0.001) by flow cytometry. In contrast, no clear association was found between the presence of numerical abnormalities of chromosome 18 and clinicobiological disease characteristics, except for a higher incidence of DNA aneuploidy by flow cytometry ( P = 0.001) and a lower median of disease‐free survival ( P = 0.06). Multivariate analysis showed that numerical abnormalities of chromosome 17, but not of chromosome 18, are an independent prognostic factor for predicting disease‐free survival in patients with colorectal cancer. Conclusions Numerical abnormalities of chromosomes 17 and 18 were relatively common findings in patients with colorectal cancer, with chromosome 17 being associated with a higher incidence of tumors localized to the rectum and a worse clinical outcome. Cytometry Part B (Clin. Cytometry) 51B:14–20, 2003. © 2002 Wiley‐Liss, Inc. |
Author | Duran, Angel Tabernero, Maria Dolores Gomez‐Alonso, Alberto Garcia, Jacinto Orfao, Alberto Flores Corral, Teresa Najera, Maria Luisa Garcia Plaza, Asunción |
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BackLink | https://www.ncbi.nlm.nih.gov/pubmed/12500293$$D View this record in MEDLINE/PubMed |
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Cites_doi | 10.1016/S0140-6736(02)07448-2 10.1038/ng0796-343 10.1002/(SICI)1097-0320(19990401)35:4<369::AID-CYTO10>3.0.CO;2-6 10.1146/annurev.genom.3.022502.103043 10.1073/pnas.92.18.8493 10.1001/jama.1989.03420210047014 10.1126/science.2294591 10.1016/0168-9525(93)90209-Z 10.1136/gut.51.1.56 10.1007/BF02234328 10.1038/ng0394-217 10.1038/sj.bjc.6690144 10.1016/0165-4608(94)90006-X 10.1016/0046-8177(94)90223-2 10.1038/359235a0 10.1002/(SICI)1097-0320(19970901)29:1<1::AID-CYTO1>3.0.CO;2-J 10.1002/gcc.2870100307 10.1002/1097-0142(19900801)66:3<491::AID-CNCR2820660315>3.0.CO;2-Q 10.1002/ijc.2910530307 10.1002/(SICI)1096-9896(199607)179:3<243::AID-PATH588>3.0.CO;2-Q 10.1038/sj.onc.1202642 10.1038/sj.onc.1203747 10.1002/1097-0142(19920315)69:6 <1589::AID-CNCR2820691314>3.0.CO;2-A 10.1016/0168-9525(91)90103-W 10.1002/1097-0142(19951001)76:7<1132::AID-CNCR2820760706>3.0.CO;2-J 10.1016/0016-5085(92)90749-O 10.1056/NEJM199407283310401 10.1056/NEJM198809013190901 10.1002/1097-0142(19920915)70:4 <1732::AID-CNCR2820701614>3.0.CO;2-# 10.1007/BF02934087 10.3322/canjclin.49.1.8 10.1056/NEJM200001133420209 10.1053/gast.1996.v111.pm8898652 10.1093/jnci/93.7.555 10.1002/gcc.2870120204 10.1016/S0140-6736(89)90537-0 |
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References | 1993; 9 2001; 93 1994; 331 1996; 428 2002; 51 1999; 49 1991; 51 1995; 76 2002; 359 1994; 25 2001; 44 1997; 3 1995; 130 1996; 149 2000; 19 1999; 18 1997; 57 1992; 359 1996; 179 1994; 71 1994; 74 1990; 50 1995; 92 1990; 247 1995; 15 1995; 12 1992; 102 1995; 10 1997; 29 2002; 3 1989; 261 1996; 13 1991; 7 1992; 70 1989; ii 1990; 66 199; 73 1997; 32 1993; 53 1999; 35 1999; 79 1994; 14 1996; 111 1992; 69 2000; 342 1995; 145 1988; 319 1998; 4 1994; 10 1994; 6 e_1_2_5_25_2 e_1_2_5_46_2 Trask BJ (e_1_2_5_40_2) 1991; 7 e_1_2_5_21_2 Steiner MG (e_1_2_5_33_2) 1993; 53 e_1_2_5_29_2 Hopman AHN (e_1_2_5_35_2) 1991; 51 Baker SJ (e_1_2_5_49_2) 1990; 50 e_1_2_5_13_2 e_1_2_5_38_2 e_1_2_5_9_2 e_1_2_5_15_2 Lino H (e_1_2_5_23_2); 73 e_1_2_5_36_2 e_1_2_5_5_2 e_1_2_5_11_2 e_1_2_5_32_2 e_1_2_5_3_2 e_1_2_5_17_2 e_1_2_5_19_2 Tabernero MD (e_1_2_5_43_2) 1996; 149 Paredes‐Zaghul A (e_1_2_5_41_2) 1998; 4 e_1_2_5_30_2 e_1_2_5_51_2 Steward N (e_1_2_5_18_2) 1995; 10 e_1_2_5_26_2 Chen TR (e_1_2_5_42_2) 1994; 14 Giaretti W (e_1_2_5_27_2) 1994; 71 e_1_2_5_24_2 e_1_2_5_47_2 e_1_2_5_22_2 e_1_2_5_20_2 e_1_2_5_28_2 Frank CJ (e_1_2_5_7_2) 1997; 57 Gerdes M (e_1_2_5_45_2) 1995; 15 e_1_2_5_14_2 e_1_2_5_37_2 e_1_2_5_16_2 e_1_2_5_10_2 e_1_2_5_6_2 e_1_2_5_12_2 e_1_2_5_31_2 e_1_2_5_4_2 e_1_2_5_2_2 Criado B (e_1_2_5_39_2) 1995; 145 Tagawa Y (e_1_2_5_34_2) 1997; 3 Takahashi DM (e_1_2_5_44_2) 1995; 130 Kern SE (e_1_2_5_48_2) 1989; 261 e_1_2_5_52_2 e_1_2_5_50_2 Oci A (e_1_2_5_8_2) 1996; 428 |
References_xml | – volume: 3 start-page: 1587 year: 1997 end-page: 1592 article-title: Clinical and pathological significance of numerical aberrations of chromosomes 11 and 17 in colorectal neoplasm publication-title: Clin Cancer Res – volume: 57 start-page: 824 year: 1997 end-page: 827 article-title: Evidence that loss of chromosome 18q associated with tumor progression publication-title: Cancer Res – volume: 359 start-page: 235 year: 1992 end-page: 237 article-title: APC mutations occur early during colorectal tumorigenesis publication-title: Nature – volume: 73 start-page: 1324 year: 199 end-page: 1331 article-title: Molecular genetic for chemical management of colorectal carcinoma 17p, 18q and 22q loss of heterozygosity and decreased DCC expression are correlated with the metastatic potential publication-title: Cancer – volume: 70 start-page: 1732 year: 1992 end-page: 1739 article-title: Current status of adjuvant chemotherapy for colorectal cancer. Can molecular markers play a role in predicting prognosis? publication-title: Cancer – volume: 18 start-page: 3098 year: 1999 end-page: 3103 article-title: Higher frequency of SMAD4 gene mutation in human colorectal cancer with distant metastsis publication-title: Oncogene – volume: 29 start-page: 1 year: 1997 end-page: 27 article-title: Common patterns of genetic evolution in human solid tumors publication-title: Cytometry – volume: 13 start-page: 343 year: 1996 end-page: 346 article-title: Evaluation of candidate tumor suppressor genes on chromosome 18 in colorectal cancer publication-title: Nat Genet – volume: ii start-page: 353 year: 1989 end-page: 356 article-title: Multiple genetic alterations in distal and proximal colorectal cancer publication-title: Lancet – volume: 342 start-page: 124 year: 2000 end-page: 125 article-title: Genetic prognostic markers for colorectal cancer publication-title: N Engl J Med – volume: 319 start-page: 525 year: 1988 end-page: 532 article-title: Genetic alterations during colorectal tumor development publication-title: N Engl J Med – volume: 331 start-page: 213 year: 1994 end-page: 221 article-title: Allelic loss of chromosome 18q and prognosis in colorectal cancer publication-title: N Engl J Med – volume: 51 start-page: 644 year: 1991 end-page: 651 article-title: Numerical chromosome 1, 7, 9 and 11 aberrations in bladder cancer detected by in situ hybridization publication-title: Cancer Res – volume: 6 start-page: 217 year: 1994 end-page: 219 article-title: Genetic steps in colorectal cancer publication-title: Nat Genet – volume: 50 start-page: 7717 year: 1990 end-page: 7722 article-title: P53 gene mutations occur in combination with 17p allelic delections as late events in colorectal tumorigenesis publication-title: Cancer Res – volume: 93 start-page: 555 year: 2001 end-page: 557 article-title: Role of transforming growth factor‐beta signaling in cancer publication-title: J Natl Cancer Inst – volume: 69 start-page: 1589 year: 1992 end-page: 1591 article-title: Molecular genetic alterations as potential prognostic indicator in colorectal carcinoma publication-title: Cancer – volume: 79 start-page: 903 year: 1999 end-page: 908 article-title: Loss of heterozygosity at 18q21 is indicative of recurrence and therefore poor prognosis in a subset of colorectal cancers publication-title: Br J Cancer – volume: 10 start-page: 190 year: 1994 end-page: 196 article-title: Clonal karyotypic abnormalities in colorectal adenomas. Clues to the early genetic events in the adenoma‐carcinoma sequence publication-title: Genes Chromosomes Cancer – volume: 74 start-page: 104 year: 1994 end-page: 108 article-title: Cytogenetic study of 30 colorectal adenomas publication-title: Cancer Genet Cytogenet – volume: 53 start-page: 382 year: 1993 end-page: 387 article-title: Concordant p53 and DCC alterations and allelic losses on chromosomes 13q and 14q associated liver metastases of colorectal carcinoma publication-title: Int J Cancer – volume: 149 start-page: 153 year: 1996 end-page: 161 article-title: Incidence of chromosome numerical changes in multiple myeloma. Fluorescence in situ hybridization analysis using chromosome‐specific probes publication-title: Am J Pathol – volume: 111 start-page: 1387 year: 1996 end-page: 1389 article-title: Somatic alterations of the DPC4 gene in human colorectal cancers in vivo publication-title: Gastroenterology – volume: 12 start-page: 97 year: 1995 end-page: 109 article-title: Karyotypic characterization of colorectal adenocarcinoma publication-title: Genes Chromosomes Cancer – volume: 4 start-page: 879 year: 1998 end-page: 886 article-title: Analysis of colorectal cancer by comparative genomic hybridization: Evidence for induction of the metastatic phenotype by loss of tumor suppressor genes publication-title: Clin Cancer Res – volume: 76 start-page: 1132 year: 1995 end-page: 1138 article-title: Monosomy of chromosome 18 detected by fluorescence in situ hybridization in colorectal tumors publication-title: Cancer – volume: 428 start-page: 243 year: 1996 end-page: 251 article-title: Numerical chromosome alterations in colorectal carcinoma detected by fluorescence in situ hybridisation. Relationship to 17p and 18q allelic losses publication-title: Virchows Arch – volume: 179 start-page: 243 year: 1996 end-page: 247 article-title: In situ hybridization and flow cytometric analysis of colorectal tumors suggests two routes of tumorigenesis characterized by gain of chromosome 7 and loss of chromosomes 17 and 18 publication-title: J Pathol – volume: 15 start-page: 13 year: 1995 end-page: 24 article-title: Recurrent deletions involving chromosomes 1,5,17 and 18 in colorectal carcinomas: possible role in biological and clinical behavior of tumors publication-title: Anticancer Res – volume: 145 start-page: 136 year: 1995 end-page: 144 article-title: Detection of numerical alterations for chromosome 7 and 12 in benign thyroid lesion by in situ hybridization publication-title: Am J Pathol – volume: 32 start-page: 487 year: 1997 end-page: 491 article-title: Aneusomy of chromosome 18 is associated with the development of colorectal carcinoma publication-title: J Gastroenterol – volume: 130 start-page: 585 year: 1995 end-page: 589 article-title: Chromosome 17p allelic loss in colorectal carcinoma publication-title: Clinical significance. Arch Surg – volume: 9 start-page: 138 year: 1993 end-page: 141 article-title: The multistep nature of cancer publication-title: Trends Genet – volume: 3 start-page: 101 year: 2002 end-page: 128 article-title: Genetic and epigenetic alterations in colon cancer publication-title: Annu Rev Genomics Hum Genet – volume: 53 start-page: 681 year: 1993 end-page: 686 article-title: Chromosomes 8,12 and 17 copy number in Astler‐Coller stage C colon cancer in relation to proliferative activity and DNA ploidy publication-title: Cancer Res – volume: 51 start-page: 59 year: 2002 article-title: Frequent loss of SMAD4/DPC4 protein in colorectal cancers publication-title: Gut – volume: 19 start-page: 3978 year: 2000 end-page: 3987 article-title: Isolation and characterization of sixteen novel p53 response genes publication-title: Oncogene – volume: 71 start-page: 904 year: 1994 end-page: 910 article-title: A model of DNA aneuploidization and evolution in colorectal cancer publication-title: Lab Invest – volume: 44 start-page: 549 year: 2001 end-page: 557 article-title: Prognostic value of K‐ras mutations and allelic imbalance on chromosome 18q in patients with resected colorectal cancer publication-title: Dis Colon Rectum – volume: 35 start-page: 369 year: 1999 end-page: 375 article-title: Intratumor heterogeneity of chromosome 1,7,17 and 18 aneusomies obtained by FISH and association with flow cytometric DNA index in human colorectal adenocarcinomas publication-title: Cytometry – volume: 66 start-page: 491 year: 1990 end-page: 497 article-title: Targeted cytogenetic analysis of gastric tumor by in situ hybridization with a set of chromosome specific DNA probes publication-title: Cancer – volume: 14 start-page: 109 year: 1994 end-page: 112 article-title: Chromosome painting and quantitative karyotyping of colon adenocarcinoma cell lines DLD‐1 and HTC‐15 publication-title: Anticancer Res – volume: 7 start-page: 149 year: 1991 end-page: 154 article-title: Fluorescence in situ hybridization publication-title: Trends Genet – volume: 25 start-page: 586 year: 1994 end-page: 590 article-title: Fluorescence in situ hybridization; a new tool for the pathologist publication-title: Hum Pathol – volume: 261 start-page: 3099 year: 1989 end-page: 3103 article-title: Allelic loss in colorectal carcinoma publication-title: JAMA – volume: 247 start-page: 49 year: 1990 end-page: 56 article-title: Identification of chromosome 18q gene that is colorectal cancers publication-title: Science – volume: 102 start-page: 1136 year: 1992 end-page: 1141 article-title: Survival and acquired genetic alterations in colorectal cancer publication-title: Gastroenterology – volume: 49 start-page: 8 year: 1999 end-page: 31 article-title: Cancer statistics 1999 publication-title: CA Cancer J Clin – volume: 359 start-page: 219 year: 2002 end-page: 225 article-title: Counting alleles to predict recurrence of early‐stage colorectal cancers publication-title: Lancet – volume: 92 start-page: 8493 year: 1995 end-page: 8497 article-title: P53 controls both G2/M and G1 cell cycle checkpoints and mediates reversible growth arrest in human fibroblast publication-title: Proc Soc Natl Acad Sci USA – volume: 10 start-page: 109 year: 1995 end-page: 115 article-title: Evidence for a second cells cycle block at G2/M by p 53 publication-title: Oncogene – ident: e_1_2_5_29_2 doi: 10.1016/S0140-6736(02)07448-2 – ident: e_1_2_5_13_2 doi: 10.1038/ng0796-343 – ident: e_1_2_5_26_2 doi: 10.1002/(SICI)1097-0320(19990401)35:4<369::AID-CYTO10>3.0.CO;2-6 – ident: e_1_2_5_25_2 doi: 10.1146/annurev.genom.3.022502.103043 – ident: e_1_2_5_17_2 doi: 10.1073/pnas.92.18.8493 – volume: 261 start-page: 3099 year: 1989 ident: e_1_2_5_48_2 article-title: Allelic loss in colorectal carcinoma publication-title: JAMA doi: 10.1001/jama.1989.03420210047014 contributor: fullname: Kern SE – volume: 71 start-page: 904 year: 1994 ident: e_1_2_5_27_2 article-title: A model of DNA aneuploidization and evolution in colorectal cancer publication-title: Lab Invest contributor: fullname: Giaretti W – ident: e_1_2_5_9_2 doi: 10.1126/science.2294591 – ident: e_1_2_5_4_2 doi: 10.1016/0168-9525(93)90209-Z – volume: 4 start-page: 879 year: 1998 ident: e_1_2_5_41_2 article-title: Analysis of colorectal cancer by comparative genomic hybridization: Evidence for induction of the metastatic phenotype by loss of tumor suppressor genes publication-title: Clin Cancer Res contributor: fullname: Paredes‐Zaghul A – ident: e_1_2_5_14_2 doi: 10.1136/gut.51.1.56 – ident: e_1_2_5_50_2 doi: 10.1007/BF02234328 – ident: e_1_2_5_6_2 doi: 10.1038/ng0394-217 – ident: e_1_2_5_28_2 doi: 10.1038/sj.bjc.6690144 – ident: e_1_2_5_31_2 doi: 10.1016/0165-4608(94)90006-X – ident: e_1_2_5_37_2 doi: 10.1016/0046-8177(94)90223-2 – ident: e_1_2_5_3_2 doi: 10.1038/359235a0 – ident: e_1_2_5_19_2 doi: 10.1002/(SICI)1097-0320(19970901)29:1<1::AID-CYTO1>3.0.CO;2-J – ident: e_1_2_5_30_2 doi: 10.1002/gcc.2870100307 – ident: e_1_2_5_36_2 doi: 10.1002/1097-0142(19900801)66:3<491::AID-CNCR2820660315>3.0.CO;2-Q – ident: e_1_2_5_22_2 doi: 10.1002/ijc.2910530307 – ident: e_1_2_5_47_2 doi: 10.1002/(SICI)1096-9896(199607)179:3<243::AID-PATH588>3.0.CO;2-Q – ident: e_1_2_5_16_2 doi: 10.1038/sj.onc.1202642 – volume: 3 start-page: 1587 year: 1997 ident: e_1_2_5_34_2 article-title: Clinical and pathological significance of numerical aberrations of chromosomes 11 and 17 in colorectal neoplasm publication-title: Clin Cancer Res contributor: fullname: Tagawa Y – volume: 15 start-page: 13 year: 1995 ident: e_1_2_5_45_2 article-title: Recurrent deletions involving chromosomes 1,5,17 and 18 in colorectal carcinomas: possible role in biological and clinical behavior of tumors publication-title: Anticancer Res contributor: fullname: Gerdes M – ident: e_1_2_5_20_2 doi: 10.1038/sj.onc.1203747 – volume: 53 start-page: 681 year: 1993 ident: e_1_2_5_33_2 article-title: Chromosomes 8,12 and 17 copy number in Astler‐Coller stage C colon cancer in relation to proliferative activity and DNA ploidy publication-title: Cancer Res contributor: fullname: Steiner MG – ident: e_1_2_5_10_2 doi: 10.1002/1097-0142(19920315)69:6 <1589::AID-CNCR2820691314>3.0.CO;2-A – volume: 7 start-page: 149 year: 1991 ident: e_1_2_5_40_2 article-title: Fluorescence in situ hybridization publication-title: Trends Genet doi: 10.1016/0168-9525(91)90103-W contributor: fullname: Trask BJ – volume: 57 start-page: 824 year: 1997 ident: e_1_2_5_7_2 article-title: Evidence that loss of chromosome 18q associated with tumor progression publication-title: Cancer Res contributor: fullname: Frank CJ – volume: 130 start-page: 585 year: 1995 ident: e_1_2_5_44_2 article-title: Chromosome 17p allelic loss in colorectal carcinoma publication-title: Clinical significance. Arch Surg contributor: fullname: Takahashi DM – ident: e_1_2_5_38_2 doi: 10.1002/1097-0142(19951001)76:7<1132::AID-CNCR2820760706>3.0.CO;2-J – ident: e_1_2_5_46_2 doi: 10.1016/0016-5085(92)90749-O – ident: e_1_2_5_5_2 doi: 10.1056/NEJM199407283310401 – ident: e_1_2_5_11_2 doi: 10.1056/NEJM198809013190901 – volume: 73 start-page: 1324 ident: e_1_2_5_23_2 article-title: Molecular genetic for chemical management of colorectal carcinoma 17p, 18q and 22q loss of heterozygosity and decreased DCC expression are correlated with the metastatic potential publication-title: Cancer contributor: fullname: Lino H – ident: e_1_2_5_51_2 doi: 10.1002/1097-0142(19920915)70:4 <1732::AID-CNCR2820701614>3.0.CO;2-# – volume: 51 start-page: 644 year: 1991 ident: e_1_2_5_35_2 article-title: Numerical chromosome 1, 7, 9 and 11 aberrations in bladder cancer detected by in situ hybridization publication-title: Cancer Res contributor: fullname: Hopman AHN – volume: 428 start-page: 243 year: 1996 ident: e_1_2_5_8_2 article-title: Numerical chromosome alterations in colorectal carcinoma detected by fluorescence in situ hybridisation. Relationship to 17p and 18q allelic losses publication-title: Virchows Arch contributor: fullname: Oci A – volume: 145 start-page: 136 year: 1995 ident: e_1_2_5_39_2 article-title: Detection of numerical alterations for chromosome 7 and 12 in benign thyroid lesion by in situ hybridization publication-title: Am J Pathol contributor: fullname: Criado B – ident: e_1_2_5_12_2 doi: 10.1007/BF02934087 – ident: e_1_2_5_2_2 doi: 10.3322/canjclin.49.1.8 – ident: e_1_2_5_52_2 doi: 10.1056/NEJM200001133420209 – volume: 149 start-page: 153 year: 1996 ident: e_1_2_5_43_2 article-title: Incidence of chromosome numerical changes in multiple myeloma. Fluorescence in situ hybridization analysis using chromosome‐specific probes publication-title: Am J Pathol contributor: fullname: Tabernero MD – volume: 50 start-page: 7717 year: 1990 ident: e_1_2_5_49_2 article-title: P53 gene mutations occur in combination with 17p allelic delections as late events in colorectal tumorigenesis publication-title: Cancer Res contributor: fullname: Baker SJ – ident: e_1_2_5_15_2 doi: 10.1053/gast.1996.v111.pm8898652 – ident: e_1_2_5_24_2 doi: 10.1093/jnci/93.7.555 – ident: e_1_2_5_32_2 doi: 10.1002/gcc.2870120204 – volume: 14 start-page: 109 year: 1994 ident: e_1_2_5_42_2 article-title: Chromosome painting and quantitative karyotyping of colon adenocarcinoma cell lines DLD‐1 and HTC‐15 publication-title: Anticancer Res contributor: fullname: Chen TR – volume: 10 start-page: 109 year: 1995 ident: e_1_2_5_18_2 article-title: Evidence for a second cells cycle block at G2/M by p 53 publication-title: Oncogene contributor: fullname: Steward N – ident: e_1_2_5_21_2 doi: 10.1016/S0140-6736(89)90537-0 |
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In recent years important information has accumulated on the genetic alterations present in colorectal tumors. However, thus far few studies have... In recent years important information has accumulated on the genetic alterations present in colorectal tumors. However, thus far few studies have analyzed the... Abstract Background In recent years important information has accumulated on the genetic alterations present in colorectal tumors. However, thus far few... Background In recent years important information has accumulated on the genetic alterations present in colorectal tumors. However, thus far few studies have... BACKGROUNDIn recent years important information has accumulated on the genetic alterations present in colorectal tumors. However, thus far few studies have... |
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SubjectTerms | abnormalities of chromosomes 17 and 18 Adult Aged Aged, 80 and over Chromosome Aberrations Chromosomes, Human, Pair 17 Chromosomes, Human, Pair 18 clinicobiological features colorectal cancer Colorectal Neoplasms - epidemiology Colorectal Neoplasms - genetics Disease-Free Survival Female Flow Cytometry Genes, DCC - genetics Genes, p53 - genetics Humans In Situ Hybridization, Fluorescence Incidence Male Middle Aged Prognosis |
Title | Numerical abnormalities of chromosomes 17 and 18 in sporadic colorectal cancer: Incidence and correlation with clinical and biological findings and the prognosis of the disease |
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