Student or educator? Sign up with your school email and get 6 months of Pro free.
CoChat
Sign Up
Cited by 41

The DOI matches its Crossref record; 5 of the 5 references it cites were found in a registry or an index.

Mutant allele specific imbalance in oncogenes with copy number alterations: Occurrence, mechanisms, and potential clinical implications

Yu, Chih-Chieh, Qiu, Wanglong, Juang, Caroline S., Mansukhani, Mahesh M., Halmos, Balazs, Su, Gloria H.·2017·Cancer Letters
DOI 10.1016/j.canlet.2016.10.013PMC PMC5507770
Open this paper in CoChat — free account

Overview

The claims and statistics of this paper haven’t been checked yet.

Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.

A few free checks a day · papers already verified open instantly · results are public

Integrity signals

Registry

Crossref · 10.1016/j.canlet.2016.10.013

Cites

5 of 5 references verified0 citation errors · 0 not checkable

Statistics

Verification

Claims the paper makes

The claims and statistics of this paper haven’t been checked yet.

Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.

A few free checks a day · papers already verified open instantly · results are public

Claims other papers make about this one

Each is checked against this paper’s own text: does it say what the citing paper says it does?

Self-check

Percentages, sums and reported differences re-computed from the paper’s own numbers.

The self-check needs the paper’s full text.

Citations

Cites

Show all 5 references

Research works printed but not linked: 96

  1. Vogelstein, 2013, Cancer genome landscapes, Science, 339, 1546, 10.1126/science.1235122 · DOI · Paper page
  2. Levens, 2013, Cellular MYCro economics: balancing MYC function with MYC expression, Cold Spring Harb. Perspect. Med., 3, 10.1101/cshperspect.a022483 · DOI
  3. Jacot, 2013, The HER2 amplicon in breast cancer: topoisomerase IIA and beyond, Biochim. Biophys. Acta, 1836, 146
  4. Soh, 2009, Oncogene mutations, copy number gains and mutant allele specific imbalance (MASI) frequently occur together in tumor cells, PLoS One, 4, e7464, 10.1371/journal.pone.0007464 · DOI
  5. Tuna, 2009, Uniparental disomy in cancer, Trends Mol. Med., 15, 120, 10.1016/j.molmed.2009.01.005 · DOI
  6. Lapunzina, 2011, The consequences of uniparental disomy and copy number neutral loss-of-heterozygosity during human development and cancer, Biol. Cell, 103, 303, 10.1042/BC20110013 · DOI
  7. Makishima, 2011, Pathogenesis and consequences of uniparental disomy in cancer, Clin. Cancer Res. Off J. Am. Assoc. Cancer Res., 17, 3913, 10.1158/1078-0432.CCR-10-2900 · DOI
  8. Qiu, 2011, Disruption of p16 and activation of Kras in pancreas increases ductal adenocarcinoma formation and metastasis in vivo, Oncotarget, 2, 862, 10.18632/oncotarget.357 · DOI · Paper page
  9. Gandhi, 2009, Alterations in genes of the EGFR signaling pathway and their relationship to EGFR tyrosine kinase inhibitor sensitivity in lung cancer cell lines, PLoS One, 4, e4576, 10.1371/journal.pone.0004576 · DOI
  10. Davies, 2002, Mutations of the BRAF gene in human cancer, Nature, 417, 949, 10.1038/nature00766 · DOI · Paper page
  11. Samuels, 2004, High frequency of mutations of the PIK3CA gene in human cancers, Science, 304, 554, 10.1126/science.1096502 · DOI
  12. Schonleben, 2006, PIK3CA mutations in intraductal papillary mucinous neoplasm/carcinoma of the pancreas, Clin. cancer Res. Off J. Am. Assoc. Cancer Res., 12, 3851, 10.1158/1078-0432.CCR-06-0292 · DOI
  13. Santos, 1984, Malignant activation of a K-ras oncogene in lung carcinoma but not in normal tissue of the same patient, Science, 223, 661, 10.1126/science.6695174 · DOI · Paper page
  14. Bos, 1989, Ras oncogenes in human cancer: a review, Cancer Res., 49, 4682
  15. Siegel, 2014, Cancer statistics, 2014, CA Cancer J. Clin., 64, 9, 10.3322/caac.21208 · DOI · Paper page
  16. Almoguera, 1988, Most human carcinomas of the exocrine pancreas contain mutant c-K-ras genes, Cell, 53, 549, 10.1016/0092-8674(88)90571-5 · DOI
  17. Smit, 1988, K-ras codon 12 mutations occur very frequently in pancreatic adenocarcinomas, Nucleic Acids Res., 16, 7773, 10.1093/nar/16.16.7773 · DOI
  18. Kobunai, 2010, The frequency of KRAS mutation detection in human colon carcinoma is influenced by the sensitivity of assay methodology: a comparison between direct sequencing and real-time PCR, Biochem. Biophys. Res. Commun., 395, 158, 10.1016/j.bbrc.2010.03.167 · DOI
  19. Cejas, 2009, KRAS mutations in primary colorectal cancer tumors and related metastases: a potential role in prediction of lung metastasis, PLoS One, 4, e8199, 10.1371/journal.pone.0008199 · DOI
  20. Rodenhuis, 1988, Incidence and possible clinical significance of K-ras oncogene activation in adenocarcinoma of the human lung, Cancer Res., 48, 5738
  21. Suzuki, 1990, Detection of ras gene mutations in human lung cancers by single-strand conformation polymorphism analysis of polymerase chain reaction products, Oncogene, 5, 1037
  22. Forbes, 2006, Cosmic 2005, Br. J. Cancer, 94, 318, 10.1038/sj.bjc.6602928 · DOI
  23. Yuen, 2002, Similarity of the phenotypic patterns associated with BRAF and KRAS mutations in colorectal neoplasia, Cancer Res., 62, 6451
  24. Samuels, 2004, Oncogenic mutations of PIK3CA in human cancers, Cell Cycle, 3, 1221, 10.4161/cc.3.10.1164 · DOI
  25. Schonleben, 2006, BRAF and KRAS gene mutations in intraductal papillary mucinous neoplasm/carcinoma (IPMN/IPMC) of the pancreas, Cancer Lett., 8, 8
  26. Shigematsu, 2006, Somatic mutations of epidermal growth factor receptor signaling pathway in lung cancers, Int. J. Cancer, 118, 257, 10.1002/ijc.21496 · DOI
  27. Ciardiello, 2008, EGFR antagonists in cancer treatment, N. Engl. J. Med., 358, 1160, 10.1056/NEJMra0707704 · DOI
  28. Pao, 2005, Epidermal growth factor receptor mutations, small-molecule kinase inhibitors, and non-small-cell lung cancer: current knowledge and future directions, J. Clin. Oncol. Off J. Am. Soc. Clin. Oncol., 23, 2556, 10.1200/JCO.2005.07.799 · DOI
  29. Cappuzzo, 2005, Epidermal growth factor receptor gene and protein and gefitinib sensitivity in non-small-cell lung cancer, J. Natl. Cancer Inst., 97, 643, 10.1093/jnci/dji112 · DOI
  30. Hirsch, 2007, Combination of EGFR gene copy number and protein expression predicts outcome for advanced non-small-cell lung cancer patients treated with gefitinib, Ann. Oncol., 18, 752, 10.1093/annonc/mdm003 · DOI
  31. Chen, 2014, Identification of druggable cancer driver genes amplified across TCGA datasets, PLoS One, 9, e98293, 10.1371/journal.pone.0098293 · DOI
  32. Pao, 2004, EGF receptor gene mutations are common in lung cancers from ”never smokers“ and are associated with sensitivity of tumors to gefitinib and erlotinib, Proc. Natl. Acad. Sci. U. S. A., 101, 13306, 10.1073/pnas.0405220101 · DOI · Paper page
  33. Paez, 2004, EGFR mutations in lung cancer: correlation with clinical response to gefitinib therapy, Science, 304, 1497, 10.1126/science.1099314 · DOI · Paper page
  34. Sankaranarayanan, 2015, Tensor GSVD of patient- and platform-matched tumor and normal DNA copy-number profiles uncovers chromosome arm-wide patterns of tumor-exclusive platform-consistent alterations encoding for cell transformation and predicting ovarian cancer survival, PLoS One, 10, e0121396, 10.1371/journal.pone.0121396 · DOI
  35. Winter, 1986, Oncogene amplification during tumorigenesis of established rat fibroblasts reversibly transformed by activated human ras oncogenes, Mol. Cell Biol., 6, 2562, 10.1128/MCB.6.7.2562 · DOI
  36. Winter, 1985, A method to detect and characterize point mutations in transcribed genes: amplification and overexpression of the mutant c-Ki-ras allele in human tumor cells, Proc. Natl. Acad. Sci. U. S. A., 82, 7575, 10.1073/pnas.82.22.7575 · DOI
  37. Mitsudomi, 1991, Mutations of ras genes distinguish a subset of non-small-cell lung cancer cell lines from small-cell lung cancer cell lines, Oncogene, 6, 1353
  38. Modrek, 2009, Oncogenic activating mutations are associated with local copy gain, Mol. Cancer Res., 7, 1244, 10.1158/1541-7786.MCR-08-0532 · DOI
  39. Chiosea, 2011, KRAS mutant allele-specific imbalance in lung adenocarcinoma, Mod. Pathol., 24, 1571, 10.1038/modpathol.2011.109 · DOI
  40. Villaruz, 2013, The prognostic and predictive value of KRAS oncogene substitutions in lung adenocarcinoma, Cancer, 119, 2268, 10.1002/cncr.28039 · DOI
  41. Pfarr, 2016, Copy number changes of clinically actionable genes in melanoma, non-small cell lung cancer and colorectal cancer-a survey across 822 routine diagnostic cases, Genes Chromosom. Cancer, 55, 821, 10.1002/gcc.22378 · DOI
  42. Kerr, 2016, Mutant Kras copy number defines metabolic reprogramming and therapeutic susceptibilities, Nature, 531, 110, 10.1038/nature16967 · DOI
  43. Krasinskas, 2013, KRAS mutant allele-specific imbalance is associated with worse prognosis in pancreatic cancer and progression to undifferentiated carcinoma of the pancreas, Mod. Pathol., 26, 1346, 10.1038/modpathol.2013.71 · DOI
  44. Malapelle, 2015, KRAS mutant allele-specific imbalance (MASI) assessment in routine samples of patients with metastatic colorectal cancer, J. Clin. Pathol., 68, 265, 10.1136/jclinpath-2014-202761 · DOI
  45. Hartman, 2012, Mutant allele-specific imbalance modulates prognostic impact of KRAS mutations in colorectal adenocarcinoma and is associated with worse overall survival, Int. J. Cancer, 131, 1810, 10.1002/ijc.27461 · DOI
  46. Oakley, 2011, Higher dosage of the epidermal growth factor receptor mutant allele in lung adenocarcinoma correlates with younger age, stage IV at presentation, and poorer survival, J. Thorac. Oncol., 6, 1407, 10.1097/JTO.0b013e31821d41af · DOI
  47. Malapelle, 2015, EGFR mutant allelic-specific imbalance assessment in routine samples of non-small cell lung cancer, J. Clin. Pathol., 68, 739, 10.1136/jclinpath-2015-203101 · DOI
  48. Takano, 2005, Epidermal growth factor receptor gene mutations and increased copy numbers predict gefitinib sensitivity in patients with recurrent non-small-cell lung cancer, J. Clin. Oncol. Off J. Am. Soc. Clin. Oncol., 23, 6829, 10.1200/JCO.2005.01.0793 · DOI
  49. Dahabreh, 2008, Trastuzumab in the adjuvant treatment of early-stage breast cancer: a systematic review and meta-analysis of randomized controlled trials, Oncologist, 13, 620, 10.1634/theoncologist.2008-0001 · DOI
  50. Li, 2008, EGFR mutations in lung adenocarcinomas: clinical testing experience and relationship to EGFR gene copy number and immunohistochemical expression, J. Mol. Diagn JMD, 10, 242, 10.2353/jmoldx.2008.070178 · DOI
  51. Dahabreh, 2010, Somatic EGFR mutation and gene copy gain as predictive biomarkers for response to tyrosine kinase inhibitors in non-small cell lung cancer, Clin. Cancer Res. Off J. Am. Assoc. Cancer Res., 16, 291, 10.1158/1078-0432.CCR-09-1660 · DOI
  52. Engel, 1980, A new genetic concept: the uniparental disomy and its potential effect, the isodisomy (author's transl), J. Genet. Hum., 28, 11
  53. Andersen, 2007, Frequent occurrence of uniparental disomy in colorectal cancer, Carcinogenesis, 28, 38, 10.1093/carcin/bgl086 · DOI
  54. Melcher, 2007, SNP-Array genotyping and spectral karyotyping reveal uniparental disomy as early mutational event in MSS- and MSI-colorectal cancer cell lines, Cytogenet Genome Res., 118, 214, 10.1159/000108303 · DOI
  55. Nagano, 2007, Allelic alterations in pancreatic endocrine tumors identified by genome-wide single nucleotide polymorphism analysis, Endocr. Relat. Cancer, 14, 483, 10.1677/ERC-06-0090 · DOI
  56. Murthy, 2002, Loss of heterozygosity associated with uniparental disomy in breast carcinoma, Mod. Pathol., 15, 1241, 10.1097/01.MP.0000032535.62750.D1 · DOI
  57. Tuna, 2010, Association between acquired uniparental disomy and homozygous mutations and HER2/ER/PR status in breast cancer, PLoS One, 5, e15094, 10.1371/journal.pone.0015094 · DOI
  58. Tuna, 2012, Prognostic value of acquired uniparental disomy (aUPD) in primary breast cancer, Breast Cancer Res. Treat., 132, 189, 10.1007/s10549-011-1579-y · DOI
  59. Teh, 2005, Genomewide single nucleotide polymorphism microarray mapping in basal cell carcinomas unveils uniparental disomy as a key somatic event, Cancer Res., 65, 8597, 10.1158/0008-5472.CAN-05-0842 · DOI
  60. Hagstrom, 1999, Mitotic recombination map of 13cen-13q14 derived from an investigation of loss of heterozygosity in retinoblastomas, Proc. Natl. Acad. Sci. U. S. A., 96, 2952, 10.1073/pnas.96.6.2952 · DOI
  61. Caren, 2008, High-resolution array copy number analyses for detection of deletion, gain, amplification and copy-neutral LOH in primary neuroblastoma tumors: four cases of homozygous deletions of the CDKN2A gene, BMC Genomics, 9, 353, 10.1186/1471-2164-9-353 · DOI
  62. Toma, 2008, Loss of heterozygosity and copy number abnormality in clear cell renal cell carcinoma discovered by high-density affymetrix 10K single nucleotide polymorphism mapping array, Neoplasia, 10, 634, 10.1593/neo.08160 · DOI
  63. Kawashima-Goto, 2015, Identification of a homozygous JAK3 V674A mutation caused by acquired uniparental disomy in a relapsed early T-cell precursor ALL patient, Int. J. Hematol., 101, 411, 10.1007/s12185-014-1711-y · DOI
  64. Li, 2014, Mutations in linker histone genes HIST1H1 B, C, D, and E; OCT2 (POU2F2); IRF8; and ARID1A underlying the pathogenesis of follicular lymphoma, Blood, 123, 1487, 10.1182/blood-2013-05-500264 · DOI
  65. Kato, 2013, Aggressive transformation of juvenile myelomonocytic leukemia associated with duplication of oncogenic KRAS due to acquired uniparental disomy, J. Pediatr., 162, 1285, 10.1016/j.jpeds.2013.01.003 · DOI
  66. Eldai, 2013, Novel genes associated with colorectal cancer are revealed by high resolution cytogenetic analysis in a patient specific manner, PLoS One, 8, 10.1371/annotation/3f97e271-6926-4766-8430-1b4a009e80c6 · DOI
  67. Tuna, 2015, Prognostic relevance of acquired uniparental disomy in serous ovarian cancer, Mol. Cancer, 14, 29, 10.1186/s12943-015-0289-1 · DOI
  68. Bullinger, 2010, Identification of acquired copy number alterations and uniparental disomies in cytogenetically normal acute myeloid leukemia using high-resolution single-nucleotide polymorphism analysis, Leukemia, 24, 438, 10.1038/leu.2009.263 · DOI
  69. Fitzgibbon, 2005, Association between acquired uniparental disomy and homozygous gene mutation in acute myeloid leukemias, Cancer Res., 65, 9152, 10.1158/0008-5472.CAN-05-2017 · DOI
  70. Schepeler, 2013, A high resolution genomic portrait of bladder cancer: correlation between genomic aberrations and the DNA damage response, Oncogene, 32, 3577, 10.1038/onc.2012.381 · DOI
  71. Torrance, 2001, Use of isogenic human cancer cells for high-throughput screening and drug discovery, Nat. Biotechnol., 19, 940, 10.1038/nbt1001-940 · DOI
  72. Li, 2003, LOH of chromosome 12p correlates with Kras2 mutation in non-small cell lung cancer, Oncogene, 22, 1243, 10.1038/sj.onc.1206192 · DOI
  73. Wan, 2006, Loss of heterozygosity of Kras2 gene on 12p12-13 in Chinese colon carcinoma patients, World J. Gastroenterol, 12, 1033, 10.3748/wjg.v12.i7.1037 · DOI
  74. Takeuchi, 1996, Frequent loss of heterozygosity in region of the KIP1 locus in non-small cell lung cancer: evidence for a new tumor suppressor gene on the short arm of chromosome 12, Cancer Res., 56, 738
  75. Sanchez-Cespedes, 2001, Chromosomal alterations in lung adenocarcinoma from smokers and nonsmokers, Cancer Res., 61, 1309
  76. Kibel, 1998, Identification of 12p as a region of frequent deletion in advanced prostate cancer, Cancer Res., 58, 5652
  77. Mahlamaki, 1997, Comparative genomic hybridization reveals frequent gains of 20q, 8q, 11q, 12p, and 17q, and losses of 18q, 9p, and 15q in pancreatic cancer, Genes Chromosom. Cancer, 20, 383, 10.1002/(SICI)1098-2264(199712)20:4<383::AID-GCC10>3.0.CO;2-O · DOI
  78. Hegi, 1994, Allelotype analysis of mouse lung carcinomas reveals frequent allelic losses on chromosome 4 and an association between allelic imbalances on chromosome 6 and K-ras activation, Cancer Res., 54, 6257
  79. Johnson, 2001, Somatic activation of the K-ras oncogene causes early onset lung cancer in mice, Nature, 410, 1111, 10.1038/35074129 · DOI · Paper page
  80. Junttila, 2010, Selective activation of p53-mediated tumour suppression in high-grade tumours, Nature, 468, 567, 10.1038/nature09526 · DOI
  81. Zhang, 2001, Wildtype Kras2 can inhibit lung carcinogenesis in mice, Nat. Genet., 29, 25, 10.1038/ng721 · DOI
  82. James, 2003, K-ras proto-oncogene exhibits tumor suppressor activity as its absence promotes tumorigenesis in murine teratomas, Mol. Cancer Res., 1, 820
  83. Li, 2007, Growth inhibitory effect of wild-type Kras2 gene on a colonic adenocarcinoma cell line, World J. Gastroenterol, 13, 934, 10.3748/wjg.v13.i6.934 · DOI
  84. Li, 2007, Changes in gene-expression profiles of colon carcinoma cells induced by wild type K-ras2, World J. Gastroenterol, 13, 4620, 10.3748/wjg.v13.i34.4620 · DOI
  85. Staffas, 2015, Wild-type KRAS inhibits oncogenic KRAS-induced T-ALL in mice, Leukemia, 29, 1032, 10.1038/leu.2014.315 · DOI
  86. Kong, 2016, Loss of wild-type Kras promotes activation of all Ras isoforms in oncogenic Kras-induced leukemogenesis, Leukemia, 30, 1542, 10.1038/leu.2016.40 · DOI
  87. Singh, 2005, The wild-type Ras: road ahead, FASEB J., 19, 161, 10.1096/fj.04-2584hyp · DOI
  88. Pfeifer, 2001, A new verdict for an old convict, Nat. Genet., 29, 3, 10.1038/ng0901-3 · DOI
  89. Zhou, 2016, The role of wild type RAS isoforms in cancer, Semin. Cell Dev. Biol., 58, 60, 10.1016/j.semcdb.2016.07.012 · DOI · Paper page
  90. Bentley, 2013, A requirement for wild-type Ras isoforms in mutant KRas-driven signalling and transformation, Biochem. J., 452, 313, 10.1042/BJ20121578 · DOI
  91. Grabocka, 2014, Wild-type H- and N-Ras promote mutant K-Ras-driven tumorigenesis by modulating the DNA damage response, Cancer Cell, 25, 243, 10.1016/j.ccr.2014.01.005 · DOI
  92. Ortiz-Vega, 2002, The putative tumor suppressor RASSF1A homodimerizes and heterodimerizes with the Ras-GTP binding protein Nore1, Oncogene, 21, 1381, 10.1038/sj.onc.1205192 · DOI
  93. Matallanas, 2011, Mutant K-Ras activation of the proapoptotic MST2 pathway is antagonized by wild-type K-Ras, Mol. Cell, 44, 893, 10.1016/j.molcel.2011.10.016 · DOI
  94. Romano, 2013, The differential effects of wild-type and mutated K-Ras on MST2 signaling are determined by K-Ras activation kinetics, Mol. Cell Biol., 33, 1859, 10.1128/MCB.01414-12 · DOI
  95. Walsh, 2008, Genome-wide loss of heterozygosity and uniparental disomy in BRCA1/2-associated ovarian carcinomas, Clin. Cancer Res. Off J. Am. Assoc. Cancer Res., 14, 7645, 10.1158/1078-0432.CCR-08-1291 · DOI
  96. Bacolod, 2009, Emerging paradigms in cancer genetics: some important findings from high-density single nucleotide polymorphism array studies, Cancer Res., 69, 723, 10.1158/0008-5472.CAN-08-3543 · DOI

Cited by

Metadata

Authors
Yu, C.-C., Qiu, W., Juang, C. S., Mansukhani, M. M., Halmos, B., & Su, G. H.
Venue
Cancer Letters
Publisher
Elsevier BV
Published
2017-01
Volume
384
Pages
86-93
ISSN
0304-3835
DOI
10.1016/j.canlet.2016.10.013
PMC
PMC5507770
Cited by
41
References
5
Language
en
Licence
www.elsevier.com/tdm/userlicense/1.0/ (tdm)

About these checks

Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.

Statistics and arithmetic are recomputed, not judged.

Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.

What counts as a claim ›How we measure confidence ›How we check this ›

Are you an author, or do you see a problem with this page? Request a review