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Knösel, Thomas; Yu, Youngwei; Stein, Ulf; Schwabe, Holger; Schlüns, Karsten; Schlag, Peter M.; Dietel, Manfred; Petersen, Iver

doi:10.1023/a:1016368708107

Cited by 15 publications

(7 citation statements)

References 30 publications

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“…In general, the membranous overexpression rates varied between 0% and 15%. Only Knösel et al and Park et al reported membranous overexpression of over 40% 34,36. However, Park et al only confirmed two out of 27 3+ cases with FISH, which puts their results in a different perspective.…”

Section: Scoring Proceduresmentioning

confidence: 95%

“…Of all seven studies that report a lack of clinical correlation, six of them do not split their scoring into membranous and cytoplasmic staining 20,21,33,35,44,46. In contrast, out of the six studies that report a clinical correlation, four of them do split their results in membranous and cytoplasmic staining 16,18,22,34. Although this has never been confirmed in a large multi-center trial, these studies strongly suggest a clinical relevance of cytoplasmic HER2 overexpression in colorectal cancer.…”

Section: Cytoplasmic Her2mentioning

confidence: 97%

“…Of 15 publications that analyzed clinical prognostic parameters, six showed a worse patient survival with cytoplasmic tumor overexpression of HER2 16,18,22,32,34,45. Seven studies showed no correlation with any clinical parameter 20,21,26,33,35,44,46.…”

Section: Cytoplasmic Her2mentioning

confidence: 99%

“…When analyzing all accessible papers about HER2-overexpression on colon cancer tissue for their scoring methods, it was observed that most publications follow the breast cancer protocol by examining only membranous overexpression,24,25,27–31,34,36,42,43 or split their scoring in membranous and cytoplasmic overexpression 16,18,22,23,26,41. In general, the membranous overexpression rates varied between 0% and 15%.…”

Section: Scoring Proceduresmentioning

confidence: 99%

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Cytoplasmic Overexpression of HER2: A Key Factor in Colorectal Cancer

Blok

Kuppen

Leeuwen

et al. 2013

Clin Med Insights Oncol

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Trastuzumab, a humanized mouse monoclonal antibody directed against HER2 (Human Epidermal Growth Factor Receptor 2), is currently a keystone in the treatment of breast cancer. Meanwhile, trastuzumab has been validated for use in other types of cancer too. But the data on HER2 expression in colorectal cancer are ambiguous, with reported overexpression of HER2 varying between zero and 84%. In this review these studies are evaluated and compared. It shows that many factors influence the determination of HER2-expression, especially of the intracellular fraction of HER2. It is concluded that although membranous overexpression of HER2 is low in colorectal cancer with only 5% of all patients being positive, a significant proportion of the patients (30%) shows cytoplasmic HER2 overexpression. The clinical impact of enhanced intracellular HER2 is not known, because the nature and origin have not completely been revealed yet. Enlightening this process could be a stepping stone towards targeting of intracellular HER2 as a treatment option.

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Section: Scoring Proceduresmentioning

confidence: 95%

Section: Cytoplasmic Her2mentioning

confidence: 97%

Section: Cytoplasmic Her2mentioning

confidence: 99%

Section: Scoring Proceduresmentioning

confidence: 99%

See 2 more Smart Citations

Cytoplasmic Overexpression of HER2: A Key Factor in Colorectal Cancer

Blok

Kuppen

Leeuwen

et al. 2013

Clin Med Insights Oncol

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“…As the loss of heterozygosity in the chromosome 4q28, where the human Fat4 gene is located, was observed in several cancers including colon, prostate lung, and liver (7,17,22,23,28), Fat4 could be involved in other types of tumors.…”

Section: Discussionmentioning

confidence: 99%

Identification of Novel Tumor Suppressor Genes for Breast Cancer

Qi¹

2006

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Public reporting burden for this collection of information is estimated to average 1 hour per response, including the time for reviewing instructions, searching existing data sources, gathering and maintaining the data needed, and completing and reviewing this collection of information. Send comments regarding this burden estimate or any other aspect of this collection of information, including suggestions for reducing this burden to Department of Defense, Washington Headquarters Services, Directorate for Information Operations and Reports (0704-0188), 1215 Jefferson Davis Highway, Suite 1204, Arlington, VA 22202-4302. Respondents should be aware that notwithstanding any other provision of law, no person shall be subject to any penalty for failing to comply with a collection of information if it does not display a currently valid OMB control number. PLEASE DO NOT RETURN YOUR FORM TO THE ABOVE ADDRESS. (From -To) REPORT DATE (DD-MM-YYYY) March 2006 REPORT TYPE Final DATES COVERED ABSTRACTChromosomal deletions are very common events in breast cancer. However, no TSGs have been identified from most of recurrent deletions and few identified TSGs do not account for the risk of majority of breast cancer. In additional to the classical TSGs, there are haplo-insufficient TSGs which defy the identification through mutation analysis and may be quite common. By using a new system to generate random chromosomal deletions, we identified a ~3Mbp deletion in mouse chromosome 3, which was associated with tumorigenesis. The expression of Fat4 in the deleted region was inactivated due to promoter methylation in the second allele of Fat4, and the re-expression of Fat4 suppressed the tumorigenecity, suggesting Fat4 as a strong candidate for breast tumor suppressor genes. We also found that Fat4 expression was lost in a high proportion of human breast cancers, some of which were attributed to Fat4 promoter methylation.15. Subject Terms (keywords previously assigned to proposal abstract or terms which apply to this award) However, no TSGs have been identified from most of recurrent deletions and few identified TSGs do not account for the risk of majority of breast cancer. In additional to the classical TSGs, there are haplo-insufficient TSGs which defy the identification through mutation analysis and may be quite common. Moreover, as chromosomal deletions in breast tumors are often large and encompass many genes, one deletion may include two or more related genes, a combined haplo-insufficient effect of which could contribute to the development of breast cancer. By using a system to generate random chromosomal deletions, we proposed to identify these haplo-insufficient TSGs. The identification of new TSGs is crucial for our understanding of breast cancer biology and breast cancer management PI: CHAO QI 5 BODY Task 1. Identify the chromosome regions causing transformation of the non-transformed, immortal breast cells when deleted. By using a random chromosome deletion method based on LoxP/Cre mediated homologous recombination, w...

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Chromosomal imbalances in wood dust‐related adenocarcinomas of the inner nose and their associations with pathological parameters

Korinth

Pacyna-Gengelbach

Deutschmann

et al. 2005

The Journal of Pathology

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Comparative genomic hybridization (CGH) was used to screen 42 wood dust-related sinonasal adenocarcinomas for chromosomal alterations. The tumour collection comprised 39 papillary-tubular cylinder cell adenocarcinomas (PTCCs; six cases G1, 23 G2, and ten G3), two alveolar goblet cell adenocarcinomas (AGCs), and one signet ring cell adenocarcinoma (SRC), according to the Kleinsasser and Schroeder classification. Copy number changes were detected in 41 tumours (97.6%). The one carcinoma without imbalances was a PTCC-G1. DNA gains were most frequently seen on chromosomes 12p (83%), 7q (74%), 8q (71%), and 20q (71%), 11q (61%), 22 (59%), and 1q (52%). Pronounced overrepresentations suggestive of high copy amplifications were detected on 8q (15 cases, 36%), 7q (six cases, 14%), 20q (five cases, 12%), 13q14 (three cases, 7%), 1q22, 5p, 12p and 20 (two cases, 5% each), and 2q24, 3q13, 3q22, 7p, 14q12, and 16q13 (one case, each 2%). Frequent chromosomal losses occurred at 5q (81%), 18q (76%), 4 (74%), 8p (61%), 9p (60%), 6q and 17p (52% each), and 3p, 13q, and 21 (50% each). There was a quantitative as well as a qualitative increase of alterations from PTCC-G1 to PTCC-G2 and finally PTCC-G3, confirming the usefulness of histopathological grading. While PTCC-G1 carried only a few alterations, namely gains on chromosomes 17 and 7 as well as losses of 4q and 13q, PTCC-G2 already carried many of the above-mentioned alterations, while PTCC-G3 showed significantly more gains of 7q, 8q, and 12p, and losses of 8p and 17p. Additionally, the latter subgroup was particularly prone to carry pronounced DNA gains. These data provide further evidence for a recurrent pattern of chromosomal imbalances in sinonasal adenocarcinomas and highlight distinct aberrations that are associated with tumour differentiation and progression.

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Untitled

Cited by 15 publications

References 30 publications

Cytoplasmic Overexpression of HER2: A Key Factor in Colorectal Cancer

Cytoplasmic Overexpression of HER2: A Key Factor in Colorectal Cancer

Identification of Novel Tumor Suppressor Genes for Breast Cancer

Chromosomal imbalances in wood dust‐related adenocarcinomas of the inner nose and their associations with pathological parameters

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