Identification of novel deletion regions on chromosome arms 2q and 6p in breast carcinomas by amplotype analysis

Piao, Zhe; Lee, Kyong Sik; Kim, Hoguen; Perucho, Manuel; Malkhosyan, Sergei

doi:10.1002/1098-2264(2000)9999:9999<::aid-gcc1069>3.0.co;2-6

Cited by 46 publications

(19 citation statements)

References 28 publications

(51 reference statements)

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“…20q13.3, frequently overexpressed in ovarian cancers, has been recently shown to localize the BRK tyrosine kinase gene (GeneID: 5753), which is thought to have an important role in the development of ovarian cancers. 16 Losses occurring at chromosome 2q have been described for various carcinomas, including head and neck squamous cell carcinoma, [17][18][19] breast carcinoma, 20 lung carcinoma, 21 neuroblastoma, 22 cervical cancer, 23 and prostate adenocarcinoma. 24 Studies using different approaches have increasingly shown that the most affected region is 2q32-q37.…”

Section: Discussionmentioning

confidence: 99%

Array comparative genomic hybridization analysis of olfactory neuroblastoma

et al. 2008

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Olfactory neuroblastoma is an unusual neuroectodermal malignancy, which is thought to arise at the olfactory membrane of the sinonasal tract. Due to its rarity, little is understood regarding its molecular and cytogenetic abnormalities. The aim of the current study is to identify specific DNA copy number changes in olfactory neuroblastoma. Thirteen dissected tissue samples were analyzed using array comparative genomic hybridization. Our results show that gene copy number profiles of olfactory neuroblastoma samples are complex. The most frequent changes included gains at 7q11.22-q21.11, 9p13.3, 13q, 20p/q, and Xp/q, and losses at 2q31.1, 2q33.3, 2q37.1, 6q16.3, 6q21.33, 6q22.1, 22q11.23, 22q12.1, and Xp/q. Gains were more frequent than losses, and high-stage tumors showed more alterations than low-stage olfactory neuroblastoma. Frequent changes in high-stage tumors were gains at 13q14.2-q14.3, 13q31.1, and 20q11.21-q11.23, and loss of Xp21.1 (in 66% of cases). Gains at 5q35, 13q, and 20q, and losses at 2q31.1, 2q33.3, and 6q16-q22, were present in 50% of cases. The identified regions of gene copy number change have been implicated in a variety of tumors, especially carcinomas. In addition, our results indicate that gains in 20q and 13q may be important in the progression of this cancer, and that these regions possibly harbor genes with functional relevance in olfactory neuroblastoma.

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Section: Discussionmentioning

confidence: 99%

Array comparative genomic hybridization analysis of olfactory neuroblastoma

et al. 2008

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“…(24) However, PTK7 expression has been shown to be decreased in metastatic melanoma (25) and clear cell renal cell carcinoma. (26) In addition, chromosome 6p, (27) on which the PTK7 gene is located, was found to be deleted in breast carcinoma (28) and malignant melanoma. (29) Although the role of PTK7 in different cancers has not been studied comprehensively, PTK7 is likely to have a tumorpromoting role in general.…”

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confidence: 99%

Oncogenic role of protein tyrosine kinase 7 in esophageal squamous cell carcinoma

et al. 2013

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Esophageal squamous cell carcinoma (ESCC) is a common subtype of esophageal cancer that is particularly prevalent in East Asian countries. Our previous expression profile analysis showed that the gene encoding protein tyrosine kinase 7 (PTK7) is upregulated in ESCC tissues. Here, we aimed to validate PTK7 as a prognostic factor and a candidate target for molecular treatment of ESCC. Both RT-PCR and Western blot analysis of tissues from ESCC patients revealed that PTK7 was significantly upregulated in tumor tissue samples of ESCC. Immunohistochemical staining of PTK7 showed that increased expression of PTK7 was inversely correlated with overall survival (P = 0.021). In vitro knockdown of PTK7 inhibited proliferation, survival, wound healing, and invasion of ESCC cells. In addition, PTK7 knockdown decreased phosphorylation of Akt, Erk, and focal adhesion kinase (FAK), important determinants of cell proliferation, survival, and migration. Therefore, our findings suggest that PTK7 has potential as a prognostic marker for ESCC and might also be a candidate for targeted therapy in the treatment of ESCC. (Cancer Sci 2013; 104: 1120-1126 E sophageal cancer is one of the most devastating malignancies. Despite recent developments in its management, advanced esophageal cancer is associated with high rates of local recurrence and distant metastasis.(1,2) Although there has been improvement in clinical outcome through multidisciplinary treatment strategies, (3)(4)(5) such as total mediastinal lymph node dissection, (6) and new diagnostic modalities such as positron emission tomography, (7) these developments have not proven satisfactory in preventing the high recurrence rates. Currently, the prognosis is only promising if the tumor is detected early and resected completely.Esophageal squamous cell carcinoma (ESCC) is the most common histologic subtype of esophageal cancer in East Asian countries.(8) It has a unique profile of clinical and anatomical characteristics that is distinct from those of esophageal adenocarcinoma, which is more prevalent in North America, UK, and Australia.(8) To develop prognostic diagnosis and effective therapeutics for ESCC, the identification of biomarkers is of vital importance. In a gene expression profiling analysis to pursue biomarkers, we identified protein tyrosine kinase 7 (PTK7; also known as colon carcinoma kinase-4 or CCK-4), as a candidate biomarker for ESCC. (9) Protein tyrosine kinase 7 is a receptor tyrosine kinase-like molecule containing an extracellular domain with seven immunoglobulin-like loops, a transmembrane domain, and a defective tyrosine kinase domain that resembles a catalytic domain but lacks catalytic activity.(10-12) Mice expressing a truncated form of PTK7 protein die perinatally, revealing a defect in neural tube closure and stereociliary bundle orientation. These findings implicate PTK7 as a regulator of planar cell polarity (PCP).(13) It has been shown that PTK7 recruits RACK1, which affects Dsh recruitment by interaction with PKCd1. (14) Interaction between PTK7...

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“…Deletions of the long arm of chromosome 6 (6q) are one of the most common chromosomal abnormalities observed in various human solid (Orphanos et al, 1995;Noviello et al, 1996;Theile et al, 1996;Makino et al, 2001;Piao et al, 2001) and lymphoid malignancies (Gerard et al, 1997;Sherratt et al, 1997;Tien et al, 1997;Wong et al, 1997;Hauptschein et al, 1998;Merup et al, 1998;Amiel et al, 1999;Stilgenbauer et al, 1999;Sinclair et al, 2000;Mancini et al, 2002). Many subchromosomal regions from 6q13 to q27 have been suggested to harbour putative tumour suppressor genes for different types of tumours, examples being 6q14-21 in prostate cancer (Cooney et al, 1996), 6q16-q21 in lymphoid leukaemia (Jackson et al, 1998(Jackson et al, , 2000, 6q23.3-q25 in breast cancer, and 6q27 in B-cell non-Hodgkin lymphoma (NHL) (Hauptschein et al, 1998) and ovarian cancers (Saito et al, 1996).…”

Section: Discussionmentioning

confidence: 99%

A 2·6 Mb interval on chromosome 6q25.2–q25.3 is commonly deleted in human nasal natural killer/T‐cell lymphoma

Sun

Lin

et al. 2003

Br J Haematol

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Summary. Natural killer (NK)/T-cell lymphoma is a special subtype of rare malignant lymphoma that is more prevalent in Asia than in America and Europe. This newly characterized haemato-lymphoid malignancy is highly aggressive and frequently present in nasal and upper aerodigestive sites. Several studies have reported the commonly deleted region of chromosome 6q21-25 in this particular type of lymphoma. To refine the smallest region of overlapping (SRO) deletion for localization of potential tumour suppressor (TS) genes, we performed loss of heterozygosity (LOH) and homozygosity mapping of deletion (HOMOD) analyses on 37 nasal and nasal-type NK/T-cell lymphoma patients using a panel of 25 microsatellite markers, covering the 6q21-q25 region. In all patients studied, LOH was detected in eight (89%) paired-sample patients, while hemizygous deletion was detected in three (11%) singlesample patients. Combination of the LOH and HOMOD results defined a distinct 3 Mb SRO on chromosome 6q25. Quantitative multiplex polymerase chain reaction analysis of 10 sequence-tagged sites further refined the putative TS-gene-containing region to a 2AE6 Mb interval between TIAM2 and SNX9. Eighteen known genes/Unigene clusters and 25 hypothetical genes are located within this 2AE6 Mb region, but none are previously identified TS genes. These results provide a framework for future positional cloning of novel TS gene(s) at 6q25.2-q25.3.

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Identification of novel deletion regions on chromosome arms 2q and 6p in breast carcinomas by amplotype analysis

Cited by 46 publications

References 28 publications

Array comparative genomic hybridization analysis of olfactory neuroblastoma

Array comparative genomic hybridization analysis of olfactory neuroblastoma

Oncogenic role of protein tyrosine kinase 7 in esophageal squamous cell carcinoma

A 2·6 Mb interval on chromosome 6q25.2–q25.3 is commonly deleted in human nasal natural killer/T‐cell lymphoma

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