Mutation analysis of the DBC2 gene in sporadic and familial breast cancer

Ohadi, Mina; Totonchi, Mehdi; Maguire, Pierce; Lindblom, Annika; Habibi, Roshanak; Alavi, B. Afshin; Keyhani, Elahe; Najmabadi, Hossein

doi:10.1080/02841860601047752

Cited by 14 publications

(13 citation statements)

References 4 publications

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“…Tumor suppressor gene RhoBTB2 (also known as Deleted in Breast Cancer 2, DBC2) was isolated from human chromosome 8p21 where frequent deletions were observed in various carcinomas including prostate, breast, lung, colon, rectum, bladder, liver and larynx (Emi et al, 1992;Lundgren et al, 1992;Bova et al, 1993;Fujiwara et al, 1993;Sunwoo et al, 1996). The activity of RhoBTB2 has been found to be altered in human malignancy by means of deletion or loss of heterozygosity, down-regulation, or point mutation (Hamaguchi et al, 2002;Ohadi et al, 2007;Cho et al, 2008). Genetic analysis demonstrated that RhoBTB2 was homozygously deleted in 3.5% of primary breast cancers, gene expression was silenced in 50% of breast and lung cancer cell lines, and several somatic missense mutations in RhoBTB2 were identified from primary tumors and cancer cell lines (Hamaguchi et al, 2002).…”

Section: Introductionmentioning

confidence: 97%

RhoBTB2 (DBC2) functions as tumor suppressor via inhibiting proliferation, preventing colony formation and inducing apoptosis in breast cancer cells

Mao

Zhang

Yang

et al. 2011

Gene

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Section: Introductionmentioning

confidence: 97%

RhoBTB2 (DBC2) functions as tumor suppressor via inhibiting proliferation, preventing colony formation and inducing apoptosis in breast cancer cells

Mao

Zhang

Yang

et al. 2011

Gene

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“…RhoBTB2/DBC2 was shown to undergo homologous deletion in a relatively small number (3.5%) of breast tumor samples; however, RhoBTB2 expression was silenced at high frequency (approximately 50%) in breast and lung tumors (Hamaguchi et al, 2002). Sporadic point mutations in RhoBTB2 were also detected in breast tumor samples and breast cancer cell lines (Hamaguchi et al, 2002), and subsequent studies have identified further sporadic mutations of the RhoBTB2 coding region and promoter in bladder (Knowles et al, 2005) and breast (Ohadi et al, 2007) tumor samples.…”

Section: Introductionmentioning

confidence: 99%

The atypical Rho GTPase RhoBTB2 is required for expression of the chemokine CXCL14 in normal and cancerous epithelial cells

et al. 2008

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The Rho family of small GTPases control cell migration, cell invasion and cell cycle. Many of these processes are perturbed in cancer and several family members show altered expression in a number of tumor types. RhoBTB2/ DBC2 is an atypical member of this family of signaling proteins, containing two BTB domains in addition to its conserved Rho GTPase domain. RhoBTB2 is mutated, deleted or silenced in a large percentage of breast and lung cancers; however, the functional consequences of this loss are unclear. Here we use RNA interference in primary human epithelial cells to mimic the loss of RhoBTB2 seen in cancer cells. Through microarray analysis of global gene expression, we show that loss of RhoBTB2 results in downregulation of CXCL14-a chemokine that controls leukocyte migration and angiogenesis, and whose expression is lost through unknown mechanisms in a wide range of epithelial cancers. Loss of RhoBTB2 expression correlates with loss of CXCL14 secretion by head and neck squamous cell carcinoma cell lines, whereas reintroduction of RhoBTB2 restores CXCL14 secretion. Our studies identify CXCL14 as a gene target of RhoBTB2 and support downregulation of CXCL14 as a functional outcome of RhoBTB2 loss in cancer.

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“…This clarifies a critical demand to investigate genetic predisposition factors in this country. Although valuable studies regarding to breast cancer germ line mutations have been done in Iran Yassaee et al, 2002;Moslehi et al, 2003;Pietschmann et al, 2005;Khadang et al, 2007;Ohadi et al, 2007), more unanswered questions still remain.…”

Section: Discussionmentioning

confidence: 99%

Familial Breast Cancer Registry Program in Patients Referred to the Cancer Institute of Iran

Sabokbar

Khajeh²,

Taghdiri³

et al. 2012

Asian Pacific Journal of Cancer Prevention

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Introduction: Annually a considerable number of people die because of breast cancer, a common disease among women also in Iran. Identifying risk factors and susceptible people can lead to prevention or at least early diagnosis. Among susceptibility risks, 5-10% of patients have a family history predisposing factor which can influence the risk of incidence among the family. Having a registry program can be a more practical way to screen high risk families for preventive planning. Method: Based on inclusion criteria, a questionnaire was prepared and after a pilot study on a small number of patients, actual data were collected on 400 patients and processed in SPSS 16.0. Results: Totally, 28.2%of the patients were younger than 40 years old and 36.8% had the included criteria for familial breast cancer (FBC). 102 patient's samples could be compared for receptor presentation. Similar to other studies, the number of triple negative breast cancers increased as the age decreased. Conclusion: The high percentage of patients with FBC among 400 cases in this study demonstrates that in order to design an infrastructural diagnostic protocol and screening of patients with FBC, a precise survey related to frequency and founder mutations of FBC is needed nationwide.

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Mutation analysis of the DBC2 gene in sporadic and familial breast cancer

Cited by 14 publications

References 4 publications

RhoBTB2 (DBC2) functions as tumor suppressor via inhibiting proliferation, preventing colony formation and inducing apoptosis in breast cancer cells

RhoBTB2 (DBC2) functions as tumor suppressor via inhibiting proliferation, preventing colony formation and inducing apoptosis in breast cancer cells

The atypical Rho GTPase RhoBTB2 is required for expression of the chemokine CXCL14 in normal and cancerous epithelial cells

Familial Breast Cancer Registry Program in Patients Referred to the Cancer Institute of Iran

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