一稿两投??



所有跟贴·加跟贴·新语丝读书论坛http://www.xys.org/cgi-bin/mainpage.pl

送交者: afa 于 2005-2-09, 21:56:38:

今天偶然在Pubmed上以“PI3K mutation”检索时,发现以下两篇文章,不知道是否是一稿两投,不过摘要题目可是几乎一样。哪位在国内有兴趣的帮忙查一些。
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Zhongguo Shi Yan Xue Ye Xue Za Zhi. 2004 Aug;12(4):420-6. Related Articles, Links


Mutation analysis of SHIP gene in acute leukemia.

Luo JM, Liu ZL, Hao HL, Wang FX, Dong ZR, Ohno R.

Department of Hematology, The Second Hospital, Hebei Medical University, Shijiazhuang 050000, China.

The SH2 domain containing inositol 5'-phosphatase (SHIP) was initially described as a 145 kD protein phosphorylated on tyrosines upon growth factor and cytokine stimulation. SHIP is predominately expressed in hematopoietic cells, and is a crucial negative regulator in the development of hematopoietic cells. To evaluate the role of the SHIP gene in human leukemogenesis, expression and mutation of SHIP gene in bone marrow and/or peripheral blood from 32 patients with acute myeloid leukemia (AML), 9 patients with acute lymphoblastic leukemia (ALL), as well as human hematopoietic cell lines were analyzed by reverse transcription-polymerase chain reaction (RT-PCR), single strand conformational polymorphism (SSCP) and sequencing. The RT-PCR showed that all samples expressed SHIP gene. Mutations of SHIP gene were detected in 7 out of 32 AML patients (22%) and one out of 9 ALL patients (12%). Interestingly, two missense mutations that had been observed in one AML patient at diagnosis disappeared after complete remission (CR). In addition, Akt phosphorylation was prolonged and increased following IL-3 stimulation in this patient sample. In conclusion, data of this study demonstrate the mutation of the SHIP gene in acute leukemia for the first time and suggest a possible role of the mutation of this gene in the development of acute leukemia. SHIP serves as a tumor suppressor by negatively regulating the PI3K/Akt signaling pathway in hematopoietic cells.

PMID: 15363123 [PubMed - indexed for MEDLINE]

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2: Zhonghua Xue Ye Xue Za Zhi. 2004 Jul;25(7):385-8. Related Articles, Links


[Mutation analysis of SHIP gene in acute leukemia]

[Article in Chinese]

Luo JM, Liu ZL, Hao HL, Wang FX, Dong ZR, Ryuzo O.

Department of Hematology, the Second Hospital of Hebei Medical University, Shijiazhuang 050000, China.

OBJECTIVE: The SH2 domain containing inositol 5'-phosphatase (SHIP) is predominately expressed in hematopoietic cells, and is a crucial negative regulator in the development of hematopoietic cells. This paper is to evaluate the role of the SHIP gene in human leukemogenesis. METHODS: Expression of SHIP gene in bone marrow and/or peripheral blood from 32 patients with acute myeloid leukemia (AML), 9 with acute lymphoblastic leukemia (ALL), as well as human hematopoietic cell lines was analyzed by reverse transcription-polymerase chain reaction (RT-PCR), single strand conformational polymorphism (SSCP) and DNA sequencing. RESULTS: RT-PCR showed that all samples expressed SHIP gene. Mutations of SHIP gene were detected in 7 (22%) of 32 AML patients and one (12%) of 9 ALL patients. Interestingly, two missense mutations that had been observed in a AML patient at diagnosis disappeared after complete remission (CR). In addition, in vitro Akt phosphorylation was prolonged and increased following IL-3 stimulation of this patient's cells. CONCLUSION: Our data demonstrate for the first time the mutation of SHIP gene in acute leukemia and suggest a possible role of the mutation of this gene in the development of acute leukemia. SHIP may serve as a tumor suppressor by negatively regulating the PI3K/Akt signaling pathway in hematopoietic cells.

PMID: 15355687 [PubMed - in process]




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