Mutational analysis of the PTEN/MMAC1 gene in non-Hodgkin’s lymphoma

Nakahara, Yoko; Nagai, Hirokazu; Kinoshita, Takafumi; Uchida, Toshiki; Hatano, Sonoko; Murate, Takashi; Saito, Hidehiko

doi:10.1038/sj.leu.2401099

Cited by 51 publications

(25 citation statements)

References 15 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…The DNA mismatch repair gene MSH2 may have importance in AML (Zhu et al, 1999). Inactivations of PTEN have been observed in a small subset of cutaneous T-cell lymphomas (Scarisbrick et al, 2000) and other NHL (Nakahara et al, 1998). Disruption of the TGFb signalling pathway by mutations of the SMA-and MAD-related protein 4 (SMAD4) can be found in AML (Imai et al, 2001).…”

Section: Discussionmentioning

confidence: 99%

Tumor suppressor genes in normal and malignant hematopoiesis

2002

View full text Add to dashboard Cite

Section: Discussionmentioning

confidence: 99%

Tumor suppressor genes in normal and malignant hematopoiesis

2002

View full text Add to dashboard Cite

“…60,253 Mutations and hemizygous deletions of PTEN have been frequently detected in AML and non-Hodgkin's Lymphoma (NHL). 254,255 PTEN inactivation is believed to occur frequently in certain hematopoietic neoplasms. Many different genetic mechanisms can result in functional inactivation or silencing of PTEN (see below).…”

Section: Roles Of the Pi3k/pten/akt/mtor Pathway In Leukemiamentioning

confidence: 99%

Contributions of the Raf/MEK/ERK, PI3K/PTEN/Akt/mTOR and Jak/STAT pathways to leukemia

et al. 2008

View full text Add to dashboard Cite

Mutations and chromosomal translocations occur in leukemic cells that result in elevated expression or constitutive activation of various growth factor receptors and downstream kinases. The Raf/MEK/ERK, PI3K/PTEN/Akt/mTOR and Jak/STAT pathways are often activated by mutations in upstream genes. The Raf/MEK/ERK and PI3K/PTEN/Akt/mTOR pathways are regulated by upstream Ras that is frequently mutated in human cancer. Recently, it has been observed that the FLT-3 and Jak kinases and the phosphatase and tensin homologue deleted on chromosome 10 ( PTEN) phosphatase are also frequently mutated or their expression is altered in certain hematopoietic neoplasms. Many of the events elicited by the Raf/MEK/ERK, PI3K/PTEN/Akt/mTOR and Jak/STAT pathways have direct effects on survival pathways. Aberrant regulation of the survival pathways can contribute to uncontrolled cell growth and lead to leukemia. In this review, we describe the Raf/MEK/ERK, PI3K/PTEN/Akt/mTOR and Jak/STAT signaling cascades and summarize recent data regarding the regulation and mutation status of these pathways and their involvement in leukemia

show abstract

“…PTEN mutations also occur in human B cell malignancies (Gronbaek et al, 1998;Hyun et al, 2000;Nakahara et al, 1998). We generated B cell-specific Pten-deficient mice (bPten flox/flox mice) by crossing Pten flox/-mice to CD19-Cre transgenic mice (Suzuki et al, in revison).…”

Section: Role Of Pten In B Cellsmentioning

confidence: 99%

Physiological Functions of Pten in Mouse Tissues.

Kishimoto

Hamada

Saunders

et al. 2003

Cell Struct. Funct.

107

View full text Add to dashboard Cite

ABSTRACT. PTEN is a tumor suppressor gene mutated in many human sporadic cancers and in hereditary cancer syndromes such as Cowden disease, Bannayan-Zonana syndrome and Lhermitte-Duclos disease. The major substrate of PTEN is PIP3, a second messenger molecule produced following PI3K activation induced by variety of stimuli. PIP3 activates the serine-threonine kinase PKB/Akt which is involved in anti-apoptosis, proliferation and oncogenesis. In mice, heterozygosity for a null mutation of Pten (Pten +/-mice) frequently leads to the development of a variety of cancers and autoimmune disease. Homozygosity for the null mutation (Pten -/-mice) results in early embryonic lethality, precluding the functional analysis of Pten in various organs. To investigate the physiological functions of Pten in viable mice, various tissue-specific Pten mutations have been generated using the Cre-loxP system. This review will summarize the phenotypes of conditional mutant mice lacking Pten function in specific tissues, and discuss how these phenotypes relate to the physiological roles of Pten in various organ systems.

show abstract

Mutational analysis of the PTEN/MMAC1 gene in non-Hodgkin’s lymphoma

Cited by 51 publications

References 15 publications

Tumor suppressor genes in normal and malignant hematopoiesis

Tumor suppressor genes in normal and malignant hematopoiesis

Contributions of the Raf/MEK/ERK, PI3K/PTEN/Akt/mTOR and Jak/STAT pathways to leukemia

Physiological Functions of Pten in Mouse Tissues.

Contact Info

Product

Resources

About