Nm23‐transfected MDA‐mB‐435 human breast carcinoma cells form tumors with altered phospholipid metabolism and pH: A 31P nuclear magnetic resonance study in vivo and in vitro

Bhujwalla, Zaver M.; Aboagye, Eric O.; Gillies, Robert J.; Chacko, V. P.; Mendola, Charmaine E.; Backer, Joseph M.

doi:10.1002/(sici)1522-2594(199905)41:5<897::aid-mrm7>3.3.co;2-k

Cited by 37 publications

(52 citation statements)

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“…22,59 Additional functions of two known isoforms, namely Nm23-H1 and Nm23-H2, are independent of their NDP kinase activity. 2,17 They also form homo-and heterohexamers by randomly associating with each other. 9 Nm23-H1 expression has been shown to be localized primarily in the cytoplasm, whereas Nm23-H2 was shown to be localized in the nucleus, have DNA binding capabilities 50 and can interact with the human telomeric repeat binding factor protein (TRF1).…”

Section: Introductionmentioning

confidence: 99%

The suppressor of metastasis Nm23-H1 interacts with the Cdc42 Rho family member and the pleckstrin homology domain of oncoprotein Dbl-1 to suppress cell migration

Murakami

Meneses²,

Lan³

et al. 2008

Cancer Biology & Therapy

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Section: Introductionmentioning

confidence: 99%

The suppressor of metastasis Nm23-H1 interacts with the Cdc42 Rho family member and the pleckstrin homology domain of oncoprotein Dbl-1 to suppress cell migration

Murakami

Meneses²,

Lan³

et al. 2008

Cancer Biology & Therapy

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“…Reduced levels of nm23 family proteins in the primary tumour have been reported to correlate with more aggressive phenotype in breast cancer patients (Galani, Sgouros et al 2002;Terasaki-Fukuzawa, Kijima et al 2002;Steeg, Ouatas et al 2003;Peihong and Perry 2007), although conflicting results have also been presented (Charpin, Garcia et al 1998;Belev, Aleric et al 2002;Sgouros, Galani et al 2007). The results seen in mouse models are more straightforward, where breast cancer cells with low expression of nm23 are more metastatic than those with high levels (Leone, Flatow et al 1993;Bhujwalla, Aboagye et al 1999;Tseng, Vicent et al 2001). In vitro models have revealed that nm23 acts by reducing breast cancer cell motility and invasiveness (MacDonald, Freije et al 1996;Russell, Pedersen et al 1998;Steeg, Ouatas et al 2003;Horak, Lee et al 2007).…”

Section: Metastasis Suppressor Genesmentioning

confidence: 99%

Breast Cancer Metastasis: Advances Through the Use of In Vitro Co-Culture Model Systems

Magliocco¹,

Egan²

2011

Breast Cancer - Focusing Tumor Microenvironment, Stem Cells and Metastasis

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“…There are now eleven transfection papers that confirm nm23 as a metastasis suppressor. [2][3][4][5][6][7][8][9][10][11][12] The field has expanded to ten or so known metastasis suppressor genes. [13][14][15] It's a collegial group of investigators who help each other with strategies and provide moral support.…”

Section: Biographical Informationmentioning

confidence: 99%

The Gift of Absorption Patricia S. Steeg

Steeg¹

2004

Cancer Biology & Therapy

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The Gift of Absorption I live, eat, sleep, research. I love my family, read voraciously and have a few hobbies. But most nights after dinner, I choose to go upstairs and log onto email to see what's new. I could go out into the backyard and plant another rosebush, but its too shaded and the bushes don't do well anyway. In earlier phases of my career when my kids were young, time demands were different. Now the kids are almost grown and I have this gift of freedom which I choose to spend hunched over a computer. To be absorbed in one's work is a blessing; how many people on this earth are bored by what they do? To completely jump into a project and lose track of time and surroundings are gifts. The subject might be an experiment that a postdoc is working on or a concept with which I have been struggling. Or it might be the problem of how to get government research to work a bit more efficiently. Minor successes in any of these areas are very satisfying. As one's career progresses, life is increasingly a series of meetings, and time to be absorbed in science is at a premium. BIOGRAPHICAL INFORMATIONI am from a working class part of Baltimore and the first of my family to attend college. I attended Towson State University in Baltimore, with a BS in Biology. My classes were split between field biology and cell biology. After graduation, it was just a matter of what type of job came along first. For three years I worked as an environmental consultant for engineering firms, doing environmental impact statements for roads, strip mines, parks. But the degree to which decisions were made politically angered me and I realized that this was not a good career. Plan B was to go back to school and see what I could contribute. Cancer was always on my mind. My cousin Cindy, a year older than I, died of oral cancer while I was in college. She had a "toothache" at 16, which turned into never-ending radiation, surgery and misery. I vowed to do something about it, and that vow helped to shape my future. My Ph.D. research was in cellular immunology at the University of Maryland under the direction of Joe Oppenheim, then at the National Institute for Dental Research (NIDR) at NIH. A quick postdoc with George Martin was completed at NIDR, and then a move to the Laboratory of Pathology at the National Cancer Institute (NCI). I've been there ever since.George was interested in basement membranes, which brought up the subject of tumor cell invasion and metastasis. How tumor cells metastasized seemed to be a question worth my effort. I modeled my work after a paper, in which differential colony hybridization was used to identify genes over-and under-expressed between serum-starved and serum-fed cells. Can we do the same between nonmetastatic and metastatic tumor cells? Expecting to find genes that were turned on in metastasis such as proteases and adhesion molecules, I was bewildered when the best candidate was turned off in the highly metastatic cell lines. The discovery of Rb as a tumor suppressor stimulated my thinking: if genes could ...

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Nm23‐transfected MDA‐mB‐435 human breast carcinoma cells form tumors with altered phospholipid metabolism and pH: A 31P nuclear magnetic resonance study in vivo and in vitro

Cited by 37 publications

References 0 publications

The suppressor of metastasis Nm23-H1 interacts with the Cdc42 Rho family member and the pleckstrin homology domain of oncoprotein Dbl-1 to suppress cell migration

The suppressor of metastasis Nm23-H1 interacts with the Cdc42 Rho family member and the pleckstrin homology domain of oncoprotein Dbl-1 to suppress cell migration

Breast Cancer Metastasis: Advances Through the Use of In Vitro Co-Culture Model Systems

The Gift of Absorption Patricia S. Steeg

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