PMID: 15388892Sep 25, 2004Paper

Comparison of vitamin E derivatives alpha-TEA and VES in reduction of mouse mammary tumor burden and metastasis

Experimental Biology and Medicine
Karla A LawsonK Kline

Abstract

A novel nonhydrolyzable ether derivative of RRR-alpha-tocopherol, RRR-alpha-tocopherol ether acetic acid analog [2,5,7,8-tetramethyl-2R-(4R,8R,12-trimethyltridecyl)chroman-6-yloxyacetic acid (alpha-TEA)], and a hydrolyzable ester derivative RRR-alpha-tocopheryl succinate (vitamin E succinate; VES) inhibited BALB/c mouse 66cl-4-GFP mammary tumor cell growth in vitro and in vivo. Treatment of 66cl-4-GFP cells in culture with alpha-TEA or VES induced dose-dependent DNA synthesis arrest and apoptosis and inhibited colony formation. Liposomal formulations of alpha-TEA delivered orally or by aerosol significantly reduced subcutaneous 66cl-4-GFP tumor burden and metastasis to lung and lymph nodes. Liposomal formulations of VES delivered by aerosol significantly reduced tumor burden and lung metastasis, but not lymph node metastasis. Unlike alpha-TEA, VES was ineffective in reducing tumor burden and metastasis to lungs and lymph nodes when administered orally. Analyses of tumor sections showed that alpha-TEA delivered by either method significantly reduced tumor cell proliferation as measured by Ki67, and increased apoptosis as measured by terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick-end labeling (TUNEL), whereas VES...Continue Reading

References

Aug 24, 1999·Cancer Chemotherapy and Pharmacology·V KnightB E Gilbert
Aug 18, 2000·The Journal of Surgical Research·M P Malafa, L T Neitzel
Jan 5, 2001·British Journal of Cancer·J NeuzilC Weber
Feb 7, 2001·FASEB Journal : Official Publication of the Federation of American Societies for Experimental Biology·J NeuzilC Weber
Feb 24, 2001·The Journal of Nutrition·K KlineB G Sanders
Jul 20, 2001·Free Radical Biology & Medicine·M F AndreasenM T Garcia-Conesa
Nov 21, 2001·Journal of Agricultural and Food Chemistry·M F AndreasenM T Garcia-Conesa
Jan 29, 2002·Surgery·Mokenge P MalafaMichele King
Aug 15, 2002·The Journal of Surgical Research·Kevin T BarnettMokenge P Malafa
Nov 1, 2003·Journal of Mammary Gland Biology and Neoplasia·Kimberly KlineBob G Sanders

❮ Previous
Next ❯

Citations

Jul 26, 2005·Rapid Communications in Mass Spectrometry : RCM·Zeyad A Al-Talla, Luke T Tolley
May 31, 2008·International Journal of Cancer. Journal International Du Cancer·Constantina ConstantinouAndreas I Constantinou
Dec 17, 2008·Molecular Nutrition & Food Research·Yan ZhaoKun Wu
Jan 15, 2011·Breast Cancer Research : BCR·Tobias HahnEmmanuel T Akporiaye
Jul 26, 2005·Cancer Immunology, Immunotherapy : CII·Lalitha V RamanathapuramEmmanuel T Akporiaye
Dec 25, 2013·Nutrition and Cancer·Aracely Angulo-MolinaJesús Hernández
Jul 13, 2006·Molecular Nutrition & Food Research·Xiu-Fang WangJiri Neuzil
Jul 20, 2006·Apoptosis : an International Journal on Programmed Cell Death·Weiping YuKimberly Kline
Jun 3, 2005·Current Opinion in Clinical Nutrition and Metabolic Care·Christopher A Jolly
Apr 3, 2008·Molecular Nutrition & Food Research·Weiping YuKimberly Kline
May 15, 2010·Nature Reviews. Drug Discovery·Simone FuldaGuido Kroemer
Oct 12, 2007·Nutrition and Cancer·Nanjoo SuhHarold L Newmark
Feb 4, 2009·Clinical Cancer Research : an Official Journal of the American Association for Cancer Research·Jing NiShuyuan Yeh

❮ Previous
Next ❯

Related Concepts

Related Feeds

Cancer Cell Invasion: Nanomedicine

Nanomedicine is a promising alternative for cancer detection and therapy that utilizes nanoparticles, such as liposomes. Nanoparticles can potentially target cancer cell invasion and metastasis. Discover the latest research on Cancer Cell Invasion: Nanomedicine here.

Apoptosis in Cancer

Apoptosis is an important mechanism in cancer. By evading apoptosis, tumors can continue to grow without regulation and metastasize systemically. Many therapies are evaluating the use of pro-apoptotic activation to eliminate cancer growth. Here is the latest research on apoptosis in cancer.

Apoptosis

Apoptosis is a specific process that leads to programmed cell death through the activation of an evolutionary conserved intracellular pathway leading to pathognomic cellular changes distinct from cellular necrosis