Liposome-delivered angiostatin strongly inhibits tumor growth and metastatization in a transgenic model of spontaneous breast cancer.

نویسندگان

  • M G Sacco
  • M Caniatti
  • E M Catò
  • A Frattini
  • G Chiesa
  • R Ceruti
  • F Adorni
  • L Zecca
  • E Scanziani
  • P Vezzoni
چکیده

The possibility to inhibit tumor growth by interfering with the formation of new vessels, which most neoplasias depend on, has recently raised considerable interest. An angiogenic switch, in which proliferating cells acquire the ability to direct new vessel formation, is thought to be an early step in the natural history of solid tumors. Using a transgenic model of breast cancer, which shows many similarities to its human counterpart, including ability to metastasize, we targeted angiostatin production to an early stage of tumor formation. Liposome-delivered angiostatin considerably delayed primary tumor growth and, more importantly, inhibited the appearance of lung metastases. These findings can be relevant to the design of therapeutic intervention in humans.

برای دانلود متن کامل این مقاله و بیش از 32 میلیون مقاله دیگر ابتدا ثبت نام کنید

ثبت نام

اگر عضو سایت هستید لطفا وارد حساب کاربری خود شوید

منابع مشابه

Effects of Enoxaparin Emulsion on Dimethylbenzanthracene-induced Breast Cancer in Female Rats

Background : Enoxaparin is an anticoagulant medication. Anticoagulation inhibits tumor cell–mediated release of angiogenic proteins and diminishes angiogenic response. Angiogenesis is an important event in various cancers such as breast cancer. Angiogenesis provide oxygen and nutrients to tumor cells and causes tumor progression. The aim of the present study was to evaluate the anti-angio...

متن کامل

An Agent- based Modeling for Breast Tissue Simulation and the Growth and Spread of Tumor in Various Breast Cancer States

Introduction: Breast cancer is a cancer that is caused by abnormal growth of breast cells. Modeling  and simulation of the growth and treatment of breast cancer, along with providing the possibility of doing experiments and research, can reduce the time and cost of treatment by predicting some cases. The purpose of the present research was to develop an agent-based model for the simulation of b...

متن کامل

An Agent- based Modeling for Breast Tissue Simulation and the Growth and Spread of Tumor in Various Breast Cancer States

Introduction: Breast cancer is a cancer that is caused by abnormal growth of breast cells. Modeling  and simulation of the growth and treatment of breast cancer, along with providing the possibility of doing experiments and research, can reduce the time and cost of treatment by predicting some cases. The purpose of the present research was to develop an agent-based model for the simulation of b...

متن کامل

Long non-coding RNA FOXO1 inhibits lung cancer cell growth through down-regulating PI3K/AKT signaling pathway

Objective(s): Lung cancer is one of the most common malignant tumors, which seriously threatens the health and life of the people. Recently, a novel long non-coding RNA (lncRNA) termed lncFOXO1 was found and investigated in breast cancer. However, the effect of lncFOXO1 on lung cancer is still ambiguous. The current study aimed to uncover the functions of lncFOXO1 in l...

متن کامل

Treatment of Murine Tumor Models of Breast Adenocarcinoma by Continuous Dual-Frequency Ultrasound

Introduction: Acoustic transient cavitation is the primary mechanism of sonochemical reaction and has potential use for tumor treatment. In this study, the in vivo anti-tumor effect of simultaneous dual-frequency ultrasound at low-level intensity (ISATA < 6 W/cm2) was investigated in a spontaneous murine model of breast adenocarcinoma in Balb/c mice. Materials and Methods: Forty tumor bearing m...

متن کامل

ذخیره در منابع من


  با ذخیره ی این منبع در منابع من، دسترسی به آن را برای استفاده های بعدی آسان تر کنید

برای دانلود متن کامل این مقاله و بیش از 32 میلیون مقاله دیگر ابتدا ثبت نام کنید

ثبت نام

اگر عضو سایت هستید لطفا وارد حساب کاربری خود شوید

عنوان ژورنال:
  • Cancer research

دوره 60 10  شماره 

صفحات  -

تاریخ انتشار 2000