Surgical injury enhances the expression of genes that mediate breast cancer metastasis to the lung.

Objective: This study was conducted to test the hypothesis that surgery induces changes at the expression level of genes implicated in metastasis, thus leading to accelerated postoperative metastatic tumor growth.

Summary Background Data: Surgical resection of the primary tumor is a necessary and effective treatment for breast cancer patients. However, studies from both animals and humans have shown that surgery potentiates the growth of minimal residual neoplastic disease.

The targeting of phosphoinositide-3 kinase attenuates pulmonary metastatic tumor growth following laparotomy.

Objective: We aimed to characterize a potential role for phosphatidylinositol 3-kinase (PI3k) in leading to accelerated postoperative metastatic tumor growth.

Background: PI3k enhances tumor cell survival in part by phosphorylating Akt and reducing apoptosis. Postoperatively, apoptosis is reduced within local recurrences and distant metastases.

Phosphoinositide 3-kinase accelerates postoperative tumor growth by inhibiting apoptosis and enhancing resistance to chemotherapy-induced apoptosis. Novel role for an old enemy.

Tumor removal remains the principal treatment modality in the management of solid tumors. The process of tumor removal may potentiate the resurgent growth of residual neoplastic tissue. Herein, we describe a novel murine model in which flank tumor cytoreduction is followed by accelerated local tumor recurrence.