Tarceva (erlotinib) New chemo

Here is some of the info I found online about this drug.

Check out this article where they talk about Her3 and Her4??  Will that be one of our (TN) new receptors?

First Article

http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=pmc549180

Second Article

 Sensitivity of breast cancer cells to erlotinib depends on cyclin-dependent kinase 2 activity

Fumiyuki Yamasaki^1,2,4, Dongwei Zhang^1,2, Chandra Bartholomeusz^1,2, Tamotsu Sudo^1,2, Gabriel N. Hortobagyi³, Kaoru Kurisu⁴ and Naoto T. Ueno^1,2,3

¹ Breast Cancer Translational Research Laboratory and Departments of ² Stem Cell Transplantation and Cellular Therapy and ³ Breast Medical Oncology, The University of Texas M. D. Anderson Cancer Center, Houston, Texas and ⁴ Department of Neurosurgery, Graduate School of Biomedical Sciences, Hiroshima University, Hiroshima, Japan

Requests for reprints: Naoto T. Ueno, Department of Stem Cell Transplantation and Cellular Therapy, The University of Texas M. D. Anderson Cancer Center, 1515 Holcombe Boulevard, Unit 448, Houston, TX 77030-4009. Phone: 713-792-8754; Fax: 713-794-4747. E-mail: nueno@mdanderson.org

Abstract

Inhibitors of epidermal growth factor receptor (EGFR) tyrosinekinases, such as erlotinib and gefitinib, have not been veryeffective in the treatment of breast cancer although many breastcancer cells express EGFR. To address this apparent paradox,we examined possible predictors of the sensitivity of 10 breastcancer cell lines to erlotinib in light of cyclin-dependentkinase 2 (CDK2), considered the farthest downstream kinase thatcontrols cell cycling in the EGFR signaling pathway. Expressionof EGFR and HER2 were not associated with sensitivity to erlotinib.Expression of phosphorylated (p-)tyrosine, p-Akt, phosphorylatedextracellular signal-regulated kinase (p-ERK) 1/ERK2 (p42/p44),and p27 after treatment of erlotinib was not associated witherlotinib sensitivity. However, suppression of CDK2 activityafter erlotinib treatment correlated with erlotinib sensitivity(P < 0.0001). Restoration of CDK2 activity partially restoredproliferation and induced erlotinib resistance in erlotinib-sensitivecell lines, indicating that sensitivity to erlotinib in thesebreast cancer cells depends, at least in part, on CDK2 activity.p27, an inhibitor of CDK2, was not translocated into the nucleusin erlotinib-resistant cell lines. Knocking down p27 proteinpartially blocked erlotinib-induced cell death and cell cyclearrest. These findings indicate that the ability of erlotinibto suppress CDK2 activity is critical for cellular sensitivityto erlotinib, regardless of EGFR expression level, and thatthe presence of p27 in the cytoplasm also participates in erlotinibresistance. [Mol Cancer Ther 2007;6(8):2168-77

Third Article

Erlotinib is a new drug that is used to treat non-small cell lung cancer and pancreatic cancer. It is also being studied for use in other cancers, including breast cancer.

Approved by the FDA in November 2004, Erlotinib is one of a new group of drugs that target tiny flaws in the cell's communication system. Many cells have receptors on their surfaces for epidermal growth factor (EGF), which is a protein produced by the body that induces growth and multiplication of cells. This protein causes an enzyme called tyrosine kinase to become active within the cells. Erlotinib blocks the cancer cell from getting the message that tells the cell to grow and divide, and the cells stop growing. Doctors have begun to prescribe Erlotinib - in combination with gemcitabine, a standard chemothrapy - for patients with metastatic or locally advanced non-small cell lung cancer who have failed at least one previous round of chemotherapy, and for patients with pancreatic cancer.

A prescription drug, Erlotinib comes in pill form and is taken orally with water at least an hour or two before eating.