scispace - formally typeset
J

James N. Ingle

Researcher at Mayo Clinic

Publications -  403
Citations -  52917

James N. Ingle is an academic researcher from Mayo Clinic. The author has contributed to research in topics: Breast cancer & Tamoxifen. The author has an hindex of 82, co-authored 387 publications receiving 47883 citations. Previous affiliations of James N. Ingle include McMaster University & University of Rochester.

Papers
More filters
Journal ArticleDOI

A prospective, randomized controlled trial of megestrol acetate among high-risk patients with resected malignant melanoma.

TL;DR: A possible role for megestrol acetate as adjuvant therapy for selected patients with malignant melanoma is suggested, and the most noteworthy side effects were weight gain and impotence.
Journal ArticleDOI

Raf-1 oncogenic signaling is linked to activation of mesenchymal to epithelial transition pathway in metastatic breast cancer cells.

TL;DR: It is demonstrated for the first time that amplification of Raf/MEK/MAPK oncogenic signaling during tumor growth promotes the genesis of metastatic lesions from primary tumors by activating the mesenchymal to epithelial transition (MET) pathway, although the molecular mechanisms remain elusive.
Journal ArticleDOI

Randomized trial to evaluate the addition of tamoxifen to cyclophosphamide, 5-fluorouracil, prednisone adjuvant therapy in premenopausal women with node-positive breast cancer.

TL;DR: This study does not establish a significant advantage for the concurrent administration of tamoxifen with the CFP regimen, and the importance of examination of clinically important prognostic factors, even those not utilized in stratification, and consideration of these factors in covariate analysis if imbalances are present is clearly demonstrated.
Journal ArticleDOI

An optimized five-gene multi-platform predictor of hormone receptor negative and triple negative breast cancer metastatic risk

TL;DR: An optimized five-gene Integrated Cytokine Score (ICS) with multi-platform capability of predicting metastatic outcome from primary HRneg/Tneg tumors independent of nodal status, adjuvant chemotherapy use, and Tneg molecular subtype is derived.