June Biedler

She received a Ph.D. degree from Cornell University Graduate school of Medical Sciences in 1959 on "Chromosomal Heterogeneity and Tumor Producing Capacity of Mouse Sarcoma: Isolation of Five single Cell Clones in vitro .

Cornelius Rhoads, the director of the institute, had assembled a group of medical researchers to find drugs that could inhibit growth of cancer cells.

Biedler, working in Burchenal's laboratory as a technical assistant, published her first paper in 1950 on effect of 4-amino-N10 methyl-pteroylglutamic acid on the leukocytes of the normal and leukemic mouse.

Her sponsor John Biesele, another of Rhoads' recruits, was a pioneer in the fields of mammalian cell culture and cytogenetic analysis [8] Biedler spent a postdoctoral year in the laboratory of Georges Barski at L'Institut Gustave-Roussy (Villejuif, France) studying cell-cell hybridization techniques.

[6] She also held the rank Professor at the Cornell-Well Graduate School of Medical Sciences; She worked at SKMCC for 35 years until her retirement in 1994.

John J. Biesele, who became Biedler's thesis advisor, found unique chromosomal alterations in mouse leukemia L1210 sublines selected with various anticancer drugs.

Using her skills in cytogenetics, Biedler, along with Dr. Dorris Hutchison, found that as resistance to methotrexate developed, unique patterns of chromosomal abnormalities were observed [11][12] In 1976 Biedler and Barbara Spengler discovered the presence of an unusual banding pattern in chromosome 2 of cells that had been made resistant to methotrexate or other anti-folate drugs.

[16] This study directly led to the concept of multi-drug resistance being mediated by changes in plasma membrane proteins that transport drugs.

[18] In addition, Biedler found that important phenotypic changes including altered ganglioside composition and increased EGF receptor number,[19] characterized multi-drug resistant cells.

[20][21] The group postulated that these regions represented areas of duplicate genes that encode proteins important in the malignant phenotype.

[23] Biedler's group also noted the presence of cytoplasmic chromosomal fragments "double minutes" in neuroblastoma cell lines were the products of gene amplification.