Dr. McLane's research
groups
2004-2005
2005-2006

2006-2007

2004-2005: front row: Claire Zelinskas
('05), Jing
Tian (PhD graduate student), Apoorva
Srivastava ('05), back row: Xiaoming Zhang (research specialist), Carrie
Paquette-Straub (research associate, along with her soon-to-be born Rachel!),
Dr. McLane, Bryn
Werbos ('05)
2005-2006: front row: as in 2004-2005, with the addition of Dara Missan
('06, back row, far right) and Brett Hensley
('07, front far right). Collaborator Dr. Mary Beth Miele is next to Dr. McLane
in the front row.
2006-2007: Stephanie
DiRosato ('08), Carrie Paquette-Straub, Dr. McLane, Jing Tian
Cancer metastasis is the major obstacle to cancer cure. Melanoma is one of the most rapidly increasing types of cancer, and malignant melanoma is particularly aggressive in its ability to metastasize and the lack of any successful treatment. In 1990, I started working with a group of naturally occurring protein from viper venom, called DISINTEGRINS. Some of these proteins can be injected into a mouse along with melanoma cells and prevent the tumor cells from forming new colonies within the lungs.

The snake pictured above is Eristocophis macmahoni, which originates
from the deserts of southwestern Asian, and which produces a very unique
disintegrin, called eristostatin. This
disintegrin can inhibit melanoma cell lung colonization in a mouse model. The
mechanism by which it accomplishes this is still unknown. My research is looking
into the motifs within eristostatin's sequence which gives it the ability to
have this anti-cancer property. Undergraduate students (Alice Wong '03, Melissa
Kuchar '01) in my lab have described the receptors found on the surface of four
different types of melanoma cells1, and the effect of using mutated
forms of eristostatin in interactions with those melanoma cells2. Claire
Zelinskas ('05) and Apoorva Srivastava ('05) created a series of alanine
mutations within eristostatin's sequence and expressed these mutations as
recombinant fusion proteins. Bryn Werbo ('05)sinvestigated how
we can improve the recombinant protein yield by purifying inclusion
bodies. Jing Tian's graduate studies are focusing on characterizing
the recombinant proteins' interactions with 1205-LU, C8161, M24met and MV3
melanoma cells using confocal microscopy, flow cytometry and in vivo
hematogenous metastasis. In addition, she isl investigating whether eristostatin
is able to make the melanoma cells better targets for natural killer cells in
vivo.
Brett Hensley ('07) did the first studies ever on intracellular signalling within melanoma cells following eristostatin exposure. Dara Missan ('06) studied how melanoma cells can vary in their metastatic potential as well as their tumor suppressor and tumor promoter gene expression.
Stephanie DiRosato ('08) studyied how five groups of melanoma cells have their intracellular phosphorylation change when incubated with eristostatin.
Mollie Kostielney ('09) did cytotoxicity assays using NK cells and six types of melanoma cells. Alaa Mahmoud ('10) has continued those experiments with a flow cytometric method. Liana Sherrod ('10) did the first ever adhesion exepriments with atomic force microscopy.
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1Effect of the disintegrin eristostatin on hematogenous
metastasis in three models of human malignant melanoma. Poster #5911,
Proceedings of the American Association for Cancer Research 44: 1180, 2003.
2 McLane MA, Kuchar, MA, Brando C, Santoli D, Paquette-Straub CA,
Miele ME. New insights on disintegrin-receptor interactions: Eristostatin and
melanoma cells, Haemostasis 31: 3-6, 177-182, 2001.