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) is studying how
five groups of melanoma cells have their intracellular phosphorylation
change when incubated with eristostatin.
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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.