i thought i'd post the HGSI release on their Hodgkins discovery. To my untrained eye, it supports the effect of the GNTA compound because it helps supports the ID of the protein. what do others think/
Human Genome Sciences Announces Advance in Hodgkin's Lymphoma
Discovery Opens Path to Similar Progress for Improved Diagnosis and Treatment of Hodgkin's Lymphoma, Other Diseases
ROCKVILLE, Md., July 14 /PRNewswire/ -- Human Genome Sciences, Inc.
(Nasdaq: HGSI) confirmed today that in conjunction with an international team
of scientists, they have characterized the cell that causes Hodgkin's
Lymphoma. The discovery opens new hope for early diagnosis and treatment of
the disease, which affects more than 58,000 people, worldwide, per year.
In making the discovery, the scientists from HGSI, Georgetown University
Medical School, the National Cancer Institute, the National Institutes of
Health and the University of Milano-Bicocca, in Italy, applied powerful new
methods to a single cancer cell to reveal that the Reed-Sternberg cell, the
cause of the disease, originates in B cells, a type of immune cell that
normally produces antibodies. The discovery is described in the cover story
of the July 15, 1999 issue of Blood. The article may be accessed at the
journal's web site bloodjournal.org.
The abnormal Reed-Sternberg cell of Hodgkin's Lymphoma has long been
recognized to be responsible for the disease. Characterization of the cell
itself is difficult as fewer than one in one thousand cells of the lymphoma
are cancer cells themselves. The great majority of cells in the lymphoma are
normal immune cells that react to the few cancer cells present in the tumor.
The origin of the Reed-Sternberg cell has been debated ever since the cell was
discovered a century ago. Two advances made the solution of this mystery
possible. First, micro-dissection methods made it possible to isolate the
Reed-Sternberg cells from the study patients' tumor tissues. Second, ultra
high-throughput sequence analysis was used to identify the genes present in
the cells. The study determined a total of more than 11 million nucleotide
sequences, representing 27,000 genes. Then, powerful computer programs were
used to compare these genes of the Reed-Sternberg cell with those used in
normal human cells. The results were clear.
The gene usage of the Reed-Sternberg cell is very similar to that of the
antibody producing B-cell and is distinctly different from all other cells of
the immune system and those found in other tissues of the human body.
The study also provides a clue to why the Reed-Sternberg cells cause
cancer. Normal cells of the immune system contain a self-destruct system that
causes them to die when they begin to grow out of control. Critical
components of the self-destruct system, notably the Rb gene as well as others,
are missing in the Reed-Sternberg cell.
A surprise finding of the study is the relatively high concentration of a
gene that has heretofore been associated with melanomas only -- the melanoma
associated tumor antigen MAGE-4a. It is possible that the MAGE-4a and other
genes specifically over expressed by the Reed-Sternberg cells identified in
this study can be used for early detection and as targets for improved
treatment of the disease.
Jeffrey Cossman, M.D., of Georgetown University Medical School, first
author of the study said, "This work answers an important and hotly debated
question in cancer research, the identity of the Reed-Sternberg cell of
Hodgkin's Lymphoma. The methods used for the analysis of genes expressed in a
single cancer cell are a technical tour-de-force. The work is important not
only because it provides new hope for the diagnosis and treatment of Hodgkin's
Lymphoma, but also because it demonstrates the combined power of two new
methodologies, single cell analysis and ultra high-throughput gene sequencing
to answer complex medical questions. I believe this work opens a new chapter
in the study of pathophysiology of disease and that such studies will have a
profound impact on medical science and the search for new ways to understand,
treat and cure disease."
Craig Rosen, Ph.D., Senior Vice President of Research and Development at
Human Genome Sciences and another author of the paper, said, "I believe that
this work validates the systematic approach to the study of disease by ultra
high-throughput analysis of expressed genes. For this study we determined the
sequence of more than 11 million nucleotides comprising more than 27,000
genes. The long-standing question of the nature of the cell responsible for
Hodgkin's Lymphoma was quickly solved using this approach. We have used
similar methods to identify genes uniquely used by a variety of cancers
including prostate cancer, breast cancer, colon cancer and lung cancer. I
believe these studies will contribute to substantial improvement of the
diagnosis, treatment, and hopefully cure of these diseases."
William A. Haseltine, Ph.D., Chairman and Chief Executive Officer of Human
Genome Sciences, Inc. said, "Human Genome Sciences is developing a specific
expertise in cancer, finding new ways to detect and treat this disease. Two
of the three HGS drugs now in clinical trials are cancer drugs -- MPIF-1, to
alleviate cancer-induced damage to the blood forming tissues, and KGF-2 to
treat damage to mucous membranes (mucositis) induced by chemo and radiation
therapy. In addition, last week's announcement of the discovery of B-
lymphocyte stimulator protein, or BLyS which is a human growth factor specific
for B cells, may lead to better ways to treat B cell lymphoma. We hope to
have BLyS in human clinical trials early in 2000. HGSI already is
manufacturing all four of these genomic drug products. Additionally, we have
used methods similar to those described in the study of Hodgkin's Lymphoma to
discover new genes that are uniquely expressed in most common cancers
including cancers of the lung, prostate, colon, ovary and breast."
The data and analysis that supports this study are available on the World
Wide Web at hodgkins.georgetown.edu under the table entitled, "Hodgkin's
Cells/Tissues" via entire database.
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