ASH News Daily 2013 - Day 1 - (Page A1)
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11:15 a.m. - 12:15 p.m.
Grassroots Network Lunch
Riverbend Ballroom, New Orleans Downtown
Marriott at the Convention Center
11:15 a.m. - 12:15 p.m.
How I Treat: Bringing Science to Clinical
11:15 a.m. - 12:15 p.m.
Meet the Scientist
12:30 - 1:30 p.m.
Speaker: Clara Camaschella, MD
Topic: Iron and Hepcidin
2:00 - 3:00 p.m.
Special Symposium: Clinical Practice
Room 393-396, Convention Center
4:00 - 5:30 p.m.
Special Scientific Symposium: Approaches
for Inhibiting "Undruggable"
Targets in Cancer
New Orleans Theater C, Convention Center
5:30 - 7:30 p.m.
Poster Halls E and G
Dr. Janis Abkowitz, ASH President, welcomes attendees and highlights special
programming and new meeting offerings.
Who Puts the Quality in Quality?
BY JULIE KANTER, MD
uality improvement" has become
a commonplace term
in medicine today. New
Medicare programs and private insurance
companies have tied measurements
of quality to monetary
and professional reimbursement.
Quality improvement projects are
required as part of maintenance of
certification (licensure) in many disciplines.
Thus, with all of this discussion,
it would seem that "quality"
should be easily defined, implemented,
and measured. However,
this is not necessarily the case.
This afternoon from 2:00 to 3:30
p.m., the issues surrounding quality-of-care
implementation will be
discussed during the Special Symposium
on Quality: Clinical Practice
Guidelines. This session, which will
take place in Room 393-396 in the
Ernest N. Morial Convention Center,
will review how clinical practice
guidelines can be developed for
blood disorders to both optimize
quality of care for patients and satisfy
ACO. The committee chairs, Dr.
Adam Cuker of the University of
Pennsylvania, and Dr. Mary Cushman
of the University of Vermont,
have assembled a program in which
speakers will define the current
challenges facing the field of guideline
development in a manner that is
both methodologically rigorous and
Dr. Holger Schünemann of McMaster
University, Hamilton, ON,
will begin the symposium with an
explanation of the history of the development
of clinical practice guidelines
and on the evolution of guideline
methodology. Having served
»» QUALITY Page A-16
The 2013 Ham-Wasserman Lecture -
BY MARK M. UDDEN, MD
IN THIS SECTION
-"Iron, cold Iron ... is ruler of them
all." Iron is critical to mitochondrial
function and heme iron is necessary
to transport oxygen; however,
iron can be a loose cannon generating
unwanted oxidation. It is a ruler
that requires protective custody by
chaperones such as transferrin and
the storage protein ferritin and careful
regulation of its entrance and exit
from the circulating iron pool.
This year, Dr. Clara Camaschella
will offer us a vision of the brave
new world of iron metabolism in her
lecture Iron and Hepcidin: A Story of
Recycling and Balance. The lecture
will be held today in Hall F in the
Ernest N. Morial Convention Center
Iron in the Balance
from 12:30 to 1:30 p.m. As Dr. Camaschella
will show us, it turns out
that iron has its own master since it
is ruled by the hepcidin ferroportin
axis that regulates flux of iron from
enterocytes and macrophages to the
circulating iron pool. Iron availability
must be closely regulated to avoid
excess or deficiency. To achieve this,
there is a delicate balance between
hepcidin degradation and upregulation.
Hepcidin degrades the iron exporter
ferroportin thereby inhibiting
iron flux to the plasma, and hepcidin
upregulation is linked to an important
signaling cascade in which
bone morphogenic protein receptor
(BMPR) complex activates SMAD,
which then upregulates hepcidin.
When BMP is diminished, as it is in
hemochromatosis types 1, 2, and 3,
hepcidin is reduced and iron accumulates
because ferroportin is un-
udyard Kipling famously
observed that of the metals
gold, silver, and copper
checked. For effective erythropoiesis,
an adequate amount of iron must be
provided, and hepcidin must be suppressed
when there is a call for more
red cells. A desirable increase in iron
availability occurs in iron deficiency
and during hypoxia, and an unwanted
iron overload occurs in thalassemia
because hepcidin is typically
suppressed in these states.
Another area of interest that Dr.
Camaschalla will discuss is her
lab's investigation of the role of TMPRSS6,
a serum protease that inhibits
hepcidin. Matriptase-2, a serine
protease encoded by TMPRSS6, is
mutated in the Mask mouse, which
suffers from a microcytic anemia,
high hepcidin, and inability to absorb
oral iron. Thus, TMPRSS6 is the
key to understanding how hypoxia
»» HAM-WASSERMAN Page A-16
Table of Contents for the Digital Edition of ASH News Daily 2013 - Day 1
Table of Contents
ASH News Daily 2013 - Day 1