Subject: psoriasis
Semin Oncol 1998 Aug;25(4 Suppl 10):31-6
Phase I trials of dexrazoxane and other potential applications for the agent.
Von Hoff DD
Institute for Drug Development, Cancer Therapy & Research Center, and
the Department of Medicine, The University of Texas Health Science
Center at San Antonio, 78245, USA.
The clinical development of dexrazoxane (DEX; ICRF-187; Zinecard,
Pharmacia and Upjohn, Kalamazoo, MI) was originally begun using it as
an antineoplastic agent. It had a unique mechanism of action and
activity in a variety of in vitro and in vivo models. Phase I trials
with the agent began in January 1979. The phase I trials indicated
that DEX could be safely administered, with leukopenia and
thrombocytopenia being the dose-limiting toxicities, on a number of
different schedules of administration. Some hints of antitumor
activity were also noted. In the phase I studies it was also noted,
based on the chelating abilities of DEX, that the compound caused
marked increases in urine clearance of iron and zinc in patients
receiving the agent. That information, plus the information being
generated in preclinical studies that DEX could protect against the
cardiotoxicity induced by anthracyclines (through a decrease in free
radical formation), led to the use of DEX as a cardioprotective agent
(as thoroughly discussed in this supplement). However, in addition to
working as a cardioprotective agent, DEX has other potential
applications that are outlined below and include (1) treatment of
patients with acquired immunodeficiency syndrome-related Kaposi's
sarcoma, based on its activity as an angiogenesis inhibitor; (2)
enhancement of the effects of cisplatin, based on its ability to
increase the antiproliferative effects of cisplatin on human ovarian
cancer cells; (3) use for treatment of iron overload states in
patients who are allergic to deferoxamine; (4) treatment of patients
with psoriasis; (5) protection from hyperoxic effects on the lungs;
(6) protection from bleomycin-induced pulmonary fibrosis; (7)
attenuation of acetaminophen-induced hepatotoxicity; (8) prevention of
mucositis; and (9) other applications. Clearly, there should be
additional investigations to maximize the usefulness of the very
interesting DEX molecule.
Publication Types:
* Review
* Review, tutorial
PMID: 9768821, UI: 98439757
_________________________________________________________________
_________________________________________________________________
Med Clin (Barc) 2001 Jun 16;117(2):49-51
Analysis of the susceptibility regions to psoriasis in Spanish population:
evidence of a major gene involved in psoriasis in 6p21
de Cid R, Volpini V, Almasy L, Otero D, Estivil X, Lazaro C
Centre de Genetica Medica i Molecular. Institut de Recerca Oncologica.
L'Hospitalet de Llobregat. Barcelona.
[Record supplied by publisher]
Background: Identification of the susceptibility regions to psoriasis
in Spanish population. Analysis of the chromosomal regions 6p, 17q, 4q
and 1cen-q21.Patients and method: Analysis of 27 Spanish families with
psoriasis. Parametric and non-parametric linkage analysis with 22
polymorphic microsatellite markers in the candidate regions.Results:
Evidence of linkage (p < 0,05) using non-parametric methods in
chromosome 6p. Absence of linkage in 17q, 4q and 1cen-q21
regions.Conclusion: We present the evidence of a major gene in 6p21.3
involved in psoriasis in Spanish population.
PMID: 11446925
_________________________________________________________________
_________________________________________________________________
Links: American journal of epidemiology.
Am J Epidemiol 2001 Aug 1;154(3):193-206
HFE Gene and Hereditary Hemochromatosis: A HuGE Review.
Hanson EH, Imperatore G, Burke W
United States Air Force School of Aerospace Medicine, Brooks Air Force
Base, San Antonio, TX. Division of Diabetes Translation, Centers for
Disease Control and Prevention, Atlanta, GA. Department of Medical
History and Ethics, University of Washington, Seattle, WA. Department
of Medicine, University of Washington, Seattle, WA.
[Record supplied by publisher]
Hereditary hemochromatosis (HHC) is an autosomal recessive disorder of
iron metabolism characterized by increased iron absorption and
deposition in the liver, pancreas, heart, joints, and pituitary gland.
Without treatment, death may occur from cirrhosis, primary liver
cancer, diabetes, or cardiomyopathy. In 1996, HFE, the gene for HHC,
was mapped on the short arm of chromosome 6 (6p21.3). Two of the 37
allelic variants of HFE described to date (C282Y and H63D) are
significantly correlated with HHC. Homozygosity for the C282Y mutation
was found in 52-100% of previous studies on clinically diagnosed
probands. In this review, 5% of HHC probands were found to be compound
heterozygotes (C282Y/H63D), and 1.5% were homozygous for the H63D
mutation; 3.6% were C282Y heterozygotes, and 5.2% were H63D
heterozygotes. In 7% of cases, C282Y and H63D mutations were not
present. In the general population, the frequency of the C282Y/C282Y
genotype is 0.4%. C282Y heterozygosity ranges from 9.2% in Europeans
to nil in Asian, Indian subcontinent, African/Middle Eastern, and
Australasian populations. The H63D carrier frequency is 22% in
European populations. Accurate data on the penetrance of the different
HFE genotypes are not available. Extrapolating from limited clinical
observations in screening studies, an estimated 40-70% of persons with
the C282Y homozygous genotype will develop clinical evidence of iron
overload. A smaller proportion will die from complications of iron
overload. To date, population screening for HHC is not recommended
because of uncertainties about optimal screening strategies, optimal
care for susceptible persons, laboratory standardization, and the
potential for stigmatization or discrimination.
PMID: 11479183
_________________________________________________________________
_________________________________________________________________