<?xml version="1.0" encoding="UTF-8"?>
<rss version="2.0"
	xmlns:content="http://purl.org/rss/1.0/modules/content/"
	xmlns:wfw="http://wellformedweb.org/CommentAPI/"
	xmlns:dc="http://purl.org/dc/elements/1.1/"
	xmlns:atom="http://www.w3.org/2005/Atom"
	xmlns:sy="http://purl.org/rss/1.0/modules/syndication/"
	xmlns:slash="http://purl.org/rss/1.0/modules/slash/"
	>

<channel>
	<title>CMLHope.Com</title>
	<atom:link href="http://cmlhope.com/feed/" rel="self" type="application/rss+xml" />
	<link>http://cmlhope.com</link>
	<description>A Worldwide Support Network For Chronic Myelogenous Leukemia</description>
	<lastBuildDate>Thu, 17 May 2012 17:47:46 +0000</lastBuildDate>
	<generator>http://wordpress.org/?v=2.9.2</generator>
	<language>en</language>
	<sy:updatePeriod>hourly</sy:updatePeriod>
	<sy:updateFrequency>1</sy:updateFrequency>
			<item>
		<title>E2F1?dependent pathways are involved in amonafide analogue 7?d?induced DNA damage, G2/M arrest and apoptosis in p53?deficient K562 cells</title>
		<link>http://cmlhope.com/2012/05/17/e2f1%e2%80%90dependent-pathways-are-involved-in-amonafide-analogue-7%e2%80%90d%e2%80%90induced-dna-damage-g2m-arrest-and-apoptosis-in-p53%e2%80%90deficient-k562-cells/</link>
		<comments>http://cmlhope.com/2012/05/17/e2f1%e2%80%90dependent-pathways-are-involved-in-amonafide-analogue-7%e2%80%90d%e2%80%90induced-dna-damage-g2m-arrest-and-apoptosis-in-p53%e2%80%90deficient-k562-cells/#comments</comments>
		<pubDate>Thu, 17 May 2012 17:47:46 +0000</pubDate>
		<dc:creator>rob</dc:creator>
				<category><![CDATA[Uncategorized]]></category>

		<guid isPermaLink="false">http://cmlhope.com/2012/05/17/e2f1%e2%80%90dependent-pathways-are-involved-in-amonafide-analogue-7%e2%80%90d%e2%80%90induced-dna-damage-g2m-arrest-and-apoptosis-in-p53%e2%80%90deficient-k562-cells/</guid>
		<description><![CDATA[AbstractThe E2F1 gene well known is its pivotal role in regulating the entry from G1 to S phase, while the salvage anti?tumoral pathway which implicates it, especially in the absence of p53, is not fully characterized. We therefore attempted to identify the up? and down?stream events involved in the activation of the E2F1?dependent pro?apoptotic pathway. [...]]]></description>
			<content:encoded><![CDATA[<p>AbstractThe E2F1 gene well known is its pivotal role in regulating the entry from G1 to S phase, while the salvage anti?tumoral pathway which implicates it, especially in the absence of p53, is not fully characterized. We therefore attempted to identify the up? and down?stream events involved in the activation of the E2F1?dependent pro?apoptotic pathway. For this purpose, a amonafide analogue, 7?d (2?(3?(2?(Dimethylamino)ethylamino)propyl)?6?(dodecylamino)?1H?benzo[de]isoquinoline?1,3(2H)?dione) was screened, which exhibited high antitumor activity against p53?deficient human Chronic Myelogenous Leukemia K562 cells. Analysis of flow cytometry and western blots of K562 cells treated with 7?d revealed an appreciable G2/M cycle arrest and apoptosis in a dose &#8230;<br />
<a href="http://www.medworm.com/rss/userss.php?qu=%2Bchronic+%2Bmyelogenous+%2Bleukemia&amp;title=MedWorm+Query%3A+%2Bchronic+%2Bmyelogenous+%2Bleukemia">More</a></p>
]]></content:encoded>
			<wfw:commentRss>http://cmlhope.com/2012/05/17/e2f1%e2%80%90dependent-pathways-are-involved-in-amonafide-analogue-7%e2%80%90d%e2%80%90induced-dna-damage-g2m-arrest-and-apoptosis-in-p53%e2%80%90deficient-k562-cells/feed/</wfw:commentRss>
		<slash:comments>0</slash:comments>
		</item>
		<item>
		<title>Medical conditions and risk of adult myeloid leukemia</title>
		<link>http://cmlhope.com/2012/05/17/medical-conditions-and-risk-of-adult-myeloid-leukemia/</link>
		<comments>http://cmlhope.com/2012/05/17/medical-conditions-and-risk-of-adult-myeloid-leukemia/#comments</comments>
		<pubDate>Thu, 17 May 2012 17:47:46 +0000</pubDate>
		<dc:creator>rob</dc:creator>
				<category><![CDATA[Uncategorized]]></category>

		<guid isPermaLink="false">http://cmlhope.com/2012/05/17/medical-conditions-and-risk-of-adult-myeloid-leukemia/</guid>
		<description><![CDATA[Conclusion&#160;&#160;Certain inflammatory medical conditions and a personal history of cancer, independent from therapy, are associated with an
 increased risk of myeloid leukemia.
	Content Type Journal ArticleCategory Original paperPages 1-7DOI 10.1007/s10552-012-9977-yAuthors
		Kimberly J. Johnson, Brown School, Washington University in St. Louis, St. Louis, MO 63130, USACindy M. Blair, Department of Nutrition Sciences, University of Alabama at Birmingham, Birmingham, [...]]]></description>
			<content:encoded><![CDATA[<p>Conclusion&nbsp;&nbsp;Certain inflammatory medical conditions and a personal history of cancer, independent from therapy, are associated with an<br />
 increased risk of myeloid leukemia.</p>
<p>	Content Type Journal ArticleCategory Original paperPages 1-7DOI 10.1007/s10552-012-9977-yAuthors<br />
		Kimberly J. Johnson, Brown School, Washington University in St. Louis, St. Louis, MO 63130, USACindy M. Blair, Department of Nutrition Sciences, University of Alabama at Birmingham, Birmingham, AL 35294, USAJames M. Fink, Department of Laboratory Medicine and Pathology, Hennepin Faculty Associates, Minneapolis, MN 55415, USAJames R. Cerhan, Division of Epidemiology, Department of Health Sciences Research, Mayo Clinic, Rochester, MN 55905, USAMichelle A. Roesler, Division of Epidemiology and Clinical Resea&#8230;<br />
<a href="http://www.medworm.com/rss/userss.php?qu=%2Bchronic+%2Bmyelogenous+%2Bleukemia&amp;title=MedWorm+Query%3A+%2Bchronic+%2Bmyelogenous+%2Bleukemia">More</a></p>
]]></content:encoded>
			<wfw:commentRss>http://cmlhope.com/2012/05/17/medical-conditions-and-risk-of-adult-myeloid-leukemia/feed/</wfw:commentRss>
		<slash:comments>0</slash:comments>
		</item>
		<item>
		<title>Hematopoietic Interferon Regulatory Factor 8-Deficiency Accelerates Atherosclerosis in Mice.</title>
		<link>http://cmlhope.com/2012/05/17/hematopoietic-interferon-regulatory-factor-8-deficiency-accelerates-atherosclerosis-in-mice/</link>
		<comments>http://cmlhope.com/2012/05/17/hematopoietic-interferon-regulatory-factor-8-deficiency-accelerates-atherosclerosis-in-mice/#comments</comments>
		<pubDate>Thu, 17 May 2012 17:47:46 +0000</pubDate>
		<dc:creator>rob</dc:creator>
				<category><![CDATA[Uncategorized]]></category>

		<guid isPermaLink="false">http://cmlhope.com/2012/05/17/hematopoietic-interferon-regulatory-factor-8-deficiency-accelerates-atherosclerosis-in-mice/</guid>
		<description><![CDATA[CONCLUSIONS: These findings indicate that a chronic myelogenous leukemia-like phenotype contributes to accelerated atherosclerosis in mice. Among proatherosclerotic effects of other cell types, this, in part, is linked to an expansion of functionally intact PMN.
    PMID: 22556330 [PubMed - as supplied by publisher] (Source: Arteriosclerosis, Thrombosis and Vascular Biology)
More
]]></description>
			<content:encoded><![CDATA[<p>CONCLUSIONS: These findings indicate that a chronic myelogenous leukemia-like phenotype contributes to accelerated atherosclerosis in mice. Among proatherosclerotic effects of other cell types, this, in part, is linked to an expansion of functionally intact PMN.<br />
    PMID: 22556330 [PubMed - as supplied by publisher] (Source: Arteriosclerosis, Thrombosis and Vascular Biology)<br />
<a href="http://www.medworm.com/rss/userss.php?qu=%2Bchronic+%2Bmyelogenous+%2Bleukemia&amp;title=MedWorm+Query%3A+%2Bchronic+%2Bmyelogenous+%2Bleukemia">More</a></p>
]]></content:encoded>
			<wfw:commentRss>http://cmlhope.com/2012/05/17/hematopoietic-interferon-regulatory-factor-8-deficiency-accelerates-atherosclerosis-in-mice/feed/</wfw:commentRss>
		<slash:comments>0</slash:comments>
		</item>
		<item>
		<title>BCR-JAK2 fusion as a result of a translocation
(9;22)(p24;q11.2) in a patient with CML-like
myeloproliferative disease</title>
		<link>http://cmlhope.com/2012/05/08/bcr-jak2-fusion-as-a-result-of-a-translocation922p24q11-2-in-a-patient-with-cml-likemyeloproliferative-disease/</link>
		<comments>http://cmlhope.com/2012/05/08/bcr-jak2-fusion-as-a-result-of-a-translocation922p24q11-2-in-a-patient-with-cml-likemyeloproliferative-disease/#comments</comments>
		<pubDate>Tue, 08 May 2012 16:28:30 +0000</pubDate>
		<dc:creator>rob</dc:creator>
				<category><![CDATA[Uncategorized]]></category>

		<guid isPermaLink="false">http://cmlhope.com/2012/05/08/bcr-jak2-fusion-as-a-result-of-a-translocation922p24q11-2-in-a-patient-with-cml-likemyeloproliferative-disease/</guid>
		<description><![CDATA[We present clinical-pathological and cytogenetic evaluation of a patient withPhiladelphia-chromosome negative CML/MPD harboring a t(9;22)(p24;q11.2) resulting inBCR-JAK2 fusion. Fluorescence in situ hybridization and molecular characterization of thetranslocation confirmed a BCR-JAK2 fusion and helped delineate the breakpoints upstreamof exon 1 of minor cluster region of BCR gene and likely intron 18 of the JAK2 gene,resulting in [...]]]></description>
			<content:encoded><![CDATA[<p>We present clinical-pathological and cytogenetic evaluation of a patient withPhiladelphia-chromosome negative CML/MPD harboring a t(9;22)(p24;q11.2) resulting inBCR-JAK2 fusion. Fluorescence in situ hybridization and molecular characterization of thetranslocation confirmed a BCR-JAK2 fusion and helped delineate the breakpoints upstreamof exon 1 of minor cluster region of BCR gene and likely intron 18 of the JAK2 gene,resulting in an in-frame transcript This case provides convincing support, along with twoprevious case-reports, for a role for activation of the Janus kinase 2 in evolution ofmyeloproliferative disease. The recurrent, albeit rare, nature of the breakpoints within BCRand JAK2 suggests a potential new diagnostic target that should be interrogated in PhnegativeCML/MPD patients. (&#8230;<br />
<a href="http://www.medworm.com/rss/userss.php?qu=%2Bchronic+%2Bmyelogenous+%2Bleukemia&amp;title=MedWorm+Query%3A+%2Bchronic+%2Bmyelogenous+%2Bleukemia">More</a></p>
]]></content:encoded>
			<wfw:commentRss>http://cmlhope.com/2012/05/08/bcr-jak2-fusion-as-a-result-of-a-translocation922p24q11-2-in-a-patient-with-cml-likemyeloproliferative-disease/feed/</wfw:commentRss>
		<slash:comments>0</slash:comments>
		</item>
		<item>
		<title>A novel five-way translocation t(7;11;9;22;9)(q22;q13;q34;q11.2;q34) involving Ph chromosome in a patient of chronic myeloid leukemia: a case report</title>
		<link>http://cmlhope.com/2012/05/08/a-novel-five-way-translocation-t7119229q22q13q34q11-2q34-involving-ph-chromosome-in-a-patient-of-chronic-myeloid-leukemia-a-case-report/</link>
		<comments>http://cmlhope.com/2012/05/08/a-novel-five-way-translocation-t7119229q22q13q34q11-2q34-involving-ph-chromosome-in-a-patient-of-chronic-myeloid-leukemia-a-case-report/#comments</comments>
		<pubDate>Tue, 08 May 2012 16:28:30 +0000</pubDate>
		<dc:creator>rob</dc:creator>
				<category><![CDATA[Uncategorized]]></category>

		<guid isPermaLink="false">http://cmlhope.com/2012/05/08/a-novel-five-way-translocation-t7119229q22q13q34q11-2q34-involving-ph-chromosome-in-a-patient-of-chronic-myeloid-leukemia-a-case-report/</guid>
		<description><![CDATA[We report a CML case with a novel five-way complex translocation. Although the result of initial G-banding was 46,XY,t(7;11;9)(q22;q13;q34),t(9;22)(q34;q11.2), fluorescence in situ hybridization (FISH) demonstrated t(7;11;9;22;9)(q22;q13;q34;q11.2;q34) consisting of sequential rearrangements involving five chromosomes. The patient was successfully treated by imatinib and obtained a major molecular response. To our knowledge, this is the tenth CML case [...]]]></description>
			<content:encoded><![CDATA[<p>We report a CML case with a novel five-way complex translocation. Although the result of initial G-banding was 46,XY,t(7;11;9)(q22;q13;q34),t(9;22)(q34;q11.2), fluorescence in situ hybridization (FISH) demonstrated t(7;11;9;22;9)(q22;q13;q34;q11.2;q34) consisting of sequential rearrangements involving five chromosomes. The patient was successfully treated by imatinib and obtained a major molecular response. To our knowledge, this is the tenth CML case with a complicated Ph translocation involving five chromosomes and the third one treated by imatinib. Good response with imatinib therapy suggested that a single-event rearrangement was involved in the chromosomal changes. (Source: Molecular Cytogenetics)<br />
<a href="http://www.medworm.com/rss/userss.php?qu=%2Bchronic+%2Bmyelogenous+%2Bleukemia&amp;title=MedWorm+Query%3A+%2Bchronic+%2Bmyelogenous+%2Bleukemia">More</a></p>
]]></content:encoded>
			<wfw:commentRss>http://cmlhope.com/2012/05/08/a-novel-five-way-translocation-t7119229q22q13q34q11-2q34-involving-ph-chromosome-in-a-patient-of-chronic-myeloid-leukemia-a-case-report/feed/</wfw:commentRss>
		<slash:comments>0</slash:comments>
		</item>
		<item>
		<title>Reduced intensity conditioning is superior to nonmyeloablative conditioning for older chronic myelogenous leukemia patients undergoing hematopoietic cell transplant during the tyrosine kinase inhibitor era</title>
		<link>http://cmlhope.com/2012/05/08/reduced-intensity-conditioning-is-superior-to-nonmyeloablative-conditioning-for-older-chronic-myelogenous-leukemia-patients-undergoing-hematopoietic-cell-transplant-during-the-tyrosine-kinase-inhibito/</link>
		<comments>http://cmlhope.com/2012/05/08/reduced-intensity-conditioning-is-superior-to-nonmyeloablative-conditioning-for-older-chronic-myelogenous-leukemia-patients-undergoing-hematopoietic-cell-transplant-during-the-tyrosine-kinase-inhibito/#comments</comments>
		<pubDate>Tue, 08 May 2012 16:28:30 +0000</pubDate>
		<dc:creator>rob</dc:creator>
				<category><![CDATA[Uncategorized]]></category>

		<guid isPermaLink="false">http://cmlhope.com/2012/05/08/reduced-intensity-conditioning-is-superior-to-nonmyeloablative-conditioning-for-older-chronic-myelogenous-leukemia-patients-undergoing-hematopoietic-cell-transplant-during-the-tyrosine-kinase-inhibito/</guid>
		<description><![CDATA[Tyrosine kinase inhibitors (TKIs) and reduced intensity conditioning (RIC)/nonmyeloablative (NMA) conditioning hematopoietic cell transplants (HCTs) have changed the therapeutic strategy for chronic myelogenous leukemia (CML) patients. We analyzed post-HCT outcomes of 306 CML patients reported to the Center for International Blood and Marrow Transplant Research aged 40 years and older undergoing RIC/NMA HCT from 2001 [...]]]></description>
			<content:encoded><![CDATA[<p>Tyrosine kinase inhibitors (TKIs) and reduced intensity conditioning (RIC)/nonmyeloablative (NMA) conditioning hematopoietic cell transplants (HCTs) have changed the therapeutic strategy for chronic myelogenous leukemia (CML) patients. We analyzed post-HCT outcomes of 306 CML patients reported to the Center for International Blood and Marrow Transplant Research aged 40 years and older undergoing RIC/NMA HCT from 2001 to 2007: 117 (38%) aged 40 to 49 years, 119 (39%) 50 to 59 years, and 70 (23%) 60 years or older. The majority (74%) had treatment with imatinib before HCT. At HCT, most patients aged 40 to 49 years were in chronic phase (CP) 1 (74%), compared with 31% aged 60 years or older. Siblings were donors for 56% aged 40 to 49 years; older cohorts had more unrelated donors. The majorit&#8230;<br />
<a href="http://www.medworm.com/rss/userss.php?qu=%2Bchronic+%2Bmyelogenous+%2Bleukemia&amp;title=MedWorm+Query%3A+%2Bchronic+%2Bmyelogenous+%2Bleukemia">More</a></p>
]]></content:encoded>
			<wfw:commentRss>http://cmlhope.com/2012/05/08/reduced-intensity-conditioning-is-superior-to-nonmyeloablative-conditioning-for-older-chronic-myelogenous-leukemia-patients-undergoing-hematopoietic-cell-transplant-during-the-tyrosine-kinase-inhibito/feed/</wfw:commentRss>
		<slash:comments>0</slash:comments>
		</item>
		<item>
		<title>Gastric Antral Vascular Ectasia in a Patient with GIST after Treatment with Imatinib: Case Report and Literature Review</title>
		<link>http://cmlhope.com/2012/05/08/gastric-antral-vascular-ectasia-in-a-patient-with-gist-after-treatment-with-imatinib-case-report-and-literature-review/</link>
		<comments>http://cmlhope.com/2012/05/08/gastric-antral-vascular-ectasia-in-a-patient-with-gist-after-treatment-with-imatinib-case-report-and-literature-review/#comments</comments>
		<pubDate>Tue, 08 May 2012 16:28:30 +0000</pubDate>
		<dc:creator>rob</dc:creator>
				<category><![CDATA[Uncategorized]]></category>

		<guid isPermaLink="false">http://cmlhope.com/2012/05/08/gastric-antral-vascular-ectasia-in-a-patient-with-gist-after-treatment-with-imatinib-case-report-and-literature-review/</guid>
		<description><![CDATA[We present a previously unreported adverse effect of imatinib, gastric antral vascular ectasia, in a 74-year-old woman with gastrointestinal stromal tumor in remission treated with adjuvant imatinib. Endoscopy performed prior to starting imatinib showed normal gastric mucosa, but 8 months after starting imatinib showed diffuse gastric inflammation. Repeat endoscopy 1 month after discontinuing imatinib showed [...]]]></description>
			<content:encoded><![CDATA[<p>We present a previously unreported adverse effect of imatinib, gastric antral vascular ectasia, in a 74-year-old woman with gastrointestinal stromal tumor in remission treated with adjuvant imatinib. Endoscopy performed prior to starting imatinib showed normal gastric mucosa, but 8 months after starting imatinib showed diffuse gastric inflammation. Repeat endoscopy 1 month after discontinuing imatinib showed significant improvement in gastric inflammation. (Source: Japanese Journal of Clinical Oncology)<br />
<a href="http://www.medworm.com/rss/userss.php?qu=%2Bchronic+%2Bmyelogenous+%2Bleukemia&amp;title=MedWorm+Query%3A+%2Bchronic+%2Bmyelogenous+%2Bleukemia">More</a></p>
]]></content:encoded>
			<wfw:commentRss>http://cmlhope.com/2012/05/08/gastric-antral-vascular-ectasia-in-a-patient-with-gist-after-treatment-with-imatinib-case-report-and-literature-review/feed/</wfw:commentRss>
		<slash:comments>0</slash:comments>
		</item>
		<item>
		<title>Spinophilin: a new tumor suppressor at 17q21.</title>
		<link>http://cmlhope.com/2012/05/08/spinophilin-a-new-tumor-suppressor-at-17q21/</link>
		<comments>http://cmlhope.com/2012/05/08/spinophilin-a-new-tumor-suppressor-at-17q21/#comments</comments>
		<pubDate>Tue, 08 May 2012 16:28:30 +0000</pubDate>
		<dc:creator>rob</dc:creator>
				<category><![CDATA[Uncategorized]]></category>

		<guid isPermaLink="false">http://cmlhope.com/2012/05/08/spinophilin-a-new-tumor-suppressor-at-17q21/</guid>
		<description><![CDATA[Authors: Carnero A
    Abstract
    The scaffold protein spinophilin (SPN) is a regulatory subunit of phosphatase 1a (PP1a) located at 17q21.33. This region is frequently associated with microsatellite instability and LOH and contains a relatively high density of known tumor suppressor genes, and several unidentified candidate tumor suppressor genes located [...]]]></description>
			<content:encoded><![CDATA[<p>Authors: Carnero A<br />
    Abstract<br />
    The scaffold protein spinophilin (SPN) is a regulatory subunit of phosphatase 1a (PP1a) located at 17q21.33. This region is frequently associated with microsatellite instability and LOH and contains a relatively high density of known tumor suppressor genes, and several unidentified candidate tumor suppressor genes located distal to BRCA1. Spn is located in this locus and proposed to be a new tumor suppressor. Loss of Spn induces a proliferative response by increasing pRb phosphorylation, which in turn activates p53, thereby, neutralizing the proliferative response. The absence of p53 bypasses this barrier and enhances the malignant phenotype. Furthermore, the ectopic expression of SPN in human tumor cells from different types of malignancies greatly redu&#8230;<br />
<a href="http://www.medworm.com/rss/userss.php?qu=%2Bchronic+%2Bmyelogenous+%2Bleukemia&amp;title=MedWorm+Query%3A+%2Bchronic+%2Bmyelogenous+%2Bleukemia">More</a></p>
]]></content:encoded>
			<wfw:commentRss>http://cmlhope.com/2012/05/08/spinophilin-a-new-tumor-suppressor-at-17q21/feed/</wfw:commentRss>
		<slash:comments>0</slash:comments>
		</item>
		<item>
		<title>Metastatic basal cell carcinoma in the era of hedgehog signaling pathway inhibitors</title>
		<link>http://cmlhope.com/2012/05/08/metastatic-basal-cell-carcinoma-in-the-era-of-hedgehog-signaling-pathway-inhibitors/</link>
		<comments>http://cmlhope.com/2012/05/08/metastatic-basal-cell-carcinoma-in-the-era-of-hedgehog-signaling-pathway-inhibitors/#comments</comments>
		<pubDate>Tue, 08 May 2012 16:28:30 +0000</pubDate>
		<dc:creator>rob</dc:creator>
				<category><![CDATA[Uncategorized]]></category>

		<guid isPermaLink="false">http://cmlhope.com/2012/05/08/metastatic-basal-cell-carcinoma-in-the-era-of-hedgehog-signaling-pathway-inhibitors/</guid>
		<description><![CDATA[The objective of the current review, in which the authors evaluated the time from the first BCC diagnosis to metastasis, location of disease, and radiographic features, was to contribute to the general knowledge and awareness among providers, patients, and support groups about mBCC and to provide an outlook for the future of treatments for mBCC. [...]]]></description>
			<content:encoded><![CDATA[<p>The objective of the current review, in which the authors evaluated the time from the first BCC diagnosis to metastasis, location of disease, and radiographic features, was to contribute to the general knowledge and awareness among providers, patients, and support groups about mBCC and to provide an outlook for the future of treatments for mBCC. A literature review on mBCC and a review of records from patients with mBCC who presented to Virginia G. Piper Cancer Center Clinical Trials (an oncology clinical trials center) were conducted. The clinical and radiographic findings of 22 patients with mBCC who were evaluated at that center from the initiation of smoothened (SMO) antagonist trials were analyzed along with a review of BCC epidemiology and pathogenesis, the HHSP, and current and futu&#8230;
<div>
<p><b><i>MedWorm Message:</i></b> Please support the <a href="http://www.doctorsinchains.org/" target="_blank">Doctors In Chains</a> campaign for the <a href="http://www.doctorsinchains.org/">medics</a> tortured and sentenced for up to 15 years in <a href="http://www.doctorsinchains.org/">Bahrain</a>. <a href="https://twitter.com/#!/search/%23FreeDoctors">#FreeDoctors</a></p>
</div>
<p><a href="http://www.medworm.com/rss/userss.php?qu=%2Bchronic+%2Bmyelogenous+%2Bleukemia&amp;title=MedWorm+Query%3A+%2Bchronic+%2Bmyelogenous+%2Bleukemia">More</a></p>
]]></content:encoded>
			<wfw:commentRss>http://cmlhope.com/2012/05/08/metastatic-basal-cell-carcinoma-in-the-era-of-hedgehog-signaling-pathway-inhibitors/feed/</wfw:commentRss>
		<slash:comments>0</slash:comments>
		</item>
		<item>
		<title>Genetic testing behavior and reporting patterns in electronic medical records for physicians trained in a primary care specialty or subspecialty.</title>
		<link>http://cmlhope.com/2012/05/08/genetic-testing-behavior-and-reporting-patterns-in-electronic-medical-records-for-physicians-trained-in-a-primary-care-specialty-or-subspecialty/</link>
		<comments>http://cmlhope.com/2012/05/08/genetic-testing-behavior-and-reporting-patterns-in-electronic-medical-records-for-physicians-trained-in-a-primary-care-specialty-or-subspecialty/#comments</comments>
		<pubDate>Tue, 08 May 2012 16:28:30 +0000</pubDate>
		<dc:creator>rob</dc:creator>
				<category><![CDATA[Uncategorized]]></category>

		<guid isPermaLink="false">http://cmlhope.com/2012/05/08/genetic-testing-behavior-and-reporting-patterns-in-electronic-medical-records-for-physicians-trained-in-a-primary-care-specialty-or-subspecialty/</guid>
		<description><![CDATA[ConclusionsIn this study, genetic tests were often ordered by a diverse group of physicians for women of childbearing age being evaluated for diseases that may affect potential offspring. EMRs currently serve primarily as a storage warehouse for textual reports that could potentially be transformed into meaningful structured data for next-generation clinical decision support. Further studies [...]]]></description>
			<content:encoded><![CDATA[<p>ConclusionsIn this study, genetic tests were often ordered by a diverse group of physicians for women of childbearing age being evaluated for diseases that may affect potential offspring. EMRs currently serve primarily as a storage warehouse for textual reports that could potentially be transformed into meaningful structured data for next-generation clinical decision support. Further studies are needed to address the design, development, and implementation of EMRs capable of managing the critical genetic health information challenges of the future.<br />
    PMID: 22511017 [PubMed - as supplied by publisher] (Source: Journal of the American Medical Informatics Association)<br />
<a href="http://www.medworm.com/rss/userss.php?qu=%2Bchronic+%2Bmyelogenous+%2Bleukemia&amp;title=MedWorm+Query%3A+%2Bchronic+%2Bmyelogenous+%2Bleukemia">More</a></p>
]]></content:encoded>
			<wfw:commentRss>http://cmlhope.com/2012/05/08/genetic-testing-behavior-and-reporting-patterns-in-electronic-medical-records-for-physicians-trained-in-a-primary-care-specialty-or-subspecialty/feed/</wfw:commentRss>
		<slash:comments>0</slash:comments>
		</item>
	</channel>
</rss>

