{"id":3211,"date":"2020-12-22T18:07:14","date_gmt":"2020-12-22T16:07:14","guid":{"rendered":"https:\/\/meddists.com\/learn\/pre-clinical\/pathology\/blood-cancers\/chronic-leukemias\/"},"modified":"2020-12-22T19:52:13","modified_gmt":"2020-12-22T17:52:13","slug":"chronic-leukemias","status":"publish","type":"page","link":"https:\/\/meddists.com\/learn\/pre-clinical\/pathology\/blood-cancers\/chronic-leukemias\/","title":{"rendered":"Chronic leukemias"},"content":{"rendered":"\n<p class=\"wp-block-paragraph\"><div class=\"intro\">Leukemias are tumors of the bone marrow. In acute leukemias, the neoplastic cells are late hematopoietic cells (-cytes).<\/div><\/p>\n\n\n\n<hr class=\"wp-block-separator\"\/>\n\n\n<span class=\"block-heading\" id=\"header_1\">\n<h4 class=\"wp-block-heading\" class=\"wp-block-heading\" class=\"title_collection title3\">Description<\/h4>\n<\/span><span class=\"block-content\" id=\"contents_1\">\n\n\n<p class=\"wp-block-paragraph\">In chronic leukemias, we see an accumulation of mature, <strong>mutated myeloid cells<\/strong>. The cells will undergo\u00a0uncontrolled proliferation due to<strong>\u00a0hyperactivated tyrosine kinases<\/strong> or other signaling pathway alterations.<\/p>\n\n\n\n<ul class=\"wp-block-list\"><li>Chronic leukemias have a slow progression, and they can progress into acute leukemias (but not the other way around!)<\/li><li>Incutable<\/li><li>Mostly affect older patients.<\/li><\/ul>\n\n\n<\/span><span class=\"block-heading\" id=\"header_2\">\n<h2 class=\"wp-block-heading\" class=\"wp-block-heading\" class=\"title_collection title1\">CML, polycythemia vera, essential thrombocythemia, and primary myelofibrosis<\/h2>\n<\/span><span class=\"block-content\" id=\"contents_2\">\n\n<\/span><span class=\"block-heading\" id=\"header_3\">\n<h3 class=\"wp-block-heading\" class=\"wp-block-heading\" class=\"title_collection title2\"><strong>Chronic Myeloid Leukemia (CML)<\/strong><\/h3>\n<\/span><span class=\"block-content\" id=\"contents_3\">\n\n\n<p class=\"wp-block-paragraph\">Increased proliferation of (mainly) granulocytes.<\/p>\n\n\n\n<ul class=\"wp-block-list\"><li>Caused by&nbsp;<strong>t(9;22)<\/strong>&nbsp;&#8212; fusion&nbsp;gene&nbsp;<strong>BCR-ABL1 <\/strong>&#8212;&nbsp;known as<strong> Philadelphia chromosome<\/strong><ul><li>Increases TK activity<\/li><\/ul><\/li><li>Slow onset<\/li><li>Nearly half of the patients are asymptomatic<ul><li>If present, the symptoms are non-specific (fatigue, weight loss)<\/li><\/ul><\/li><li>Increased <strong>white blood count<\/strong> (WBC)<ul><li>Must be differentiated from&nbsp;<strong>lekemoid reaction&nbsp;<\/strong>(a normal response to infection)<\/li><\/ul><\/li><li>Consists of 3 phases:<ul><li>Indolent, chronic phase<\/li><li>Accelerated phase<\/li><li>Blastic phase<\/li><\/ul><\/li><li>Decreased levels of blood <strong>neutrophil alkaline phosphatase<\/strong> (LAP)<\/li><li>Treatments include tyrosine kinase inhibitors and bone marrow transplantation<\/li><\/ul>\n\n\n<\/span><span class=\"block-heading\" id=\"header_4\">\n<h3 class=\"wp-block-heading\" class=\"wp-block-heading\" class=\"title_collection title2\">Polycythemia vera<\/h3>\n<\/span><span class=\"block-content\" id=\"contents_4\">\n\n\n<p class=\"wp-block-paragraph\">Increased production of (mainly) RBCs.<\/p>\n\n\n\n<ul class=\"wp-block-list\"><li>RBC production regardless of the levels of erythropoietin<\/li><li>Most commonly due to point mutations in <strong>JAK2<\/strong><\/li><li>Symptoms include redness (or blueness) of the skin, hemorrhages, and splenomegaly<\/li><li>In blood analysis:<ul><li>6-10T\/L RBC count<\/li><li>Over 60% hematocrit<\/li><li>Abnormal platelet functionality which may cause thrombosis<\/li><li>Basophilia (increased number basophils in the blood)<\/li><li>Decreased serum erythropoietin&nbsp;levels<\/li><\/ul><\/li><\/ul>\n\n\n<\/span><span class=\"block-heading\" id=\"header_5\">\n<h3 class=\"wp-block-heading\" class=\"wp-block-heading\" class=\"title_collection title2\">Essential thrombocythemia<\/h3>\n<\/span><span class=\"block-content\" id=\"contents_5\">\n\n\n<p class=\"wp-block-paragraph\">Increased production of (mainly) platelets.<\/p>\n\n\n\n<ul class=\"wp-block-list\"><li>The platelets produced are dysplastic and defective<\/li><li>Most commonly due to point mutations in <strong>JAK2<\/strong><\/li><li>Symptoms include hemorrhages and splenomegaly<\/li><li>In blood analysis:<ul><li>&gt;600G\/L platelet count<\/li><li>Abnormal platelet morphology<\/li><li>Basophilia<\/li><\/ul><\/li><\/ul>\n\n\n<\/span><span class=\"block-heading\" id=\"header_6\">\n<h3 class=\"wp-block-heading\" class=\"wp-block-heading\" class=\"title_collection title2\">Primary myelofibrosis<\/h3>\n<\/span><span class=\"block-content\" id=\"contents_6\">\n\n\n<p class=\"wp-block-paragraph\"><strong>Decreased hematopoiesis<\/strong> due to&nbsp;<strong>fibrosis of the bone marrow<\/strong> (hence the name).<\/p>\n\n\n\n<ul class=\"wp-block-list\"><li>Most probably, <strong>megakaryocytes <\/strong>releasing PDGF and TGF-\u03b2, activating fibroblasts<ul><li>Resulting in increased ECM deposition = fibrosis<\/li><li>Angiogenesis<\/li><\/ul><\/li><li>Most commonly due to point mutations in <strong>JAK2<\/strong><\/li><li>Consists of 2 stages:<ul><li>Hypercellular stage<ul><li>Cellular proliferation due to the mutation<\/li><\/ul><\/li><li>Hypocellular stage<ul><li>Due to bone marrow fibrosis<\/li><\/ul><\/li><\/ul><\/li><li>Fibrosis will lead to<strong> extramedullary hematopoiesis<\/strong><ul><li>Liver<\/li><li>Spleen<\/li><\/ul><\/li><li>Symptoms include cytopenic symptoms, hepatosplenomegaly, and splenic infarctions<\/li><\/ul>\n<\/span><div id=\"the_titles\" style=\"display:none;\"><h4 class=\"wp-block-heading\" class=\"wp-block-heading\">Description<\/h4><h2 class=\"wp-block-heading\" class=\"wp-block-heading\">CML, polycythemia vera, essential thrombocythemia, and primary myelofibrosis<\/h2><h3 class=\"wp-block-heading\" class=\"wp-block-heading\"><strong>Chronic Myeloid Leukemia (CML)<\/strong><\/h3><h3 class=\"wp-block-heading\" class=\"wp-block-heading\">Polycythemia vera<\/h3><h3 class=\"wp-block-heading\" class=\"wp-block-heading\">Essential thrombocythemia<\/h3><h3 class=\"wp-block-heading\" class=\"wp-block-heading\">Primary myelofibrosis<\/h3><\/div>","protected":false},"excerpt":{"rendered":"<p>Description In chronic leukemias, we see an accumulation of mature, mutated myeloid cells. The cells will undergo\u00a0uncontrolled proliferation due to\u00a0hyperactivated tyrosine kinases or other signaling pathway alterations. Chronic leukemias have a slow progression, and they can progress into acute leukemias (but not the other way around!) Incutable Mostly affect older patients. CML, polycythemia vera, essential [&hellip;]<\/p>\n","protected":false},"author":1,"featured_media":0,"parent":3209,"menu_order":2,"comment_status":"closed","ping_status":"closed","template":"","meta":{"footnotes":""},"class_list":["post-3211","page","type-page","status-publish","hentry"],"yoast_head":"<!-- This site is optimized with the Yoast SEO plugin v27.8 - https:\/\/yoast.com\/product\/yoast-seo-wordpress\/ -->\n<title>Chronic leukemias &#8211; Meddists<\/title>\n<meta name=\"robots\" content=\"index, follow, max-snippet:-1, max-image-preview:large, max-video-preview:-1\" \/>\n<link rel=\"canonical\" href=\"https:\/\/meddists.com\/learn\/pre-clinical\/pathology\/blood-cancers\/chronic-leukemias\/\" \/>\n<meta name=\"twitter:label1\" content=\"Est. reading time\" \/>\n\t<meta name=\"twitter:data1\" content=\"2 minutes\" \/>\n<script type=\"application\/ld+json\" class=\"yoast-schema-graph\">{\"@context\":\"https:\\\/\\\/schema.org\",\"@graph\":[{\"@type\":\"WebPage\",\"@id\":\"https:\\\/\\\/meddists.com\\\/learn\\\/pre-clinical\\\/pathology\\\/blood-cancers\\\/chronic-leukemias\\\/\",\"url\":\"https:\\\/\\\/meddists.com\\\/learn\\\/pre-clinical\\\/pathology\\\/blood-cancers\\\/chronic-leukemias\\\/\",\"name\":\"Chronic leukemias &#8211; 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