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	<title>Cancer Treatment Today &#187; Rituximab</title>
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	<description>Knowledge is Power</description>
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		<title>Rituxan or Rituxan with cladribine for Variant Hairy Cell Leukemia &#8211; pro</title>
		<link>http://cancertreatmenttoday.org/11572/</link>
		<comments>http://cancertreatmenttoday.org/11572/#comments</comments>
		<pubDate>Fri, 18 Oct 2013 14:01:45 +0000</pubDate>
		<dc:creator>M Levin, MD</dc:creator>
				<category><![CDATA[Cancer Treatment]]></category>
		<category><![CDATA[Chronic Lymphocytic Leukemia]]></category>
		<category><![CDATA[New Drugs]]></category>
		<category><![CDATA[Non-Hodgkin's Lymphoma]]></category>
		<category><![CDATA[Professional]]></category>
		<category><![CDATA[Rituxan]]></category>
		<category><![CDATA[CHronic Leukemia]]></category>
		<category><![CDATA[Hairy Cell]]></category>
		<category><![CDATA[Haury Cell Leukemia. Rituxan. RituximabAnti CD20]]></category>
		<category><![CDATA[Leukemic REticuloendotheliosis]]></category>
		<category><![CDATA[Rituximab]]></category>
		<category><![CDATA[Varian Hairy Cell Leukemia]]></category>

		<guid isPermaLink="false">http://cancertreatmenttoday.org/?p=11572</guid>
		<description><![CDATA[Recent literature suggests that a subgroup of Hairy Cell Leukemia(NCL), sometimes called Variant Hairy Cell Leukemia(HCL-V)l  my in fact be a different disease not related to HCL at all and which my respond to rituximab to a much higher extent than common Hairy Cell does. It is thought that this variant is what used to [...]]]></description>
			<content:encoded><![CDATA[<p>Recent literature suggests that a subgroup of Hairy Cell Leukemia(NCL), sometimes called Variant Hairy Cell Leukemia(HCL-V)l  my in fact be a different disease not related to HCL at all and which my respond to rituximab to a much higher extent than common Hairy Cell does. It is thought that this variant is what used to be called Leukemic Reticuloendotheliosis in the past. It is an uncommon disorder accounting for approximately 0.4% of chronic lymphoid malignancies and 10% of all HCl cases. In contrast to HCl-C, HCl-V is a more aggressive disease and according to the new WHO classification it is no longer considered to be biologically related to HCl-C. Patients with HCl-V have an elevated white blood count, easy-to-aspirate bone marrow, unlike HCL which is difficult to aspirate,  and weak reactivity to tartrate &#8211; resistant acid phosphatase (TRAP). Immunophenotypically, HCl-V cells are positive for CD103 and CD11c and negative for CD25. The HCl-V cells express also the B-cell antigens, CD19, CD20 and CD22. The HCl-V patients have frequently an unmutated Ig gene configuration. Currently, the principles of therapy for this rare disease derive from uncontrolled single institutional studies, or even single case reports. In contrast to HCl-C, the HCl-V response to purine nucleoside analogs (PNA) is limited to partial responses in approximately 50% of patients. However, complete responses were observed in patients treated with rituximab and anti-CD22 immunotoxins.</p>
<p>For non-variant type, the use fo the first two together is based on a study reported very recently in ASCO on 3/2020 byKreitmen et al as reported in ASCO 2020. This regimen is for patients who have minimal residual disease after 6 months. In the trial, 68 patients with purine analog-naive classic hairy cell leukemia were randomly assigned to receive 0.15 mg/kg of cladribine intravenously on days 1 to 5 with eight weekly doses of rituximab at 375 mg/m2 started on day 1 (concurrent group, n = 34) or 6 months later after detection of minimal residual disease in their blood (delayed group, n = 34). Minimal residual disease tests included blood and bone marrow flow cytometry and bone marrow immunohistochemistry.</p>
<p>Patients in either group could receive a second course of rituximab 6 months after the first. The primary endpoint was 6-month minimal residual diseasefree complete remission rates with concurrent treatment vs cladribine monotherapy in the delayed group. THe delayed group did better nad ahd less toxicity. In the trial, 68 patients with purine analognaive classic hairy cell leukemia were randomly assigned to receive 0.15 mg/kg of cladribine intravenously on days 1 to 5 with eight weekly doses of rituximab at 375 mg/m2 started on day 1 (concurrent group, n = 34) or 6 months later after detection of minimal residual disease in their blood (delayed group, n = 34). Minimal residual disease tests included blood and bone marrow flow cytometry and bone marrow immunohistochemistry.</p>
<p>Patients in either group could receive a second course of rituximab 6 months after the first. The primary endpoint was 6-month minimal residual disease-free complete remission rates with concurrent treatment vs cladribine monotherapy in the delayed group, which favored the concurrent group, but with more thrmbocytopenia..<br />
The investigators concluded: “Achieving minimal residual disease-free complete remission of hairy cell leukemia after first-line cladribine is greatly enhanced by concurrent rituximab and less so by delayed rituximab. Longer follow-up will determine if minimal residual disease-free survival leads to less need for additional therapy or cure of hairy cell leukemia.”</p>
<p>NCCN lists single-agent cladribine or pentostatin in first line and a purine analog with rituximab for recurrent or refractory disease only. and Elitek, not in combination.</p>
<p>Jones G, Parry-Jones N, Wilkins B, Else M, Catovsky D, British Committee for Standards in Haematology. Revised guidelines for the diagnosis and management of hairy cell leukaemia and hairy cell leukaemia variant. Br J Haematol. 2012 Jan;156(2):186-95. [60 references]</p>
<p>Jones G, Parry-Jones N, Wilkins B, et al. Revised guidelines for the diagnosis and management of hairy cell leukaemia and hairy cell leukaemia variant. Br J Haematol 2012; 156:186.</p>
<p>Hagberg H, Lundholm L. Rituximab, a chimaeric anti-CD20 monoclonal antibody, in the treatment of hairy cell leukaemia. Br J Haematol 2001; 115:609.</p>
<p>Robak T. Current treatment options in hairy cell leukemia and hairy cell leukemia variant. Cancer Treat Rev 2006; 32:365.</p>
<p>Arons E, Suntum T, Stetler-Stevenson M, Kreitman RJ. VH4-34+ hairy cell leukemia, a new variant with poor prognosis despite standard therapy. Blood 2009; 114:4687.</p>
<p>Robak T. Hairy-cell leukemia variant: recent view on diagnosis, biology and treatment. Cancer Treat Rev 2011; 37:3.</p>
<p>Grever MR, Abdel-Wahab O, Andritsos LA, et al. Consensus guidelines for the diagnosis and management of patients with classic hairy cell leukemia. Blood 2017; 129:553.</p>
<p>https://www.ascopost.com/news/march-2020/first-line-cladribine-with-concurrent-or-delayed-rituximab-for-hairy-cell-leukemia/</p>
<p>nccn, hcl-1, A- 2020</p>
<p>For Lay Version see<a title="Rituxan for Hairy Cell Leukemia" href="http://cancertreatmenttoday.org/rituxan-for-hairy-cell-leukemia/"><span style="color: #ff0000;"> here</span></a></p>
<p>&nbsp;</p>
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		<item>
		<title>Rituxan to prevent post transplant lymphocyte proliferation</title>
		<link>http://cancertreatmenttoday.org/rituxan-to-prevent-post-transplant-lymphocyte-proliferation/</link>
		<comments>http://cancertreatmenttoday.org/rituxan-to-prevent-post-transplant-lymphocyte-proliferation/#comments</comments>
		<pubDate>Sun, 28 Apr 2013 14:27:12 +0000</pubDate>
		<dc:creator>M Levin, MD</dc:creator>
				<category><![CDATA[Immune System]]></category>
		<category><![CDATA[Immunology]]></category>
		<category><![CDATA[Layperson]]></category>
		<category><![CDATA[Alllogeneic Transplantation]]></category>
		<category><![CDATA[EBv]]></category>
		<category><![CDATA[Epstein Barr Virus]]></category>
		<category><![CDATA[Post Transplant Lymphocyte]]></category>
		<category><![CDATA[PTLD]]></category>
		<category><![CDATA[Rituxan]]></category>
		<category><![CDATA[Rituximab]]></category>
		<category><![CDATA[TIters]]></category>

		<guid isPermaLink="false">http://cancertreatmenttoday.org/?p=11074</guid>
		<description><![CDATA[Post-transplant lymphoproliferative disease (PTLD) remains a major complication after solid organ and allogeneic stem cell transplantation. It usually is caused by growth of lymphocytes infected with Epstein-Barr virus (EBV) in patients whose immune system is suppressed after transplantation to prevent rejection. Following titers and an individualized treatment plan including decreased immunosuppression and other agents should [...]]]></description>
			<content:encoded><![CDATA[<p>Post-transplant lymphoproliferative disease (PTLD) remains a major complication after solid organ and allogeneic stem cell transplantation. It usually is caused by growth of lymphocytes infected with Epstein-Barr virus (EBV) in patients whose immune system is suppressed after transplantation to prevent rejection. Following titers and an individualized treatment plan including decreased immunosuppression and other agents should be chosen based on the severity and extent of disease.</p>
<p>There are different kinds of PTLD.  Rituxan appears to have some role in the management of this condition. Several studies show that it reduces both the EBV titers and severity of PTLD. It can be given by itself of with low dose chemotherapy.</p>
<p>Some physicians advocte following the EBV titers and treating when they rise.  The strategy of following titers and giving prophylactic Rituxan has not been formally studied.  Most published studies have dealt with treating patients who already have PTLD.</p>
<p>For Professional version see <a title="Rituxan for PTLD -pro" href="http://cancertreatmenttoday.org/rituxan-for-ptld-pro/"><span style="color: #ff0000;">here</span></a></p>
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