Cardiac tumors medical therapy: Difference between revisions

	Cardiac tumors Microchapters
Home
Patient Information
Overview
Historical Perspective
Classification
Pathophysiology
Causes
Differentiating Cardiac Tumors from other Diseases
Epidemiology and Demographics
Risk Factors
Screening
Natural History, Complications and Prognosis
Diagnosis
Diagnostic Study of Choice
History and Symptoms
Physical Examination
Laboratory Findings
Electrocardiogram
Chest X Ray
CT
MRI
Echocardiography or Ultrasound
Other Imaging Findings
Other Diagnostic Studies
Treatment
Medical Therapy
Surgery
Primary Prevention
Secondary Prevention
Cost-Effectiveness of Therapy
Future or Investigational Therapies
Case Studies
Case #1
Cardiac tumors medical therapy On the Web
Most recent articles
Most cited articles
Review articles
CME Programs
Powerpoint slides
Images
American Roentgen Ray Society Images of Cardiac tumors medical therapy All Images X-rays Echo & Ultrasound CT Images MRI
Ongoing Trials at Clinical Trials.gov
US National Guidelines Clearinghouse
NICE Guidance
FDA on Cardiac tumors medical therapy
CDC on Cardiac tumors medical therapy
Cardiac tumors medical therapy in the news
Blogs on Cardiac tumors medical therapy
Directions to Hospitals Treating Cardiac tumors
Risk calculators and risk factors for Cardiac tumors medical therapy

VisualWikitext

Latest revision as of 20:22, 4 July 2022

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Dheeraj Makkar, M.D.[2]

Overview

Most of the Cardiac tumors are treated with surgical management. Malignant primary cardiac tumors have a predisposition for rapid metastasis spread.

Systemic neoadjuvant therapy should be aggressively explored in hemodynamically stable patients with localized disease because it permits: (a) quicker removal by shrinking the tumor size and (b) a decrease in the likelihood of systemic recurrence

Medical Treatment of Cardiac Tumors

Malignant recurrent effusions may require the use of a sclerosing agent or drainage with a subxiphisternal windows or percutaneous approach.

Cardiac Tumors Medical Management
Tumor	Treatment
Cardiac Lymphoma	Rituximab is an anti-CD20 monoclonal antibody that typically produces remission in a wide range of B-cell non-Hodgkin lymphomas. MOA: Activation of antibody-dependent, cell-mediated cytotoxicity, complement-mediated lysis, phagocytosis of antibody-coupled tumor cells, and activation of cell death appear to constitute its mode of action.^[1]
Sarcoma	Doxorubicin and Ifosfamide alternative regimen Gemcitabine/Docetaxel Gemcitabine: MOA :Gemcitabine is a nucleoside analogue that induces apoptosis in cancerous cells during DNA formation to exert its antitumor effects.^[2] Docetaxel: MOA: Stabilizes microtubule assembly.^[2]
Angiosarcoma	Paclitaxel MOA: Dr. Horwitz found that Paclitaxel inhibits cell division by promoting the assembly of stable microtubules, particularly from -tubulin heterodimers. It inhibits their depolymerization; as a result, vulnerable cells are detained in the G2/M stage of mitosis.^[3] Other Vinca alkaloids block microtubule arrangement.^[3]
Prominent targeted therapy	Anti-angiogenic agents Pazopanib MOA suppression of the intracellular tyrosine kinase of VEGF receptor (VEGFR) and PDGF receptor (PDGFR) (PDGFR).^[4] Sorafenib MOA a potent soluble epoxide hydrolase inhibitor.^[4]
Undifferentiated pleomorphic sarcomas	Pembrolizumab MOA:blocks a protein called PD-1 on the surface of certain immune cells called T-cells. Blocking PD-1 triggers the T-cells to find and kill cancer cells.^[5]

References

↑ Nakagawa Y, Ikeda U, Hirose M, Ubukata S, Katsuki TA, Kaminishi Y; et al. (2004). "Successful treatment of primary cardiac lymphoma with monoclonal CD20 antibody (rituximab)". Circ J. 68 (2): 172–3. doi:10.1253/circj.68.172. PMID 14745155.
↑ ^2.0 ^2.1 Seddon B, Strauss SJ, Whelan J, Leahy M, Woll PJ, Cowie F; et al. (2017). "Gemcitabine and docetaxel versus doxorubicin as first-line treatment in previously untreated advanced unresectable or metastatic soft-tissue sarcomas (GeDDiS): a randomised controlled phase 3 trial". Lancet Oncol. 18 (10): 1397–1410. doi:10.1016/S1470-2045(17)30622-8. PMC 5622179. PMID 28882536.
↑ ^3.0 ^3.1 Schiff PB, Horwitz SB (1980). "Taxol stabilizes microtubules in mouse fibroblast cells". Proc Natl Acad Sci U S A. 77 (3): 1561–5. doi:10.1073/pnas.77.3.1561. PMC 348536. PMID 6103535.
↑ ^4.0 ^4.1 Germano D, Daniele B (2014). "Systemic therapy of hepatocellular carcinoma: current status and future perspectives". World J Gastroenterol. 20 (12): 3087–99. doi:10.3748/wjg.v20.i12.3087. PMC 3964381. PMID 24696596.
↑ Keung EZ, Burgess M, Salazar R, Parra ER, Rodrigues-Canales J, Bolejack V; et al. (2020). "Correlative Analyses of the SARC028 Trial Reveal an Association Between Sarcoma-Associated Immune Infiltrate and Response to Pembrolizumab". Clin Cancer Res. 26 (6): 1258–1266. doi:10.1158/1078-0432.CCR-19-1824. PMC 7731262 Check |pmc= value (help). PMID 31900276.

Template:WH Template:WS

[pmid14745155-1] Nakagawa Y, Ikeda U, Hirose M, Ubukata S, Katsuki TA, Kaminishi Y; et al. (2004). "Successful treatment of primary cardiac lymphoma with monoclonal CD20 antibody (rituximab)". Circ J. 68 (2): 172–3. doi:10.1253/circj.68.172. PMID 14745155.

[pmid28882536-2] 2.0 ^2.1 Seddon B, Strauss SJ, Whelan J, Leahy M, Woll PJ, Cowie F; et al. (2017). "Gemcitabine and docetaxel versus doxorubicin as first-line treatment in previously untreated advanced unresectable or metastatic soft-tissue sarcomas (GeDDiS): a randomised controlled phase 3 trial". Lancet Oncol. 18 (10): 1397–1410. doi:10.1016/S1470-2045(17)30622-8. PMC 5622179. PMID 28882536.

[pmid6103535-3] 3.0 ^3.1 Schiff PB, Horwitz SB (1980). "Taxol stabilizes microtubules in mouse fibroblast cells". Proc Natl Acad Sci U S A. 77 (3): 1561–5. doi:10.1073/pnas.77.3.1561. PMC 348536. PMID 6103535.

[pmid24696596-4] 4.0 ^4.1 Germano D, Daniele B (2014). "Systemic therapy of hepatocellular carcinoma: current status and future perspectives". World J Gastroenterol. 20 (12): 3087–99. doi:10.3748/wjg.v20.i12.3087. PMC 3964381. PMID 24696596.

[pmid31900276-5] Keung EZ, Burgess M, Salazar R, Parra ER, Rodrigues-Canales J, Bolejack V; et al. (2020). "Correlative Analyses of the SARC028 Trial Reveal an Association Between Sarcoma-Associated Immune Infiltrate and Response to Pembrolizumab". Clin Cancer Res. 26 (6): 1258–1266. doi:10.1158/1078-0432.CCR-19-1824. PMC 7731262 Check |pmc= value (help). PMID 31900276.

[1]

[2]

[3]

[4]

[5]

@@ Line 1: / Line 1: @@
+__NOTOC__
 {{Cardiac tumors}}
-{{CMG}}
+{{CMG}}; {{AE}} {{DMakkar}}
+==Overview==
+Most of the Cardiac tumors are treated with surgical management.
+Malignant primary cardiac tumors have a predisposition for rapid metastasis spread.
+*Systemic neoadjuvant therapy should be aggressively explored in hemodynamically stable patients with localized disease because it permits: (a) quicker removal by shrinking the tumor size and (b) a decrease in the likelihood of systemic recurrence
+==Medical Treatment of Cardiac Tumors==
+Malignant recurrent effusions may require the use of a sclerosing agent or drainage with a subxiphisternal windows or percutaneous approach.
-==Overview==
+{| class="wikitable"
+|+ Cardiac Tumors Medical Management
+|-
+! Tumor || Treatment
+|-
+| '''[[Cardiac Lymphoma]]''' || Rituximab is an '''[[anti-CD20 monoclonal antibody]]''' that typically produces remission in a wide range of B-cell non-Hodgkin lymphomas.
+MOA: Activation of antibody-dependent, [[cell-mediated cytotoxicity]], [[complement-mediated lysis]], [[phagocytosis]] of antibody-coupled tumor cells, and activation of cell death appear to constitute its mode of action.<ref name="pmid14745155">{{cite journal| author=Nakagawa Y, Ikeda U, Hirose M, Ubukata S, Katsuki TA, Kaminishi Y | display-authors=etal| title=Successful treatment of primary cardiac lymphoma with monoclonal CD20 antibody (rituximab). | journal=Circ J | year= 2004 | volume= 68 | issue= 2 | pages= 172-3 | pmid=14745155 | doi=10.1253/circj.68.172 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=14745155  }} </ref>
+|-
+|'''[[Sarcoma]]''' || Doxorubicin and Ifosfamide alternative regimen Gemcitabine/Docetaxel
+*Gemcitabine: MOA :Gemcitabine is a nucleoside analogue that induces apoptosis in cancerous cells during DNA formation to exert its antitumor effects.<ref name="pmid28882536">{{cite journal| author=Seddon B, Strauss SJ, Whelan J, Leahy M, Woll PJ, Cowie F | display-authors=etal| title=Gemcitabine and docetaxel versus doxorubicin as first-line treatment in previously untreated advanced unresectable or metastatic soft-tissue sarcomas (GeDDiS): a randomised controlled phase 3 trial. | journal=Lancet Oncol | year= 2017 | volume= 18 | issue= 10 | pages= 1397-1410 | pmid=28882536 | doi=10.1016/S1470-2045(17)30622-8 | pmc=5622179 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=28882536  }} </ref>
+*Docetaxel: MOA:  Stabilizes microtubule assembly.<ref name="pmid28882536">{{cite journal| author=Seddon B, Strauss SJ, Whelan J, Leahy M, Woll PJ, Cowie F | display-authors=etal| title=Gemcitabine and docetaxel versus doxorubicin as first-line treatment in previously untreated advanced unresectable or metastatic soft-tissue sarcomas (GeDDiS): a randomised controlled phase 3 trial. | journal=Lancet Oncol | year= 2017 | volume= 18 | issue= 10 | pages= 1397-1410 | pmid=28882536 | doi=10.1016/S1470-2045(17)30622-8 | pmc=5622179 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=28882536  }} </ref>
+|-
+|'''[[Angiosarcoma]]''' || Paclitaxel
+*MOA: Dr. Horwitz found that Paclitaxel inhibits cell division by promoting the assembly of stable microtubules, particularly from -tubulin heterodimers. It inhibits their depolymerization; as a result, vulnerable cells are detained in the G2/M stage of mitosis.<ref name="pmid6103535">{{cite journal| author=Schiff PB, Horwitz SB| title=Taxol stabilizes microtubules in mouse fibroblast cells. | journal=Proc Natl Acad Sci U S A | year= 1980 | volume= 77 | issue= 3 | pages= 1561-5 | pmid=6103535 | doi=10.1073/pnas.77.3.1561 | pmc=348536 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=6103535  }} </ref>
+Other Vinca alkaloids block microtubule arrangement.<ref name="pmid6103535">{{cite journal| author=Schiff PB, Horwitz SB| title=Taxol stabilizes microtubules in mouse fibroblast cells. | journal=Proc Natl Acad Sci U S A | year= 1980 | volume= 77 | issue= 3 | pages= 1561-5 | pmid=6103535 | doi=10.1073/pnas.77.3.1561 | pmc=348536 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=6103535  }} </ref>
+|-
+| '''[[Prominent targeted therapy]]''' ||  Anti-angiogenic agents
+*Pazopanib MOA suppression of the intracellular '''tyrosine kinase''' of VEGF receptor (VEGFR) and PDGF receptor (PDGFR) (PDGFR).<ref name="pmid24696596">{{cite journal| author=Germano D, Daniele B| title=Systemic therapy of hepatocellular carcinoma: current status and future perspectives. | journal=World J Gastroenterol | year= 2014 | volume= 20 | issue= 12 | pages= 3087-99 | pmid=24696596 | doi=10.3748/wjg.v20.i12.3087 | pmc=3964381 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=24696596  }} </ref>
+*Sorafenib MOA a potent soluble epoxide hydrolase inhibitor.<ref name="pmid24696596">{{cite journal| author=Germano D, Daniele B| title=Systemic therapy of hepatocellular carcinoma: current status and future perspectives. | journal=World J Gastroenterol | year= 2014 | volume= 20 | issue= 12 | pages= 3087-99 | pmid=24696596 | doi=10.3748/wjg.v20.i12.3087 | pmc=3964381 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=24696596  }} </ref>
+|-
+|'''[[Undifferentiated pleomorphic sarcomas]]''' || Pembrolizumab
+*MOA:blocks a protein called PD-1 on the surface of certain immune cells called T-cells. Blocking PD-1 triggers the T-cells to find and kill cancer cells.<ref name="pmid31900276">{{cite journal| author=Keung EZ, Burgess M, Salazar R, Parra ER, Rodrigues-Canales J, Bolejack V | display-authors=etal| title=Correlative Analyses of the SARC028 Trial Reveal an Association Between Sarcoma-Associated Immune Infiltrate and Response to Pembrolizumab. | journal=Clin Cancer Res | year= 2020 | volume= 26 | issue= 6 | pages= 1258-1266 | pmid=31900276 | doi=10.1158/1078-0432.CCR-19-1824 | pmc=7731262 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=31900276  }} </ref>
+|}
 ==References==
-{{reflist|2}}
+{{Reflist|2}}
+{{WH}}
+{{WS}}
+[[Category:needs english review]]
 [[Category:Disease]]
 [[Category:Cardiology]]
+[[Category:Types of cancer]]
+[[Category:Cardiovascular system]]
+[[Category:Up-To-Date]]
 [[Category:Oncology]]
-[[Category:Types of cancer]]
+[[Category:Medicine]]
+[[Category:Surgery]]
-{{WikiDoc Help Menu}}
-{{WikiDoc Sources}}

Cardiac tumors medical therapy: Difference between revisions

Latest revision as of 20:22, 4 July 2022

Overview

Medical Treatment of Cardiac Tumors

References

Navigation menu