tbuckley/cabot-search huggingface dataset:
Hunted Heretic: The Life and Death of Michael Servetus, 1511-1553
Authors: Roland Herbert Bainton
Journal: JAMA (1953)

Our website uses cookies to enhance your experience. By continuing to use our site, or clicking "Continue," you are agreeing to our Cookie Policy | Continue JAMA HomeNew OnlineCurrent IssueFor Authors Publications JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry (1919-1959) Podcasts Clinical Reviews Editors' Summary Medical News Author Interviews More JN Learning / CMESubscribeJobsInstitutions / LibrariansReprints & Permissions Terms of Use | Privacy Policy | Accessibility Statement 2023 American Medical Association. All Rights Reserved Search All JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Forum Archive JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry Input Search Term Sign In Individual Sign In Sign inCreate an Account Access through your institution Sign In Purchase Options: Buy this article Rent this article Subscribe to the JAMA journal
Abstract 2583: Intratumoral treatment of one tumor lesion with LTX-315 induces complete tumor regression and long-term specific protective immune responses in a metastatic rodent tumor model
Authors: Øystein Rekdal, Janne Nestvold, Meng Y. Wang, Ketil André Camilio, Ali Areffard, Baldur Sveinbjørnsson, Gunnar Kvalheim
Journal: Cancer Research (2014)

Abstract Host defense peptides are naturally occurring peptides that have an important function in innate immune responses in almost every life form. Recently it has been documented that several host defense peptides have anticancer activity. Based on a naturally occurring host defense peptide we have do novo designed the short chemically modified peptide LTX-315. We have demonstrated that LTX-315 induces an immunogenic type of cell death with subsequent release of danger signals (e.g. HMBG1, ATP and Cytochrome C) and tumor associated antigens (TAA`s). In addition LTX-315 also has the ability to directly modulate immune-responses. In a novel rat mescenhymal sarcoma model (rTMSC) we demonstrate that LTX-315 induces a complete tumor regression by intratumoral (i.t.) injection. Studies on treated tumor tissue confirmed massive necrosis and infiltration of immune cells. Successfully treated animals were protected against re-challenge with the tumor cell type treated, but not against other types of tumor cells. Moreover, tumor resistance could be adoptively transferred by spleen cells from LTX-315-treated animals. The resistance was abrogated by depletion of T-lymphocytes. To clarify whether intratumoral injection of LTX-315 in one tumor lesion can have an effect on metastatic disease, intraperitoneal tumor and two subcutaneous tumors were established in the animals. Thereafter, LTX-315 was injected into one of the subcutaneous lesion and tumor growth assessed by living imaging. The results showed that LTX-315 eradicated all three lesions and the animal went into durable complete remission. We propose that by targeting tumor locally LTX-315 can be used for individualized therapeutic in situ vaccination against cancer. Citation Format: Øystein Rekdal, Janne Nestvold, Meng Yu Wang, Ketil André Camilio, Ali Areffard, Baldur Sveinbjørnsson, Gunnar Kvalheim. Intratumoral treatment of one tumor lesion with LTX-315 induces complete tumor regression and long-term specific protective immune responses in a metastatic rodent tumor model. [abstract]. In: Proceedings of the 105th Annual Meeting of the American Association for Cancer Research; 2014 Apr 5-9; San Diego, CA. Philadelphia (PA): AACR; Cancer Res 2014;74(19 Suppl):Abstract nr 2583. doi:10.1158/1538-7445.AM2014-2583
Update on actinic keratosis in clinical trial experience with imiquimod
Authors: C. Ferrándiz
Journal: British Journal of Dermatology (2007)

Actinic keratoses (AK) is a sun induced cutaneous lesion, currently considered as a squamous cell carcinoma in situ that has the potential to progress to invasive SCC. To treat them, numerous, ablative and no ablative, therapeutic approaches exist. Among them, imiquimod, a toll like receptor agonist, recently approved to treat them in the US and Europe, has demonstrated to be effective and safe with an acceptable tolerability in the treatment of these lesions. In this article the results of several high quality RCT are analysed.
A fully human monoclonal antibody against VEGFR-1 inhibits growth of human breast cancers
Authors: Yan Wu, Zhaojing Zhong, Huiling Li, James Huber, Rajiv Bassi, Andrea Hooper, Bridget Finnerty, Xenia Jimenez, Henry Koo, Paul Balderes, Dale Ludwig, Paul Kussie, Larry Witte, Peter Bohlen, Daniel J. Hicklin
Journal: Cancer Research (2004)

3005  Vascular endothelial growth factor receptor 1 (VEGFR-1), a tyrosine kinase receptor, has been shown to be a potential therapeutic target for treatment of tumors and angiogenesis-associated diseases. VEGFR-1 is activated by the ligands VEGF-A, VEGF-B and placental growth factor (PlGF). Studies have shown that VEGFR-1 plays not only an important role in regulating pathological angiogenesis for tumor growth but also a functional role in directly promoting growth of certain cancer cells. Our studies have demonstrated a role of VEGFR-1 in growth of breast cancer in experimental models. Here, we report antitumor activity of a fully human neutralizing monoclonal antibody against human VEGFR-1. . A panel of human monoclonal antibodies specific to VEGFR-1 was generated from the KM strain of human Ig transgenic mice (Medarex). The variable regions of the antibodies were engineered into a high expression vector for production of fully human IgG1 κ antibody. One clone designated IMC-18F1 with high affinity (KD = 54 pM) efficiently blocked binding of PlGF and VEGF to VEGFR-1 with an IC50 of 0.5 and 0.8 nM, respectively. IMC-18F1 inhibited ligand-induced phosphorylation of VEGFR-1 and activation of MAP kinase and Akt downstream signaling pathways in VEGFR-1 expressing endothelial and human breast cancer cell lines. The antibody also inhibited VEGF and PlGF-stimulated growth of breast carcinoma cells in vitro. Treatment of mice with IMC-18F1 significantly suppressed growth of human breast tumors in several xenograft models. Histology analysis showed that the antitumor effect was a result of MAPK and /or Akt signaling inhibition and tumor cell necrosis induced by anti-VEGFR-1 treatment. These results indicate that targeting VEGFR-1 by a specific monoclonal antibody is a promising therapeutic approach to human breast cancer and warrant further investigation.
American Lake Scene
Authors: M. Therese Southgate
Journal: JAMA (2004)

Our website uses cookies to enhance your experience. By continuing to use our site, or clicking "Continue," you are agreeing to our Cookie Policy | Continue JAMA HomeNew OnlineCurrent IssueFor Authors Publications JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry (1919-1959) Podcasts Clinical Reviews Editors' Summary Medical News Author Interviews More JN Learning / CMESubscribeJobsInstitutions / LibrariansReprints & Permissions Terms of Use | Privacy Policy | Accessibility Statement 2023 American Medical Association. All Rights Reserved Search All JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Forum Archive JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry Input Search Term Sign In Individual Sign In Sign inCreate an Account Access through your institution Sign In Purchase Options: Buy this article Rent this article Subscribe to the JAMA journal
Lipid Profile, Plasma Apolipoproteins, and Risk of a First Myocardial Infarction Among Asians
Authors: Ganesan Karthikeyan, Koon K. Teo, Shofiqul Islam, Mathew J. McQueen, Prem Pais, Xingyu Wang, Hiroshi Sato, Chim Choy Lang, Chitr Sitthi-Amorn, M.R. Pandey, Khawar Kazmi, John E. Sanderson, Salim Yusuf
Journal: Journal of the American College of Cardiology (2009)
Single-agent Taxane Versus Taxane-containing Combination Chemotherapy as Salvage Therapy for Advanced Urothelial Carcinoma
Authors: Guru Sonpavde, Gregory R. Pond, Toni K. Choueiri, Stephanie Mullane, Guenter Niegisch, Peter Albers, Andrea Necchi, Giuseppe Di Lorenzo, Carlo Buonerba, Antonio Rozzi, Kazumasa Matsumoto, Jae-Lyun Lee, Hiroshi Kitamura, Haruki Kume, Joaquim Bellmunt
Journal: European Urology (2015)
Studies of Properties of the Liver Mitotic Stimulant (LMS) in Mouse Tumor Tissue
Authors: Richard A. Malmgren, Willie Mills
Journal: JNCI Journal of the National Cancer Institute (1961)

Journal Article Studies of Properties of the Liver Mitotic Stimulant (LMS) in Mouse Tumor Tissue Get access Richard A. Malmgren, Richard A. Malmgren Laboratory of Pathology, National Cancer Institute,2Bethesda, Maryland Search for other works by this author on: Oxford Academic PubMed Google Scholar Willie Mills Willie Mills Laboratory of Pathology, National Cancer Institute,2Bethesda, Maryland Search for other works by this author on: Oxford Academic PubMed Google Scholar JNCI: Journal of the National Cancer Institute, Volume 26, Issue 3, March 1961, Pages 525–532, https://doi.org/10.1093/jnci/26.3.525 Published: 01 March 1961 Article history Received: 16 March 1960 Revision received: 02 November 1960 Published: 01 March 1961
Lipid Profile Changes in Patients With Chronic Inflammatory Arthritis Treated With Biologic Agents and Tofacitinib in Randomized Clinical Trials: A Systematic Review and Meta‐Analysis
Authors: Alejandro Souto, Eva Salgado, José Ramón Maneiro, Antonio Mera, Loreto Carmona, Juan J. Gómez‐Reino
Journal: Arthritis & Rheumatology (2014)

To analyze lipid changes in patients with rheumatoid arthritis (RA) and patients with spondyloarthritis (SpA) treated with biologic agents or tofacitinib in randomized clinical trials (RCTs).A systematic literature search was performed, using the Medline, Embase, Cochrane Library, and Web of Knowledge databases. Meta-analyses were performed using random-effects models to assess changes in the percentage of patients with abnormal lipid values or in the mean percentage of increase in the cholesterol and triglycerides levels.Twenty-five of 4,527 identified articles met the inclusion criteria. Compared with RA patients treated with placebo, those treated with tocilizumab were more likely to have hypercholesterolemia (odds ratio [OR] 4.64; 95% confidence interval [95% CI] 2.71, 7.95 [P < 0.001]), increased levels of high-density lipoprotein (HDL) cholesterol (OR 2.25; 95% CI 1.14, 4.44 [P = 0.020]), and increased levels of low-density lipoprotein (LDL) cholesterol (OR 4.80; 95% CI 3.27, 7.05 [P < 0.001]); this was not observed in patients treated with tumor necrosis factor (TNF) antagonists (OR 1.54; 95% CI 0.90, 2.66 [P = 0.119]) or tofacitinib (OR 3.4; 95% CI 0.62, 18.55 [P = 0.158]). Among patients receiving tofacitinib 5 mg twice daily, the mean percentage of increases in the HDL cholesterol level (weighted mean difference [WMD] 13.00 mg/dl; 95% CI 12.08, 13.93 [P < 0.001]) and the LDL cholesterol level (WMD 11.20 mg/dl; 95% CI 10.08, 12.32 [P < 0.001]) were higher than those in the comparator groups. Among patients treated with tofacitinib 10 mg twice daily, the mean percentage of increases in the HDL cholesterol level (WMD 15.21 mg/dl; 95% CI 13.28, 17.14 [P < 0.001]) and the LDL cholesterol level (WMD 15.42 mg/dl; 95% CI 11.77, 19.06 [P < 0.001]) were also higher than those in the comparator groups. No data were available for RA treated with other biologic agents or for SpA.In patients with RA treated with tocilizumab or tofacitinib but not with TNF antagonists, moderate changes in lipids are observed. Whether these changes pertain to the control of inflammation or to the mechanism of action of the biologic agents or tofacitinib remains undetermined.
ACTINOMYCOSIS: A NEW SPECIES, PATHOGENIC FOR MAN
Authors: George C. H. Franklin
Journal: Annals of Internal Medicine (1940)

Article1 January 1940ACTINOMYCOSIS: A NEW SPECIES, PATHOGENIC FOR MANGEORGE C. H. FRANKLIN, M.D., F.A.C.P.GEORGE C. H. FRANKLIN, M.D., F.A.C.P.Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-13-7-1205 SectionsAboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail ExcerptThe diagnosis of human actinomycosis is not always made with ease, and furthermore the identification of the causative species is usually quite difficult. In medical literature cases are frequently reported as actinomycosis followed by the statement, unable to culture, culture lost, not able to identify, etc. The species in some cases is not of great interest to the physician; however, the laboratory should always attempt to identify the organism.The disease may be either localized or generalized. It is usually chronic and the duration is from several months to several years. It is thus frequently misdiagnosed "tuberculosis."In 1925, Sanford...References1. SANFORDVOELKER AHM: Actinomycosis in the United States, Arch. Surg., 1925, ii, 809-841. CrossrefGoogle Scholar2. TOPLEYWILSON WWGS: Principles of bacteriology and immunity, 2nd ed., 1936, Wm. Wood and Co., Baltimore. Google Scholar3. BRUMPT E: Précis de Parasitologie, 5th ed., Vol. ii, 1936, Masson et Cie, Paris, France. Google Scholar4. DODGE CW: Medical mycology, 1935, C. V. Mosby Co., St. Louis. Google Scholar5. BERGEY DH: Manual of determinative bacteriology, 4th ed., 1933, Williams and Wilkins Co., Baltimore. Google Scholar6. TOPLEYWILSON WWGS 2 Google Scholar7. DODGE CW 4 Google Scholar8. BRUMPT E 3 Google Scholar9. WAKSMAN SA: Principles of soil microbiology, 2nd ed., 1932, Williams and Wilkins Co., Baltimore. Google Scholar This content is PDF only. To continue reading please click on the PDF icon. Author, Article, and Disclosure InformationAffiliations: Fort Leavenworth, Kansas*Received for publication July 9, 1938.†Deceased. PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics Cited byDie AktinomykoseCritical survey of the mycological literature of the years 1939 to 1942Primary actinomycosis of the lung 1 January 1940Volume 13, Issue 7Page: 1205-1213KeywordsActinomycosisPathogensResearch laboratories Issue Published: 1 January 1940 PDF downloadLoading ...
Abstract LB-300: Reintroduction of tumor-suppressor miR-34a shows therapeutic efficacy in triple-negative breast cancer
Authors: Brian D. Adams, Vikram Wali, Chris Cheng, Sachi Inukai, David Rimm, Lajos Pusztai, Mark Saltzman, Frank Slack
Journal: Cancer Research (2015)

Abstract Triple-negative breast cancer (TNBC) accounts for a disproportionate share of the total breast cancer morbidity because of its aggressive behavior and lack of effective targeted therapies to treat the disease. MicroRNAs, global regulators of survival and proliferation pathways important in tumor development and maintenance, are highly dysregulated in cancer. We identified miR-34a to be aberrantly lost in TNBC lines when compared to both a luminal cancer subtype as well as normal breast cells. Re-introduction of miR-34a in TNBC lines results in inhibition of cell proliferation and invasion, reactivation of senescence, and enhanced sensitivity to apoptosis inducing agents. Furthermore, intratumoral delivery of miR-34a into subcutaneous tumors in nude mice, as well as systemic delivery of poly(amine-co-ester) PACE-loaded miR-34a in an orthotopic setting, delayed tumor growth. In conclusion, re-introduction of miR-34a in TNBC promotes potent anti-tumorigenic phenotypes in vitro and in vivo, and could be a promising targeted therapeutic agent to treat the disease. Citation Format: Brian D. Adams, Vikram Wali, Chris Cheng, Sachi Inukai, David Rimm, Lajos Pusztai, Mark Saltzman, Frank Slack. Reintroduction of tumor-suppressor miR-34a shows therapeutic efficacy in triple-negative breast cancer. [abstract]. In: Proceedings of the 106th Annual Meeting of the American Association for Cancer Research; 2015 Apr 18-22; Philadelphia, PA. Philadelphia (PA): AACR; Cancer Res 2015;75(15 Suppl):Abstract nr LB-300. doi:10.1158/1538-7445.AM2015-LB-300
Abstract 13969: Effect of Endothelial Shear Stress on the Serial Changes of Vein Grafts Assessed by Optical Coherence Tomography during the First Year After Coronary Artery Bypass Graft Surgery: Analysis from the CABG-PRO Study
Authors: Anna Kotsia, Michail Papafaklis, Tesfaldet Michael, Bavana Rangan, Matthias Pelz, Michele Roesle, Michael Jessen, Bernice Willis, Georgios Christopoulos, Georgios Nakas, Sofia Giannitsi, Spyros Sioros, Konstantinos Argyropoulos, Dimitris Fotiadis, Lampros Michalis, Subhash Banerjee, Emmanouil Brilakis
Journal: Circulation (2014)

Introduction: Saphenous vein grafts (SVGs) have high rates of both early (≤ 1 year) and late failure following coronary arterial bypass graft surgery (CABG). Hypothesis: Endothelial shear stress (ESS) is a critical determinant of the natural history of coronary atherosclerosis, but the influence on the structural changes of SVGs has not been studied. We evaluated the effect of ESS on the serial anatomic outcomes of SVGs assessed by optical coherence tomography (OCT) during the first postoperative year. Methods: We performed 3-dimensional SVG reconstruction in 8 SVGs using fusion of angiographic and OCT data 5-7 days after surgery (baseline) and at 12-month follow-up. Baseline ESS was assessed using computational fluid dynamics. The reconstructed SVGs were divided in consecutive 3-mm segments (n=181), and we assessed the association of baseline ESS with the anatomic outcomes in the corresponding segments at follow-up: change in lumen area and plaque burden, and neointimal area at follow-up. Baseline ESS was categorized according to the tertiles of the ESS frequency distribution. Results: Median baseline ESS in SVGs was 0.48 Pa [IQR: 0.37-0.61 Pa]). Baseline low ESS was associated with: (i) the largest decrease in lumen area (low ESS category: -8.72±0.95 mm2 vs. moderate ESS category: -5.67±0.95 mm2 vs. high ESS category: -3.64±0.95 mm2; p&lt;0.001 low vs moderate and high ESS category), (ii) the largest increase in plaque burden (low ESS category: 24.3±3.4% vs. moderate ESS category: 22.6±3.4% vs. high ESS category: 20.9±3.4%; p=0.011 low vs high ESS category), and (iii) the largest neointimal area at 12 months (low ESS category: 4.02±0.45 mm2 vs. moderate ESS category: 3.65±0.45 mm2 vs. high ESS category: -3.57±0.45 mm2; p=0.020 low vs moderate ESS category, and p=0.009 low vs high ESS category). Conclusions: SVG areas with the lowest local ESS develop the largest lumen constriction, plaque burden increase and neointima formation. These findings provide important insights into the pathogenesis of early SVG failure.
THE TREATMENT OF REFRACTORY ANEMIA WITH COBALT
Authors: E D THOMAS
Journal: Annals of Internal Medicine (1956)

ExcerptSince Waltner and Waltner1 first discovered that cobalt produces polycythemia in animals, physicians have attempted to employ this element in the therapy of anemia. One group of anemias that has attracted particular attention is that of the refractory anemias. Most investigators have found cobalt to have no therapeutic value in this type of anemia. Berk, Burchenal and Castle2 treated five patients with refractory anemia and hypercellular marrow with 300 mg. of cobaltous chloride daily with no reticulocyte response or rise in blood values. Weissbecker3 found cobalt to be of no value in six cases of aplastic anemia.However, a few...
Senate Extends Funding That Provides Health Insurance for Children
Authors: Rita Rubin
Journal: JAMA (2015)

Our website uses cookies to enhance your experience. By continuing to use our site, or clicking "Continue," you are agreeing to our Cookie Policy | Continue JAMA HomeNew OnlineCurrent IssueFor Authors Publications JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry (1919-1959) Podcasts Clinical Reviews Editors' Summary Medical News Author Interviews More JN Learning / CMESubscribeJobsInstitutions / LibrariansReprints & Permissions Terms of Use | Privacy Policy | Accessibility Statement 2023 American Medical Association. All Rights Reserved Search All JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Forum Archive JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry Input Search Term Sign In Individual Sign In Sign inCreate an Account Access through your institution Sign In Purchase Options: Buy this article Rent this article Subscribe to the JAMA journal
Peanut oral immunotherapy transiently expands circulating Ara h 2–specific B cells with a homologous repertoire in unrelated subjects
Authors: Sarita U. Patil, Adebola O. Ogunniyi, Agustin Calatroni, Vasisht R. Tadigotla, Bert Ruiter, Alex Ma, James Moon, J. Christopher Love, Wayne G. Shreffler
Journal: Journal of Allergy and Clinical Immunology (2015)
Circadian Rhythms and Reperfusion in Patients With Acute ST-Segment Elevation Myocardial Infarction
Authors: Roberto Manfredini, Benedetta Boari, Raffaella Salmi, Anna Maria Malagoni, Fabio Manfredini
Journal: JAMA (2005)

Our website uses cookies to enhance your experience. By continuing to use our site, or clicking "Continue," you are agreeing to our Cookie Policy | Continue JAMA HomeNew OnlineCurrent IssueFor Authors Publications JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry (1919-1959) Podcasts Clinical Reviews Editors' Summary Medical News Author Interviews More JN Learning / CMESubscribeJobsInstitutions / LibrariansReprints & Permissions Terms of Use | Privacy Policy | Accessibility Statement 2023 American Medical Association. All Rights Reserved Search All JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Forum Archive JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry Input Search Term Sign In Individual Sign In Sign inCreate an Account Access through your institution Sign In Purchase Options: Buy this article Rent this article Subscribe to the JAMA journal
Unrelated Hematopoietic Cell Transplantation in Aplastic Anemia
Authors: Mouhab Ayas
Journal: JAMA Oncology (2015)

Aplastic anemia is a condition in which the hematopoietic stem cells fail to function adequately leading to peripheral pancytopenia.When the cytopenia is severe, patients require intensive support with blood products and broad spectrum antibiotics, and without definitive treatment, most will eventually die of infec-tions or bleeding.Over the past 4 decades, however, these once uniformly fatal conditions have been transformed into potentially highly curable ones.Matched related hematopoietic cell transplantation (HCT) is now the standard curative modality for acquired severe aplastic anemia