Skip to main content Accessibility help
×
  1. Home
  2. Browse subjects
  3. Medicine
  4. Oncology
  5. Content listing

Refine search

Refine search

Access:
Content type:
Publication date:
Apply   From and To filters
Subject: Show more
Journals Show more
Publishers: Show more
Societies Show more
Series: Show more
Collections: Show more

Actions for selected content:

Select all | Deselect all
  • View selected items
  • Export citations
  • Download PDF (zip)
  • Save to Kindle
  • Save to Dropbox
  • Save to Google Drive

Save Search

You can save your searches here and later view and run them again in "My saved searches".

Please provide a title, maximum of 40 characters.
Cancel
×

2602 results in Oncology

Page 35 of 131

  • 19 - Graft rejection and failure

  • Joseph H. Antin, Deborah Yolin Raley
  • Book:
    Manual of Stem Cell and Bone Marrow Transplantation
    Published online:
    05 November 2013
    Print publication:
    17 October 2013, pp 121-123

  • Summary

    Graft rejection

  • Graft rejection refers to the immunologic rejection of donor hematopoietic elements by the residual host immune system. Graft rejection occurs more frequently in patients transplanted for aplastic anemia and in those receiving unrelated or mismatched transplants (because of increased donor–recipient disparity at major and minor HLA loci). Graft rejection may also be observed in reduced-intensity regimens, especially in patients who are not pretreated heavily.

  • In many patients with aplastic anemia, the underlying pathophysiology reflects an autoimmune recognition of the stem cells by an aberrant immune response. Most conditioning regimens used in aplastic anemia are reduced-intensity regimens. If the conditioning regimen does not fully eliminate the abnormal immune response, the graft may fail by the same mechanism that resulted in aplastic anemia in the first place. Prior to matched related donor transplantation, family member, directed donor transfusions should not be administered to avoid alloimmunization of the patient against minor histocompatibility antigens that are common to other family members.

  • 22 - Pulmonary complications

  • Joseph H. Antin, Deborah Yolin Raley
  • Book:
    Manual of Stem Cell and Bone Marrow Transplantation
    Published online:
    05 November 2013
    Print publication:
    17 October 2013, pp 154-161

  • Summary

    Pulmonary injury is one of themost common complications of stem cell transplantation and a major cause ofmorbidity and mortality. Damage to the lungs can be multifactorial,including infection, chemotherapy toxicity, graft-versus-host disease(GVHD), radiation injury, hemorrhage, and immune reactions. Potentialetiology can be determined by carefully considering timing of pulmonarycomplications and whether the radiographic studies are focal or diffuse.Important also to consider is history including exposure to infectiousagents, current and recent prophylaxis regimen, cytomegalovirus (CMV) statusof patient and donor, prior treatment and exposure to pulmonary/cardiotoxictherapy, and current and recent immunosuppression therapy.

    All patients should havebaseline pulmonary function tests (PFTs) before transplantation, and anaggressive diagnostic approach should be taken early after transplantationif there are pulmonary problems.

    In general, patients withdyspnea and normal chest X-ray (CXR) should undergo PFTs and arterial bloodgas analysis. Restrictive physiology should prompt a chest CT (to look forinterstitial disease). In patients with normal PFTs and CXR, cardiac causessuch as pulmonary hypertension and cardiac dysfunction should beexcluded.

    Bronchoscopy withbronchoalveolar lavage (BAL) should be performed early in the search for adiagnosis. If no diagnosis is made, lung biopsy if possible should beconsidered. Patients with focal ini ltrates should be given empiricantibiotics plus or minus fungal therapy and assessed for a response beforeinvasive measures are taken.

  • 15 - Treatment guidelines for acute graft-versus-host disease

  • Joseph H. Antin, Deborah Yolin Raley
  • Book:
    Manual of Stem Cell and Bone Marrow Transplantation
    Published online:
    05 November 2013
    Print publication:
    17 October 2013, pp 64-78

  • Summary

    Steroids ± calcineurin inhibitor

    All other therapies areinvestigational at this time and no comparative data are available.

  • Therapy is effective 30–60% of the time.

  • Typically, therapy needs to be maintained until manifestations are completely resolved; however, be careful of the risk of opportunistic infections and EBV lymphoproliferative disorders that are associated with increased immunosuppression.

  • If GVHD develops after T-cell-depleted HSCT, CSA or tacrolimus are useful additions.

    • Steroids

    Methylprednisolone 0.5 to 2mg/kg/day. The most common dose is 1 to 2 mg/kg day in grade II to IVGVHD.

  • Conversion: Hydrocortisone (1×), prednisone (4×), Solu-Medrol® (5×), Decadron (20×). For example, a patient on 100 mg of Solu-Medrol would convert to 80 mg of prednisone.

  • There is no standard method to tapering steroids once symptoms improve. A reasonable approach is to taper by 10% of original dose per week in the absence of GVHD symptoms and after GVHD has been controlled for about 1 month.

  • 14 - Graft-versus-host disease prophylactic regimens

  • Joseph H. Antin, Deborah Yolin Raley
  • Book:
    Manual of Stem Cell and Bone Marrow Transplantation
    Published online:
    05 November 2013
    Print publication:
    17 October 2013, pp 53-63

  • Summary

    Effective prophylaxis islimited by an incomplete understanding of the pathophysiology of thedisease. Drugs are often used in combination in an attempt to block severalpathways thought to cause graft-versus-host disease (GVHD). Use ofcalcineurin inhibitors in conjunction with methotrexate is the most commoncombination regimen. Institutions use a variety of combinations. The doseand toxicity of each agent are listed individually below.

  • Tacrolimus/methotrexate (MTX) or cyclosporine/MTX is superior to single-agent prophylaxis. When calcineurin inhibitors are used with lower doses of MTX, so-called “mini methotrexate” may attenuate mucositis caused by MTX.

  • Tacrolimus/mycophenolate mofetil (MMF) or cyclosporine/MMF are alternatives for patients who are unable to take MTX.

  • Sirolimus/tacrolimus/MTX or sirolimus/tacrolimus may allow for lower doses or the elimination of MTX, although there is an increased risk of veno-occlusive disease (VOD) if myeloablative conditioning is used.

    • Agents used for prophylaxis

    Methotrexate

    Mechanism of action

    Blocks the enzymedihydrofolate reductase, which inhibits the conversion of folic acid totetrahydrofolic acid, resulting in inhibition of the key precursors of DNA,RNA, and cellular protein.

  • 4 - Stem cell source

  • Joseph H. Antin, Deborah Yolin Raley
  • Book:
    Manual of Stem Cell and Bone Marrow Transplantation
    Published online:
    05 November 2013
    Print publication:
    17 October 2013, pp 9-14

  • Summary

    Hematopoietic progenitor cell products

    Hematopoietic progenitor cell(HPC) products contain hematopoietic stem and lineage-committed progenitorcells capable of providing hematopoietic and immune reconstitution aftermyeloablative, nonmyeloablative, or reduced-intensity preparative regimens.There is no unanimity on the terminology.

  • Since stem cells are difficult to identify specifically, some authors prefer the term hematopoietic cell transplantation (HCT).

  • Others call the procedure hematopoietic stem cell transplantation (HSCT) to acknowledge that most transplantations are not successful unless stem cells are transplanted.

  • The Foundation for the Accreditation of Cellular Therapy (FACT) focuses on progenitors. Cellular therapy products can be broadly categorized as being either minimally manipulated products or more than minimally manipulated products.

    • Hematopoietic progenitor cell function

    Hematopoietic progenitor cellsadministered intravenously migrate to the marrow, where they adhere, expand,self-renew (stem cells only), and differentiate. The differentiated cellsare released into the blood, restoring blood counts and immunity. The timefrom administration of HPCs to recovery of adequate or normal blood countsis variable (see Chapter 9, Engraftment).

  • 26 - Neurologic complications

  • Joseph H. Antin, Deborah Yolin Raley
  • Book:
    Manual of Stem Cell and Bone Marrow Transplantation
    Published online:
    05 November 2013
    Print publication:
    17 October 2013, pp 172-176

  • Summary

    Neurologic toxicity is commonand often multifactorial. The primary causes of neurologic injury are (1)drug toxicity, (2) infection, (3) toxic metabolic encephalopathy, and (4)hemorrhage. It is convenient to consider neurologic injury occurring earlyafter transplantation and that occurring late after transplantationseparately. Early toxicity tends to be related to immediate problems withconditioning regimen effects. Preexisting neurological problems related tomalignancy or metabolic encephalopathy are likely to increase the risk ofimmediate post-transplantation neurologic symptoms. Later events are oftenrelated to prolonged immunoincompetence and the effects of calcineurininhibitors.

    Calcineurin inhibitors

  • CNI use (cyclosporine and tacrolimus) is probably the single most frequent cause of neurologic toxicity. The most common manifestations are tremor and burning palmar and plantar dysesthesias. However, headache, depression, confusion, somnolence, and nystagmus may also be observed. Seizures may occur, especially in association with hypomagnesemia, hypertension, hypocholesterolemia, infections, and high blood levels of CNIs.

  • A unique complication of CNIs is cortical blindness and posterior leukoencephalopathy. This syndrome is known as PRES – posterior reversible encephalopathy syndrome. It is often observed in association with the new onset of hypertension, suggesting that there is cerebral edema due to abnormalities of pressure regulation in the posterior circulation. Many of the radiologic manifestations are similar to those seen in hypertensive encephalopathy. The most common pattern is white matter edema in the posterior circulation, which may or may not persist despite continued use of the drug. Although there are reports to the contrary, most clinicians believe that cyclosporine and tacrolimus are cross-reactive; therefore, substitution of one for the other may not be useful. Newer agents such as sirolimus or mycophenolate mofetil have no known neurological toxicity and may be appropriate substitutes for CNIs. Establishing a successful immunosuppressive regimen in this setting can be quite difficult, and may require persistent use of the offending agent with an effort to maintain excellent blood pressure control.

  • A frequent complication of the use of CNIs is the development of thrombotic microangiopathy. These microangiopathies are associated with evidence of hemolysis; typically, schistocytes are observed on the blood smear and there is a reduction in haptoglobin. Because of renal vascular involvement, hypertension and azotemia are generally concomitantly observed.

  • Other less common manifestations of these agents include coma, optic disc edema, aphasia, paralysis, insomnia, somnolence, and rigidity.

The BMT Data Book
  • Including Cellular Therapy
  • 3rd edition
  • Edited by Reinhold Munker, Gerhard C. Hildebrandt, Hillard M. Lazarus, Kerry Atkinson
  • Published online:
    05 August 2013
    Print publication:
    21 February 2013
  • This is an essential guide to the data, basic science, outcome studies and decision-making processes involved in blood and marrow stem cell transplantation. Organized according to disease types and procedures, it contains more than 100 tables, figures and algorithms that reflect up-to-date research and give guidance on the choices between different types of chemotherapy, autologous vs. allogeneic transplantation, peripheral blood vs. bone marrow stem cells, and standard vs. experimental treatments. This new edition summarizes the research of the last four years and gives mature data for all established indications, such as acute myeloid leukemia, myelodysplastic syndrome and Hodgkin and non-Hodgkin lymphomas. New chapters discuss global trends in stem cell transplantation, cellular therapies including donor lymphocytes, and pediatric neurologic and metabolic disorders. With an expanded complications section, links to electronic databases and discussion of new drugs and alternative stem cell sources, this text belongs in every transplant unit.

Altchek's Diagnosis and Management of Ovarian Disorders
  • 3rd edition
  • Edited by Liane Deligdisch, Nathan G. Kase, Carmel J. Cohen
  • Published online:
    05 August 2013
    Print publication:
    25 July 2013
  • Disorders of the ovary can lead to a wide range of endocrinologic and malignant conditions, many of which are linked with fertility. This comprehensive, yet succinct book presents a multidisciplinary approach to address the major issues in diagnosing and managing ovarian disorders. Beginning with the complex functioning of the normal ovary, the editors address many of the major issues in women's health. New chapters on ovarian cysts, menopause, the aging ovary, early detection and risk assessment of ovarian cancer, screening, stage I ovarian cancer and many other topics have been added to this third edition. Assisted reproductive techniques, diagnostic imaging modalities, minimally invasive surgery, and chemotherapy have advanced dramatically and the chapters have been updated accordingly. This well-documented volume has been fully updated with contemporary references and chapters written by current leaders in their field. A must-read for gynecologists, oncologists, obstetricians, pathologists and researchers in human reproductive sciences.

Page 35 of 131