PubMed Health⌕ Search
Home/Archive/PubMed

PubMed · 16416343

[Thymoma].

Stephan Gripp·Edwin Bölke·Klaus Orth
View original source ↗Export metadata ↓

Abstract

Thymoma is a rare epithelial tumor of the thymus, but the most common malignancy in the anterior mediastinum. A unique feature is its association with paraneoplastic syndromes, in particular myasthenia gravis. According to the WHO classification 6 histologic types of thymic epithelial tumors can be discriminated. Tumor stage according to MASAOKA is the most important prognostic factor. Non-invasive tumors (stage I) are usually completely resected and no further therapy is warranted. For incompletely resected tumors and locally advanced invasive thymomas (stage Ill-IV) postoperative radiotherapy with 50-60 Gy is advisable. Chemotherapy, preferably with Cisplatinum, is indicated with inoperable thymomas or metastatic disease. In general thymomas have a fair prognosis even in advanced stage. Long term follow-up is mandatory up to 10 years.

Explore related subjects

Drug TherapyHumansNeoplasm Recurrence, LocalPractice Guidelines as TopicPractice Patterns, Physicians'PrognosisRadiotherapyThymomaThymus NeoplasmsEnglish AbstractJournal ArticleReview

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

Stephan Gripp, Edwin Bölke, Klaus Orth. 2005. [Thymoma].. https://doi.org/10.1007/s00508-005-0407-y

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related citations

PubMed2006

Chronic myeloid leukemia: standard treatment options.

PURPOSE: Treatment options for chronic myeloid leukemia (CML) are discussed. SUMMARY: In the 1980s busulfan and hydroxyurea were the standards of care. These were subsequently replaced by interferon alpha (IFN alpha) based therapy. Currently, bone marrow transplant survival has improved, making this also a viable option. Five-year progression-free survival averaged above 70% for chemotherapeutic options. Transplant survival at 56 months was approximately 60%; however, these survivors were generally cured of disease. The recognition of the role for BCR-ABL in CML has led to the development of specific kinase inhibitors such as imatinib. Clinical trial evidence has demonstrated a clear superiority of imatinib over interferon plus cytarabine, making this the new standard of care in first-line treatment of CML. Resistance to imatinib has been observed, in addition to relapse. The data suggest that the probability of response may be estimated as early as six months after initiation of imatinib therapy. Although combinations of imatinib with IFN alpha show small improvements compared to imatinib therapy alone, the biggest improvements were seen when imatinib doses were doubled. Unfortunately, not all patients can tolerate this increase in dose. The most common mechanism for imatinib resistance is the presence of a mutated BCR-ABL kinase. Several of these mutants have been cloned and characterized. CONCLUSION: Molecular-targeted BCR-ABL kinase inhibitors, such as imatinib, are now first-line treatment for CML. Allogeneic stem cell transplant is still the only proven curable treatment for CML in patients with an appropriate donor. Next generation BCR-ABL kinase inhibitors hold promise for patients with mutated BCR-ABL kinase that confer resistance to imatinib.

Drug Therapy↗
PubMed2006

Novel treatment strategies for chronic myeloid leukemia.

PURPOSE: Despite dramatic advances in the treatment of chronic myeloid leukemia (CML), resistance to therapeutic agents has emerged as a significant treatment dilemma. Mutations of the BCR-ABL kinase domain, a common mechanism of resistance to imatinib in CML, are discussed. SUMMARY: Several new targeted kinase inhibitors have reached clinical trials and have proved to be efficacious in halting the oncogenic activity of most BCR-ABL mutants. Dasatinib is 300 times more potent than imatinib at BCR-ABL inhibition, has few side effects, and inhibits the SRC family kinases. Nilotinib inhibits BCR-ABL at 20-50 times more potency than imatinib. Both agents were highly effective in treating chronic phase CML but were less effective at treating accelerated phase CML in early phase clinical trials. In addition to these specific kinase inhibitors, farnesyl transferase inhibitors are actively being investigated. Vaccination strategies are undergoing clinical investigation transitioning from animal models to human clinical trials. CONCLUSION: The new kinase inhibitors, dasatinib and nilotinib, are emerging as plausible therapeutic options for the treatment of imatinib-refractory CML.

Drug Therapy↗