M.G. Sauta

Myelodysplastic syndrome appearing during imatinib mesylate therapy in a patient with GIST.

The introduction of imatinib has been a major advance in the treatment of gastrointestinal stromal tumor (GIST). However, despite its remarkable efficacy and toxicity profile little is known about the potential for long-term toxicity. This may be an important issue because some patients (pts) with chronic myelogenous leukemia (CML) develop, during imatinib treatment, chromosomal abnormalities in philadelphia chromosome (Ph) negative cells with evolution to myelodysplastic syndromes (MDS) or acute myeloid leukemia (AML), furthermore a nonrandom association between GIST and myeloid leukemia has been recently reported. We report here a case of refractory cytopenia with mutilineage dysplasia (RAEB-1) with monosomy 7 which rapidly transformed into AML in a patient with GIST during imatinib treatment.

Risk of Second Malignant Neoplasm Among Patients With Lymphoma

TO THE EDITOR: The recently published article, “Long-Term Complications of Lymphoma and Its Treatment,” by Ng et al 1 provides a much needed overview of its topic. Unfortunately, however, the article fails to emphasize two key concepts: first, the necessity of investigating the impact of associated rituximab treatment in nonHodgkin’s lymphoma on long-term complications, and second, the differences in risk of a new, second malignancy caused by a lymphoma subtype. Briefly, the monoclonal antibody rituximab has increased disease-free survival for many lymphoid malignant diseases and seems not to have a significant influence on secondary myelodysplastic syndromes/acute myeloid leukemia, whereas it has emerged as an independent risk factor for solid tumor development. 2 In addition, even if the precise role played by B cells in cancer biology remains to be defined, recent reports stress antitumor B-cell— derived immunity. 3,4 In other words, it seems conceivable that the profound immunosuppression that is secondary to B-cell deletion by rituximab may contribute to the expansion of tumor cells. Given that the occurrences of lung cancer and melanoma are limited to more indolent lymphomas, it is plausible that long-term immune dysfunction from the underlying disease or repeated treatments is responsible. Furthermore, the heightened risks immediately after chronic lymphocytic leukemia (CLL)/small lymphocytic lymphoma (SLL) and follicular lymphoma (FL) diagnoses suggest an intrinsic mechanism, possibly involving prediagnostic immune alterations or defects in a cell cycle and apoptosis, which are more characteristic of indolent rather than aggressive lymphomas. Recent findings demonstrate substantial heterogeneity in the occurrence of a second malignancy by a lymphoma subtype, which suggests differences in etiology. Specifically, significantly different patterns of second malignancy after CLL/SLL, diffuse large B-cell lymphoma (DLBCL), and FL among patients without HIV/AIDS-related lymphoma have been reported. 5 Most notable were the elevated risks for lung cancer and melanoma after the more indolent lymphomas, but not after the more aggressive DLBCL. Furthermore, survivors of CLL/SLL and FL have demonstrated a greater risk of developing other nonhematologic malignancies (ie, salivary gland, colon, anus, and thyroid), whereas, in contrast, no evidence has been reported, to our

Secondary Leukemia in a non-Hodgkin's Lymphoma Patient Presenting as Myeloid Sarcoma of the Breast

As defined by the World Health Organization classification of tumors of hematopoietic and lymphoid tissue, myeloid sarcoma (MS) is a tumor mass of myeloblasts or immature myeloid cells that can arise before, concurrent with, or following acute myeloid leukaemia. We describe a case of secondary leukemia presenting itself as MS of the breast in a patient previously treated for a non-Hodgkins Lymphoma.

Combinations of Hormonal Therapy and Chemotherapy

Prostate cancer (PC) is a heterogeneous disease, with a complex natural history, whose growth is driven by androgens and androgen receptors. In most cases, patients have localized disease at presentation, which may be successfully treated with radical prostatectomy and external beam radiation. However, many patients subsequently develop metastatic disease. De novo metastases can also occur in a minority of cases.Androgen deprivation therapy (ADT) is the standard treatment of metastatic hormone-naive (or castration-sensitive) prostatic cancer (CSPC). ADT usually determines a profound PSA decline and a radiological and clinical benefit in most patients. However, essentially all patients experience progression to castration-resistant prostate cancer (CRPC) despite persisting low testosterone levels in around 1–2 years, and overall prognosis remains disappointing, although subsequent active treatments are available. Early targeting of cells that survive hormonal therapy may potentially prevent the development of CRPC. The aim of these therapeutic strategies is the elimination of resistant cells at the time the tumor is apparently “androgen sensitive”. The large randomized studies analyzed in this chapter, addressing the early use of docetaxel in combination with ADT in men with metastatic CSPC, have shown evidence that at least a subset of patients with metastatic CSPC may benefit from the combination of ADT with docetaxel as initial therapy.