PubMed · 2644477
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J Shimazaki. 1989. [Prostatic cancer].. https://pubmed.ncbi.nlm.nih.gov/2644477/
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Occurrence of second cancers is a major concern for the care of children cured of cancer. Children treated for acute lymphoblastic leukemia (ALL) have an increased risk for developing mucoepidermoid carcinomas (MEC) of the parotid gland. The latent period ranges from 5 to 16 years. A 3-year-old boy presented with pre-B ALL. Treatment included multidrug chemotherapy and prophylactic intrathecal injections of methotrexate and prednisolone. Low-grade MEC of the left parotid gland was diagnosed at the age of 7 years, only 1 year after completing treatment. Local lymph nodes were not metastatic, and course was favorable 8 years after complete surgical excision. This case report is remarkable for the early diagnosis of second cancer, only 4 years after diagnosis of ALL, and its occurrence in parotid gland without previous head and neck irradiation. It highlights the need for concern about second cancers of the parotid gland in children treated for ALL.
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Richter's transformation denotes the development of high-grade non-Hodgkin lymphoma, prolymphocytic leukemia, Hodgkin disease, or acute leukemia in patients with chronic lymphocytic leukemia (CLL)/small lymphocytic lymphoma. A search of published articles in Medline (PubMed) and abstracts from professional meetings was performed. An electronic database search of patients with CLL at The University of Texas M. D. Anderson Cancer Center (Houston, TX) determined the incidence of Richter syndrome (RS) in patients with CLL between 1992 and 2002. RS occurs in approximately 5% of patients with CLL. The large cells of RS may arise through transformation of the original CLL clone or represent a new neoplasm. RS may be triggered by viral infections, such as Epstein-Barr virus. Trisomy 12 and chromosome 11 abnormalities are more frequent in patients with RS than in the overall population of patients with CLL. Multiple genetic defects, such as mutations of the p53 tumor suppressor gene, p16INK4A, and p21, loss of p27 expression, deletion of retinoblastoma, increased copy number of C-MYC, and decreased expression of the A-MYB gene, have been described. These abnormalities may cause CLL cells to proliferate and-by facilitating the acquisition of new genetic abnormalities-to transform into RS cells. Therapeutic strategies include intensive chemotherapy, monoclonal antibodies, and stem cell transplantation. The response rates range from 5% to 43% (complete response, 5-38%), and the median survival duration ranges from 5 months to 8 months. In conclusion, RS may be triggered by viral infections or by genetic defects. Current treatments are aggressive, but prognosis is poor. Novel curative treatment strategies are needed.