RESUMEN
Metastatic breast cancer is rarely identified in a uterine leiomyoma. Herein is reported the case of a 53-year-old patient with untreated left-sided breast cancer who later manifested abdominal symptoms and metrorrhagia. After hysterectomy, pathologic analysis revealed metastatic lobular breast carcinoma involving the uterine fundus and a leiomyoma.
Asunto(s)
Neoplasias de la Mama/patología , Carcinoma Lobular/secundario , Leiomioma/patología , Neoplasias Primarias Múltiples/patología , Neoplasias Uterinas/secundario , Neoplasias de la Mama/cirugía , Carcinoma Lobular/cirugía , Femenino , Humanos , Leiomioma/cirugía , Persona de Mediana Edad , Neoplasias Primarias Múltiples/cirugía , Neoplasias Uterinas/cirugíaRESUMEN
Acute myeloid leukemia (AML) with normal cytogenetics represents approximately 40% to 50% of de novo AML. This heterogeneous AML subgroup constitutes the single largest cytogenetic group with an intermediate prognosis. Previous studies have suggested that the Fms-like tyrosine kinase-3 internal tandem duplication (FLT3/ITD) mutation-positive de novo AML may represent a distinctive subgroup of AML. We analyzed the clinical and pathologic features of 15 cases of de novo AML with normal cytogenetics and with the FLT3/ITD mutation. In comparison with patients with AML without the FLT3/ITD mutation, patients with FLT3/ITD+ AML are relatively younger, more often have marked peripheral leukocytosis with a higher number of circulating blasts at initial examination, more often have minimal differentiation morphologic features, more frequently have abnormal CD7 coexpression, and have poorer outcome. Close association of aberrant CD7 expression and FLT3/ITD mutation in the myeloblasts of FLT3/ITD+ AML suggests that FLT3/ITD- mediated leukemic transformation occurs in the more early stage of myeloid progenitor cells.
Asunto(s)
Antígenos CD7/metabolismo , Células Precursoras de Granulocitos/metabolismo , Leucemia Mieloide Aguda/genética , Leucemia Mieloide Aguda/metabolismo , Mutación , Secuencias Repetidas en Tándem/genética , Tirosina Quinasa 3 Similar a fms/genética , Adulto , Anciano , Anciano de 80 o más Años , Células de la Médula Ósea/química , Células de la Médula Ósea/patología , California/epidemiología , Transformación Celular Neoplásica , ADN de Neoplasias/análisis , Femenino , Células Precursoras de Granulocitos/patología , Humanos , Leucemia Mieloide Aguda/mortalidad , Leucemia Mieloide Aguda/patología , Masculino , Persona de Mediana Edad , Tasa de Supervivencia , Tirosina Quinasa 3 Similar a fms/metabolismoRESUMEN
OBJECTIVES: Radiation necrosis presenting as pseudoprogression (PsP) is relatively common after radiation and temozolomide (TMZ) treatment in glioblastoma multiforme (GBM), especially among patients with GBM that harbors intrinsic increased responsiveness to TMZ (methylated O6-methylguanine-DNA methyltransferase [MGMT] promoter). Alectinib is a second generation ALK inhibitor that has significant CNS activity against brain metastases in anaplastic lymphoma kinase (ALK)-rearranged (ALK+) non-small cell lung cancer (NSCLC) patients. MATERIALS AND METHODS: We report 2 ALK+ NSCLC patients who met RECIST criteria for progressive disease by central radiologic review due to increased in size from increased contrast enhancement in previously stereotactically radiated brain metastases with ongoing extra-cranial response to alectinib. In both patients alectinib was started within 4 months of completing stereotactic radiosurgery (SRS). The enlarging lesions in both patients were resected and found to have undergone extensive necrosis with no residual tumor pathologically. PsP was incorrectly classified as progressive disease even by central independent imaging review. CONCLUSIONS: Treatment-related necrosis of previously SRS-treated brain metastasis during alectinib treatment can present as PsP. It may be impossible to distinguish PsP from true disease progression without a pathologic examination from resected sample. High degree of clinical suspicion, close monitoring and more sensitive imaging modalities may be needed to distinguish PsP versus progression in radiated brain lesions during alectinib treatment especially if there is no progression extra-cranially.