BACKGROUNDIn the current study, the authors describe the M. D. Anderson experience with adjuvant systemic therapy in male breast carcinoma patients.METHODSA total of 156 men with a diagnosis of breast carcinoma registered and were treated at the M. D. Anderson Cancer Center between 1944 and 2001. One hundred thirty‐five men had nonmetastatic breast carcinoma at diagnosis and were included in this analysis. Patients' charts were retrospectively reviewed to obtain details of patient characteristics, adjuvant therapy, and outcomes. Analysis was performed with descriptive statistics; the log rank test was used to compare outcomes.RESULTSThe median patient age was 59 years (range, 25–80 yrs). Median follow‐up was 13.8 years (range, 0.6–32.5 yrs). Sixty percent of patients had tumors 2 cm or smaller. Pathologic lymph node involvement was seen in 55% of patients. Tumors were estrogen receptor‐positive in 85% of cases and progesterone receptor‐positive in 71%. Chemotherapy was administered to 32 men (84% with adjuvant chemotherapy, 6% with neoadjuvant chemotherapy, and 9% with both). Approximately 81% received anthracycline‐based regimens; 9% received additional taxanes; and 16% were treated with cyclophosphamide, methotrexate, and 5‐fluorouracil (CMF). The median number of cycles was 6 (range, 4–14 cycles). Thirty‐eight men received adjuvant hormonal therapy (92% received tamoxifen and 8% were treated with other therapy). The 5‐year and 10‐year overall survival rates were 86% and 75%, respectively, for men with lymph node‐negative disease and 70% and 43%, respectively, for men with lymph node‐positive disease. For men with lymph node‐positive disease, adjuvant chemotherapy was associated with a lower risk of death (hazards ratio [HR] of 0.78), although this difference was not statistically significant. Overall survival was significantly better for men who received adjuvant hormonal therapy (HR of 0.45; P = 0.01).CONCLUSIONSThis relatively large series of men with breast carcinoma suggests that men benefit from adjuvant systemic therapy for breast carcinoma, with the greatest benefit from adjuvant hormonal therapy. Cancer 2005. © 2005 American Cancer Society.
Identifying elderly patients who will benefit from combination chemotherapy for pancreatic cancer remains a significant clinical challenge. An assessment of medical comorbidities and functional status plays a key role in determining fitness for intensive chemotherapeutic regimens in this important subset of patients.
Thrombotic microangiopathy is an uncommon but reported adverse effect of a variety of antineoplastic drugs, including chemotherapy agents such as mitomycin C and gemcitabine, and newer targeted agents such as the vascular endothelial growth factor inhibitors. We present a review of thrombotic microangiopathy associated with antineoplastic agents and its implications in current cancer therapy.
Tumor lysis syndrome (TLS) is a life-threatening condition which consists of a constellation of electrolyte imbalances, acute renal failure, seizure, and arrhythmias. It is most commonly seen with hematologic malignancies after the initiation of chemotherapy. However, it can also occur spontaneously, prior to treatment with cytotoxic agents. TLS has been rarely described with non-hematologic solid tumors, and it is even more uncommon to have spontaneous tumor lysis syndrome (STLS) in solid tumors. To our knowledge, only two cases of STLS in small-cell lung cancer (SCLC) were reported in the literature. Herein, we present the case of a patient with metastatic SCLC who developed STLS. Our case highlights that in the setting of metastatic solid tumors, STLS must be in the differential diagnosis, to allow prompt initiation of prophylaxis and treatment.
Essential thrombocythemia (ET) is a myeloproliferative neoplasm characterized by a clonal expansion of megakaryocytes. ET can result in both arterial and venous thrombosis. Involvement of the coronary arteries has been reported. Patients who harbor a CALR mutation are half as likely to suffer a thrombotic event as compared to patients with a JAK2 mutation. We report a case of CALR-mutated ET whose initial disease manifestation was a non-ST segment elevation myocardial infarction.
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