Sinonasal teratocarcinosarcoma (SNTCS) is a highly aggressive rare tumor of the nasal cavity. Surgery followed by concurrent chemoradiation is the mainstay of treatment in SNTCS. However, intracranial extension may complicate surgical resection, with difficulty in achieving R0 resection. Here we present two cases of SNTCS with intracranial extension; both patients were seen in skull base clinic of our hospital and deemed unsuitable for surgery. These patients then were offered neoadjuvant chemotherapy (NACT), both patients had a partial response with cisplatin and etoposide protocol; subsequently they underwent R0 resection (no macroscopic residual tumor at surgery with all margins were negative for tumor on microscopy). The present cases highlight the fact that NACT with cisplatin and etoposide protocol may be considered in technically unresectable SNTCS.
A 38-year-old female with urachal carcinoma showed extensive bone metastases 1 year after wide excision of the urachal tumor, including partial cystectomy. A combination of radiotherapy and systemic chemotherapy was offered. Local radiotherapy of 8 Gy as a single fraction or 10 Gy in two fractions was delivered to the painful regions of the skeletal system. Multiagent chemotherapy consisting of methotrexate, vinblastine, Adriamycin, and cisplatin was given for three cycles. The patient died 28 months after the initial presentation with progression of the disease to pelvis and skeletal sites. The problem of metastatic spread after initial resection should be considered in urachal carcinoma, and adjuvant chemoradiotherapy should improve the outcome in this rare neoplasm.
Chemotherapy induced nausea and vomiting (CINV) is one of the most feared and severe side effects of cancer treatment. It is broadly categorised as anticipatory (a conditioned reflex, due to past experience, generally triggered by same stimuli), acute (within 24 hours of chemotherapy administration), delayed (after 24 hours and lasting up to 7 days of chemotherapy), breakthrough (inspite of primary prophylaxis for CINV), and refractory (unresponsive to prophylactic and breakthrough medications). The chemotherapeutic regimens are having varying potential (high, moderate, low, or minimal) for CINV. Incidence and timing of CINV depends upon the emetogenic potential of chemotherapy and also patient factors. This perspective highlights the underlying mechanism of CINV, state of the art therapeutic options and nuances in the field to better control this dreaded complication and in turn enhance the quality of life of these patients.
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