ABSTRACT
The role for localized radiation to treat ovarian cancer (OC) patients with locally recurrent vaginal/perirectal lesions remains unclear, though we hypothesize these patients may be salvaged locally and gain long-term survival benefit. We describe our institutional outcomes using intensity modulated radiation therapy (IMRT) +/- high-dose rate (HDR) brachytherapy to treat this population. Our primary objectives were to evaluate complete response rates of targeted lesions after radiation and calculate our 5-year in-field control (IFC) rate. Secondary objectives were to assess radiation-related toxicities, chemotherapy free-interval (CFI), as well as post-radiation progression-free (PFS) and overall survival (OS). PFS and OS were defined from radiation start to either progression or death/last follow-up, respectively. This was a heavily pre-treated cohort of 17 recurrent OC patients with a median follow-up of 28.4 months (range 4.5-166.4) after radiation completion. 52.9% had high-grade serous histology and 4 (23.5%) had isolated vaginal/perirectal disease. Four (23.5%) patients had in-field failures at 3.7, 11.2, 24.5, and 27.5 months after start of radiation, all treated with definitive dosing of radiation therapy. Patients who were platinum-sensitive prior to radiation had similar median PFS (6.5 vs. 13.4 months, log-rank p = 0.75), but longer OS (71.1 vs 18.8 months, log-rank p = 0.05) than their platinum-resistant counterparts. Excluding patients with low-grade histology or who were treated with palliative radiation, median CFI was 14.2 months (range 4.7 - 33.0). Radiation was well tolerated with 2 (12.0%) experiencing grade 3/4 gastrointestinal/genitourinary toxicities. In conclusion, radiation to treat locally recurrent vaginal/perirectal lesions in heavily pre-treated OC patients is safe and may effectively provide IFC.
Subject(s)
Down Syndrome/genetics , Keratin-8/genetics , Placenta/metabolism , TNF-Related Apoptosis-Inducing Ligand/genetics , Blotting, Northern , Cell Membrane/metabolism , Down Syndrome/metabolism , Female , GPI-Linked Proteins , Gene Expression Profiling , Humans , Immunohistochemistry , Karyotyping , Keratin-8/metabolism , Pregnancy , Receptors, TNF-Related Apoptosis-Inducing Ligand , Receptors, Tumor Necrosis Factor/genetics , Receptors, Tumor Necrosis Factor, Member 10c , TNF-Related Apoptosis-Inducing Ligand/metabolism , Trophoblasts/metabolism , Tumor Necrosis Factor Decoy Receptors/genetics , Tumor Necrosis Factor-alpha/geneticsABSTRACT
BACKGROUND: Breast cancer is the most commonly diagnosed cancer in pregnancy. Though the prognosis by stage is not different from that in nonpregnant women, it is more likely to present at an advanced stage in pregnancy. CASE: A 28-year-old primigravida presented with dyspnea and pleuritic chest pain. The workup revealed cardiac tamponade. Pericardiocentesis and subsequent pericardial window were performed. Cytology of the pericardial fluid revealed poorly differentiated adenocarcinoma. Ultrasonography displayed a right breast mass, and biopsy identified it as the primary source of the cancer. CONCLUSION: Cardiac tamponade is an unusual presentation of advanced breast cancer. To the best of our knowledge, it has not previously been described as occurring in pregnancy.
Subject(s)
Adenocarcinoma/complications , Breast Neoplasms/complications , Cardiac Tamponade/etiology , Pregnancy Complications, Neoplastic/diagnosis , Adenocarcinoma/diagnosis , Adenocarcinoma/pathology , Adult , Breast Neoplasms/diagnosis , Breast Neoplasms/pathology , Chest Pain/etiology , Dyspnea/etiology , Fatal Outcome , Female , Humans , PregnancyABSTRACT
In a previous report, we have shown that acute activation of the hypothalamo-pituitary-adrenal (HPA) axis by the cytokine interleukin-1 alpha (IL-1 alpha) in the ovariectomized (OVX) rhesus monkey results in an inhibition of LH secretion. Here, we study whether estradiol (E) replacement therapy, at a level that reproduces E concentrations typical of the late follicular phase, modifies the gonadotropin and cortisol responses to IL-1 alpha administration. For E replacement, two Silastic capsules containing E were implanted sc 5 days before the experiment. The serum E concentration increased from less than 5 in OVX to 103.0 +/- 5.2 pg/ml in OVX and E-replaced monkeys. The experimental protocols were carried out 24 h or more after the LH surge that had been induced by E. In Exp 1, the effects of an intracerebroventricular (icv) infusion of physiological saline (group 1) or IL-1 alpha (2.1 or 4.2 micrograms/30 min; group 2) on LH, FSH, and cortisol were compared. IL-1 alpha administration resulted in a progressive release of LH (to 159.0 +/- 8.3% of baseline at 5 h; P < 0.05, 3-5 h vs. saline). Cortisol decreased in group 1 (84.5 +/- 1.3% by 5 h), but increased after IL-1 alpha (147.3 +/- 12.6%; P < 0.05 vs. saline). In Exp 2, we determined whether the stimulatory effects of IL-1 alpha on LH result from the central activation of CRH release (group 3). Infusion of the CRH antagonist, D-Phe12, Nle21,38, CaMe,Leu37-CRF-(12-41) (240 or 360 micrograms/2 h) prevented the increase in LH seen after IL-1 alpha treatment (67.3 +/- 12.5% at 5 h, NS vs. saline). The CRH antagonist also prevented the increase in cortisol and progesterone induced by IL-1 alpha. In Exp 3, we tested whether the stimulatory effect of IL-1 alpha on LH secretion can be simulated by ACTH infusion (group 4). ACTH-(1-24) (10-micrograms bolus plus 50 micrograms/5 h, iv) induced a progressive increase in LH secretion (to 221.5 +/- 27.8% of baseline by 5 h; P < 0.05, 3-5 h vs. saline). ACTH also stimulated cortisol secretion (to 203.3 +/- 30.7% by 5 h). In Exp 4, we investigated the role of adrenal progesterone in the LH response observed in groups 2 and 4. This increase in LH did not occur after pretreatment with RU486, a progesterone antagonist (5 mg Mifepristone; 77 +/- 24.2% by 5 h; P = NS vs. saline), although the increases in cortisol and progesterone were not prevented.(ABSTRACT TRUNCATED AT 400 WORDS)
