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An outbreak ofClostridium difficile-associated disease (CDAD) caused by the epidemic North American pulsed-field gel electrophoresis type 1 (NAP1) strain began after a formulary change from levofloxacin to moxifloxacin. Cases of CDAD were associated with moxifloxacin use, but a formulary change back to levofloxacin failed to reduce rates of disease. Substituting use of one fluoroquinolone with use of another without also controlling the overall use of drugs from this class is unlikely to control outbreaks caused by the NAP1 strain ofC. difficile.

Background Internal medicine (IM) residents participate in cardiopulmonary resuscitation events (or “codes”), stressful events that involve the death or near death of patients. Experiencing traumatic stress can lead to posttraumatic stress disorder (PTSD). Objective We examined whether IM residents who participate in codes developed PTSD symptoms. Methods We conducted this research as a 2-phase, mixed methods study. In the first phase, we analyzed interview transcripts from 25 IM residents at 9 institutions for content relevant to PTSD. In the second phase, we surveyed 82 IM residents at 1 midwestern institution for symptoms reported post-code that are associated with PTSD (post-code PTSD symptoms). Results A total of 7 of 25 residents (28%) interviewed characterized codes as traumatic or described experiencing PTSD symptoms, including intrusive thoughts about the code, avoidance and emotional numbing, and hyperarousal, irritability, or hypervigilance. Of the 82 residents, 51 (62%) responded to the questionnaire. Of the 42 respondents who had participated in a code, 6 (14%) reported at least 1 PTSD symptom, and 3 (7%) women screened positive for potential PTSD with 2 or more PTSD symptoms. Endorsing any PTSD symptom was associated with residents' perception that code participation negatively affected their work performance. Conclusions Our study found that some IM residents reported symptoms of PTSD after being involved in a code.

The immunohistochemical detection of epithelially derived cells in the bone marrow of patients with primary breast cancer has been shown to be associated with increased risk of distant relapse as well as higher rates of cancer-related death. Despite the correlation between bone marrow micrometastases and poor outcome in breast cancer patients, bone marrow status does not yet have an established role in patient management. In this prospective study, adjuvant therapy recommendations for 43 patients with stage I, II, or III breast cancer treated with lumpectomy or mastectomy, sentinel lymph node biopsy and/or axillary dissection, and intraoperative bone marrow aspiration were recorded. Recommendations were made by a multidisciplinary tumor board both blinded and unblinded to the results of the bone marrow aspiration. In our study, 10 of the 43 breast cancer patients were found to have bone marrow micrometastases. Four of these patients (40%) had axillary lymph node metastases. When blinded to the results of the bone marrow aspiration, the tumor board recommended adjuvant chemotherapy for these four node-positive patients, as well as two node-negative patients. When unblinded to the results of the bone marrow aspiration, the tumor board did not change its recommendations for any of these six patients. The remaining four node-negative, bone marrow-positive patients were not advised to have adjuvant chemotherapy by the tumor board when blinded to bone marrow status. However, once the tumor board was informed of the presence of bone marrow micrometastases, adjuvant chemotherapy was recommended for all of these patients. The results of this pilot study indicate that the presence of bone marrow micrometastases in breast cancer patients with stage I, II, or III disease does influence recommendations for adjuvant chemotherapy, particularly in patients with node-negative disease.

Skin-sparing mastectomy (SSM), which involves the resection of the nipple/areolar complex with the breast parenchyma, improves the aesthetic outcome for breast cancer patients. Most patients undergoing SSM desire reconstruction of the nipple/areolar complex for symmetry. These data explore the possibility of preserving the areola in selected mastectomy patients.A retrospective analysis of 217 mastectomy patients was conducted to determine the frequency of malignant nipple and/or areola involvement. The association between nipple and/or areola involvement and prognostic factors, including tumor size, stage, nuclear grade, axillary nodal status, and tumor location, was evaluated.The overall frequency of malignant nipple involvement was 23 of 217 (10.6%). In a subgroup of patients with tumors2 cm, peripheral tumors, and with two positive nodes or less, the incidence of nipple involvement was 6.7%. When the nipple and areolar involvement were analyzed separately, only 2 of 217 patients had involvement of the areola (0.9%). All patients with areolar involvement had stage 3 breast cancer and were located centrally in the breast.We conclude from these data that nipple preservation is not a reasonable option for mastectomy patients. However, preservation of the areola with mastectomy in selected patients warrants further study.

Importance The results of the American College of Surgeons Oncology Group Z0011 (ACOSOG Z0011) trial were first reported in 2005 with a median follow-up of 6.3 years. Longer follow-up was necessary because the majority of the patients had estrogen receptor–positive tumors that may recur later in the disease course (the ACOSOG is now part of the Alliance for Clinical Trials in Oncology). Objective To determine whether the 10-year overall survival of patients with sentinel lymph node metastases treated with breast-conserving therapy and sentinel lymph node dissection (SLND) alone without axillary lymph node dissection (ALND) is noninferior to that of women treated with axillary dissection. Design, Setting, and Participants The ACOSOG Z0011 phase 3 randomized clinical trial enrolled patients from May 1999 to December 2004 at 115 sites (both academic and community medical centers). The last date of follow-up was September 29, 2015, in the ACOSOG Z0011 (Alliance) trial. Eligible patients were women with clinical T1 or T2 invasive breast cancer, no palpable axillary adenopathy, and 1 or 2 sentinel lymph nodes containing metastases. Interventions All patients had planned lumpectomy, planned tangential whole-breast irradiation, and adjuvant systemic therapy. Third-field radiation was prohibited. Main Outcomes and Measures The primary outcome was overall survival with a noninferiority hazard ratio (HR) margin of 1.3. The secondary outcome was disease-free survival. Results Among 891 women who were randomized (median age, 55 years), 856 (96%) completed the trial (446 in the SLND alone group and 445 in the ALND group). At a median follow-up of 9.3 years (interquartile range, 6.93-10.34 years), the 10-year overall survival was 86.3% in the SLND alone group and 83.6% in the ALND group (HR, 0.85 [1-sided 95% CI, 0-1.16]; noninferiorityP = .02). The 10-year disease-free survival was 80.2% in the SLND alone group and 78.2% in the ALND group (HR, 0.85 [95% CI, 0.62-1.17];P = .32). Between year 5 and year 10, 1 regional recurrence was seen in the SLND alone group vs none in the ALND group. Ten-year regional recurrence did not differ significantly between the 2 groups. Conclusions and Relevance Among women with T1 or T2 invasive primary breast cancer, no palpable axillary adenopathy, and 1 or 2 sentinel lymph nodes containing metastases, 10-year overall survival for patients treated with sentinel lymph node dissection alone was noninferior to overall survival for those treated with axillary lymph node dissection. These findings do not support routine use of axillary lymph node dissection in this patient population based on 10-year outcomes. Trial Registration clinicaltrials.gov Identifier:NCT00003855

Background: Although breast conservation with lumpectomy and radiation treatment has become a commonly used treatment for breast cancer, there are little data to support the use of lumpectomy for central and retroareolar breast cancers. In this study, we investigate the local and distant recurrence rates of patients with central or retroareolar breast cancers treated with lumpectomy compared with mastectomy Methods: This study provides a retrospective analysis of 99 patients, from 1981 to 2000, with central or retroareolar breast cancers treated with mastectomy or lumpectomy to determine the frequency of local and distant recurrence. The mastectomy and lumpectomy patients were compared with respect to recurrence and other prognostic factors including: tumor location, tumor size, axillary nodal status, and final surgical margins. Results: The overall frequency of local recurrence was 5 of 99 (5.0%) in the entire group, 3 of 67 (4.5%) and 2 of 32 (6.3%) of patients who underwent mastectomy and lumpectomy, respectively ( P >0.99). Overall, 3 patients experienced a distant recurrence as a first event, with 2 patients (3.0%) in the mastectomy group and 1 patient (3.1%) in the lumpectomy group ( P >0.99). The type of surgical management was not statistically significant related to either local or distant disease recurrence, with median time to local recurrence of 3.0 years for the mastectomy patients and 5.0 years for lumpectomy patients. Of the patients with central tumors who underwent mastectomy 2 of 42 (4.8%) developed local recurrences compared with those who had a lumpectomy, 1 of 21 (4.8%). Similarly for retroareolar tumors, the local recurrence rate was 1 of 25 (4.0%) for patients undergoing mastectomy and 1 of 11 (9.1%) for those undergoing lumpectomy ( P >0.99). Conclusions: In this study there was no significant difference in local or distant failure rates of those patients with central or retroareolar tumors treated with mastectomy versus lumpectomy. We conclude lumpectomy to be a reasonable treatment option for selected patients with central or retroareolar breast cancers.

BACKGROUND Widespread use of mammography has increased the detection of ductal carcinoma in situ with microinvasion (DCISM) in pathology specimens. Currently there is disagreement regarding the incidence of axillary metastasis from DCISM. The controversy centers on whether complete lymphadenectomy is indicated for axillary staging, given its morbidity and the reportedly minimal rate of axillary involvement in these patients. Intraoperative lymphatic mapping and sentinel lymphadenectomy (SLND) may obviate complete axillary lymph node dissection in selected breast carcinoma patients. In intraoperative lymphatic mapping, isosulfan blue dye is used to demonstrate the course of lymphatic flow from the breast tumor to the first draining or sentinel lymph node. This blue-stained lymph node is selectively excised for pathologic examination; its tumor status is used to predict the tumor status of the other axillary lymph nodes. The authors examined whether SLND would be suitable for staging DCISM. METHODS From February 1992 to January 1997, 14 patients with DCISM underwent intraoperative lymphatic mapping and SLND at the John Wayne Cancer Institute in Santa Monica, California. Clinical and pathologic data were prospectively collected. RESULTS Primary DCISM tumors ranged in size from 0.9 to 6.5 cm. Nine patients presented with mammographic abnormalities, two patients presented with Paget's disease and a palpable lesion, and three patients presented with palpable lesions. Two patients (14.3%) had tumor-involved sentinel lymph nodes. One of these patients had two sentinel lymph nodes, both of which contained single cancer cells identified by immunohistochemistry. The other patient had 1 sentinel lymph node, in which a 0.3-cm metastasis was revealed by light microscopy. Completion axillary dissection was performed on both patients and revealed no further tumor positive lymph node metastases. CONCLUSIONS SLND can detect lymph node micrometastases (tumor deposits

In a single-center cohort of surgical patients, we assessed the association between postoperative change in serum creatinine and adverse outcomes and compared the American College of Surgeons National Surgical Quality Improvement Program's definition for acute kidney injury with consensus risk, injury, failure, loss, and end-stage kidney and Kidney Disease: Improving Global Outcomes definitions.Retrospective single-center cohort.Academic tertiary medical center.Twenty-seven thousand eight hundred forty-one adult patients with no previous history of chronic kidney disease undergoing major surgery.Risk, injury, failure, loss, and end-stage kidney defines acute kidney injury as change in serum creatinine greater than or equal to 50% while Kidney Disease: Improving Global Outcomes uses 0.3 mg/dL change from the reference serum creatinine. Since National Surgical Quality Improvement Program defines acute kidney injury as serum creatinine change greater than 2 mg/dL, it may underestimate the risk associated with less severe acute kidney injury.The optimal discrimination limits for both percent and absolute serum creatinine changes were calculated by maximizing sensitivity and specificity along the receiver operating characteristic curves for postoperative complications and mortality. Although prevalence of risk, injury, failure, loss, and end-stage kidney-acute kidney injury was 37%, only 7% of risk, injury, failure, loss, and end-stage kidney-acute kidney injury patients would be diagnosed with acute kidney injury using the National Surgical Quality Improvement Program definition. In multivariable logistic models, patients with risk, injury, failure, loss, and end-stage kidney or Kidney Disease: Improving Global Outcomes-acute kidney injury had a 10 times higher odds of dying compared to patients without acute kidney injury. The optimal discrimination limits for change in serum creatinine associated with adverse postoperative outcomes were as low as 0.2 mg/dL while the National Surgical Quality Improvement Program discrimination limit of 2.0 mg/dL had low sensitivity (0.05-0.28).Current American College of Surgeons National Surgical Quality Improvement Program definition underestimates the risk associated with mild and moderate acute kidney injury otherwise captured by the consensus risk, injury, failure, loss, and end-stage kidney and Kidney Disease: Improving Global Outcomes criteria.

e20662Background: The 6 FDA drug approvals for non-small cell lung cancer (NSCLC) in 2015 included 2 programmed cell death protein 1 (PD-1) inhibitors and a 3rd generation (gen) epidermal growth fa...

Although more than 30 million patients in the United States undergo ambulatory surgery each year, it remains unclear what percentage of these patients receive a perioperative nerve block. We reviewed data from the 2006 National Survey of Ambulatory Surgery to determine the demographic, socioeconomic, geographic, and clinical factors associated with the likelihood of nerve block placement for ambulatory orthopedic surgery. The primary outcome of interest was the association between primary method of payment and likelihood of nerve block placement. In addition, we examined the association between type of surgical procedures, patient demographics, and hospital characteristics with the likelihood of receiving a nerve block.This cross-sectional study reviewed 6000 orthopedic anesthetics from the 2006 National Survey of Ambulatory Surgery data set, which accounted for more than 3.9 million orthopedic anesthetics when weighted. The primary outcome of this study addressed the likelihood of receiving a nerve block for orthopedic ambulatory surgery according to the patient's primary method of payment. Secondary end points included differences in demographics, surgical procedures, adverse effects, complications, recovery profile, anesthesia staffing model, and total perioperative charges in those with and without nerve block.Overall, 14.9% of anesthetics in this sample involved a peripheral nerve block. Length of time in postoperative recovery, total perioperative time, and total charges were less for those receiving nerve blocks. Patients were more likely to receive a nerve block if their procedures were performed in metropolitan service areas (odds ratio [OR], 1.86; 95% confidence interval [CI], 1.19-2.91; P = 0.007) or in freestanding surgical facilities (OR, 2.27; 95% CI, 1.74-2.96; P0.0001) and if payment for their surgery was supported by government programs (OR, 2.5; 95% CI, 1.01-6.21; P = 0.048) or private insurance (OR, 2.62; 95% CI, 1.12-6.13; P = 0.03) versus self-pay or charity care.For patients receiving ambulatory orthopedic surgery in the United States, our results suggest that geographic and socioeconomic factors are associated with different likelihoods of perioperative peripheral nerve block placement.

Nitrogen (N) leaching from agricultural soils is a major concern in the southeastern USA. A winter cover crop following the summer crop rotation is essential for controlling N leaching and soil run-off, thereby improving sustainable development. Rotation of peanut (Arachis hypogea L.) and cotton (Gossypium hirsutum L.) with bahiagrass (Paspalum notatum) (i.e. sod-based rotation) can greatly improve soil health and increase crop yields and profitability. In the sod-based rotation, the winter cover crop is an important component. The objective of this study was to determine effects of summer crops, cotton and peanut, on growth and physiology of a subsequent oat (Avena sativa L.) cover crop in both a conventional (Peanut-Cotton-Cotton) and sod-based (Bahiagrass-Bahiagrass-Peanut-Cotton) rotations. Two rotations with an oat cover crop were established in 2000. In the 2006-07 and 2007-08 growing seasons, oat plant height, leaf chlorophyll and sap NO3-N concentrations, shoot biomass, and N uptake were determined. Our results showed that the previous summer crop in the two rotations significantly influenced oat growth and physiology. Oat grown in the sod-based rotation had greater biomass, leaf chlorophyll and NO3-N concentrations as compared with oat grown in the conventional rotation. At pre-heading stage, oat in the sod-based rotation had 44% greater biomass and 32% higher N uptake than oat in the conventional rotation; oat following peanut produced 40 to 49% more biomass and accumulated 27 to 66% more N than oat following cotton. Therefore, the sod-based rotation improved not only summer crops, but also the winter cover crop. Increased oat growth and N status from the sod-based rotation indicated greater soil quality and sustainability. bahiagrass / crop rotation/ oat biomass / nitrogen uptake / soil quality / sustainability

Raf kinase inhibitor protein (RKIP) was originally identified as a protein that bound membrane phospholipids and was named phosphatidylethanolamine binding protein-2 (PEBP-2). RKIP was than identified as a protein that bound Raf and blocked its ability to phosphorylate MEK, thus earning its new name of RKIP. Subsequent to identification of its role in the Raf:MEK pathway, RKIP has been demonstrated to regulate several other signaling pathways including G-protein signaling and NF-kappaB signaling. Its involvement in several signaling pathways has engendered RKIP to contribute to several physiological processes including membrane biosynthesis, spermatogenesis, neural development, and apoptosis. RKIP is expressed in many tissues including brain, lung, and liver and thus, dysregulation of RKIP expression or function has potential to contribute to pathophysiology in these tissues. Loss of RKIP expression in prostate cancer cells confers a metastatic phenotype on them. Additionally, restoration of RKIP expression in a metastatic prostate cancer cell line does not effect primary tumor growth, but it does inhibit prostate cancer metastasis. These parameters identify RKIP as a metastasis suppressor gene. In this review, the biology and pathophysiology of RKIP is described.

Defining the mechanisms that confer metastatic ability on cancer cells is an important goal towards prevention of metastasis. A gene array screen between a non-metastatic prostate cancer cell and its metastatic derivative line revealed decreased expression of Raf kinase inhibitor protein (RKIP) in the metastatic cell line. This finding is consistent with the possibility that loss of RKIP is associated with metastasis. RKIP is expressed in many tissues including brain, lung, and liver. RKIP blocks Raf-induced phosphorylation of MEK. In addition to its modulation of Raf signaling, RKIP modulates both G-protein signaling and NF-kappaB activity. The impact that RKIP has on multiple signaling pathways grants it the ability to play a role in several cellular functions including membrane biosynthesis, spermatogenesis, and neural signaling. Novel cellular functions for RKIP continue to be identified, several of which contribute to cancer biology. For example, RKIP promotes apoptosis of cancer cells, which suggests that loss of RKIP in cancer will protect cancer cells against cell death. Additionally, restoration of RKIP expression ina metastatic prostate cancer cell line does not effect primary tumor growth, but it does inhibit prostate cancer metastasis. These parameters identify RKIP as a metastasis suppressor gene, which suggest that it or proteins it interacts with are putative molecular targets to control metastasis. These findings are supported by the observation that RKIP expression is decreased in metastases of prostate cancer patients, compared to normal prostate or the primary prostate tumor. In this review, RKIP biology and its role in cancer will be described.

Raf kinase inhibitor protein (RKIP) is a member of the phosphatidylethanolamine-binding protein (PEBP) family. RKIP plays a pivotal modulatory role in several protein kinase signaling cascades. RKIP binds inhibits Raf-1-mediated phosphorylation of MEK through binding to Raf-1. Protein kinase C (PKC) phosphorylates RKIP, resulting in release of Raf-1 and activation of MEK and ERK. The phosphorylated RKIP binds to and inhibits G-protein-coupled receptor kinase, resulting in sustained G-protein signaling. The regulatory role that RKIP has in cell signaling is reflected in its role in physiology and pathophysiology. RKIP is involved in neural development, cardiac function and spermatogenesis and appears to have serine protease activity. In addition to its roles in physiology, dysregulated RKIP expression has the potential to contribute to pathophysiological processes including Alzheimer's disease and diabetic nephropathy. RKIP has been shown to fit the criteria of being a metastasis suppressor gene, including having decreased expression in prostate cancer metastases and restoring RKIP expression in a prostate cancer cell line diminishes metastasis in a murine model. Clearly, RKIP has multiple molecular and cellular functions. In this review, RKIP's molecular roles in intracellular signaling, its physiological functions and its role in disease are described.

Punch biopsies of human skin were obtained 1 day after irradiation with two minimal-erythema doses (MED) from either a UVB light source or a Solar Simulator and incubated in organ culture for 72 h. Organ culture fluids obtained at 24, 48 and 72 h were analyzed for collagenolytic activity and for reactivity with antibodies to matrix metalloproteinase-1 (MMP-1; interstitial collagenase) and MMP-13 (collagenase-3). High levels of collagenolytic activity were seen in organ culture fluid from skin exposed to either light source. MMP-1 was strongly induced in parallel, increasing from less than 100 ng/ml in organ culture fluid from control skin to approximately 1.1 microg/ml in culture fluid from UV-treated skin. Whereas most of the detectable MMP-1 in control culture fluid was represented by the latent form of the enzyme, approximately 50% of the enzyme was present as the active form in organ culture fluid of UV-exposed skin. In contrast, there was no detectable MMP-13 in control organ culture fluid and very little change after UV exposure (less than 100 ng/ml in both cases). Finally, neutralization studies with a blocking antibody to MMP-1 removed 95 +/- 4% of the collagenolytic activity in the organ culture fluid from UV-treated skin. These findings strongly implicate MMP-1 rather than MMP-13 as the major collagenolytic enzyme responsible for collagen damage in photoaging.

Matrix metalloproteinase-13 (MMP-13; collagenase-3) was detected in the vasculature from 17 of 20 human basal cell carcinomas as assessed by immunohistology immediately after surgery. In contrast, MMP-1 (interstitial collagenase) was detected in the vasculature of only two of the same specimens. MMP-13 reactivity was also observed in the capillaries of normal human skin taken from the wound margin. Human dermal microvascular endothelial cells as well as human umbilical vein endothelial cells were isolated in culture and examined for MMP-13 expression. By reverse transcription-polymerase chain reaction and Southern blotting, an MMP-13 transcript was detected in unstimulated endothelial cells. The transcript was upregulated in cells treated with 50 nM phorbol myristate acetate (PMA). Western blotting demonstrated the presence of an anti-MMP-13 - immunoreactive protein in culture fluid from both cell sources. Immunoreactivity was stronger in culture fluid from cells treated with interleukin-1alpha (IL-1alpha) than in culture fluid from control cells. Tumor necrosis factor-alpha (TNF-alpha) and PMA also upregulated MMP-13 expression but these agents were not as effective as IL-1alpha. Additionally, reactivity was greater in culture fluid from endothelial cells grown on three-dimensional lattices of polymerized type I collagen than on dried collagen films. These data indicate that endothelial cells in the skin are a source of MMP-13 and that enzyme expression is upregulated under conditions that promote endothelial cell growth and vascular differentiation.

Background: EGFR inhibition is an established therapy for previously treated NSCLC. Estrogen receptors (ER) and aromatase are expressed in most NSCLC specimens in both men and women. In preclinical models, estrogen stimulates NSCLC growth, an effect blocked by F, a pure ER antagonist. Preclinical models show enhanced anti-tumor effects by combining EGFR inhibitors with F. Methods: We conducted a Phase II clinical study to evaluate whether addition of F enhances antitumor efficacy of E. Men and women with advanced NSCLC and > 1 prior chemotherapy regimen (unless patient refused) were randomized 2:1 to receive E (150 mg PO qd) + F (500 mg IM q2wk x 3, then q4wk) or E alone. Stratification for gender and ECOG (0, 1 vs. 2) was performed. Response rate (RR) was the primary endpoint. Secondary endpoints included progression free survival (PFS), overall survival (OS) and correlation between clinical endpoints and tumor tissue and blood-based biomarkers. Results: 106 patients (pts) were randomized from March 2006 to June 2010. 100 (evaluated population) received E +/- F. E + F was well tolerated, with adverse events well balanced between arms. For E + F and E respectively, RR (23.6% vs. 14.8%, p = 0.35), PFS [1.9 vs. 1.8 months, hazard ratio (HR) 0.85, 95% confidence interval 0.55, 1.33] and OS [9.4 vs. 5.7 months, HR 0.96 (0.6, 1.55)] were similar between arms. EGFR mutational data could be obtained on 69 pts. EGFR mutations were more prevalent in the E arm (35% vs. 20%). EGFR mutations strongly predicted best response, PFS and OS (p < 0.0002 for each). RR, PFS and OS were similar among EGFR mutants between arms in this small subset (17 patients). Among the 52 pts with EGFR WT tumors, 3 partial responses (PR) were seen with E + F vs. none for E alone. Clinical benefit rate [CBR (RR + stable disease): 54.8% vs. 8.3%, p = 0.0056] was significantly higher among pts with WT tumors treated with E + F. Trends were observed in favor of E + F in PFS [2.0 vs. 1.6 months, HR 0.56 (0.29, 1.07)] and OS [7.4 vs. 5.9 months, HR 0.69 (0.36, 1.31)]. Conclusion: E + F was well tolerated in previously treated NSCLC pts, including men and pre- and post-menopausal women. The study showed a high RR (23.6%) for E + F, that was not adequately explained by EGFR mutations. Among EGFR WT pts, a significantly higher CBR that included 3 PRs was seen with trends towards improved PFS and OS with E + F as compared to E alone. Evaluation of tumor tissue biomarkers (including ER-α and -β, aromatase), blood estrogen levels and EGFR ligands known to be induced by ER signaling is ongoing to determine NSCLC subpopulations most likely to benefit from antiestrogens. [Supported by 1K23CA149079, P50 CA090440, V Foundation for Cancer Research, Jonsson Comprehensive Cancer Center, Wolfen Family Lung Cancer Research Program, Stiles Program in Oncology, National Lung Cancer Partnership and One Ball Matt Memorial Golf Tournament] Citation Format: Edward B. Garon, Jill M. Siegfried, Steven M. Dubinett, Robert M. Elashoff, David J. Park, Rupesh J. Parikh, Ravi Patel, Eddie H. Hu, Karen L. Reckamp, Brad Adams, Diego Martinez, He-Jing Wang, Fairooz Kabbinavar, Sanja Dacic, Meghan Brennan, Isett Laux, Diana C. Marquez-Garban, Laura P. Stabile, Dennis J. Slamon, Richard J. Pietras. Result of TORI L-03, a randomized, multicenter phase II clinical trial of erlotinib (E) or E + fulvestrant (F) in previously treated advanced non-small cell lung cancer (NSCLC). [abstract]. In: Proceedings of the 104th Annual Meeting of the American Association for Cancer Research; 2013 Apr 6-10; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2013;73(8 Suppl):Abstract nr 4664. doi:10.1158/1538-7445.AM2013-4664