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105 results on '"Nabell, L."'

5. Pain, Weight Loss, and Quality of Life in a Supportive Care Trial for Patients With Advanced Head and Neck Cancer

Author

Lenzie, A., primary, Hoyle, J., additional, Yang, E.S., additional, Spencer, S.A., additional, Willey, C.D., additional, Bonner, J.A., additional, Dobelbower, M.C., additional, Snider, J.W., additional, McCammon, S., additional, Carroll, W., additional, Nabell, L., additional, Bhatia, S., additional, and McDonald, A.M., additional

Published
2021
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6. 961MO Safety, efficacy, immunogenicity of arenavirus-based vectors HB-201 and HB-202 in patients with HPV16+ cancers

Author

Posner, M.R., primary, Ho, A.L., additional, Niu, J., additional, Nabell, L., additional, Leidner, R.S., additional, Nieva, J., additional, Richardson, D.L., additional, Pearson, A.T., additional, Wang, D., additional, Chung, K., additional, Adkins, D.R., additional, Pimentel, A., additional, Wong, S., additional, Lacobucci, C., additional, Qing, X., additional, Katchar, K., additional, Schlienger, K., additional, Matushansky, I., additional, Fu, S., additional, and Pfister, D.G., additional

Published
2021
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10. 71P A phase II study of ADU-S100 in combination with pembrolizumab in adult patients with PD-L1+ recurrent or metastatic HNSCC: Preliminary safety, efficacy and PK/PD results

Author

Zandberg, D.P., primary, Ferris, R., additional, Laux, D., additional, Mehra, R., additional, Nabell, L., additional, Kaczmar, J., additional, Gibson, M.K., additional, Kim, Y.J., additional, Neupane, P., additional, Bauman, J., additional, Julian, R., additional, Adkins, D., additional, Cohen, E., additional, Burtness, B., additional, Bermingham, C., additional, Dupage, A., additional, Desbien, A., additional, Loi, A., additional, Nuyten, D.S.A., additional, and Saba, N.F., additional

Published
2020
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12. A Phase 1b Presurgical Window Study to Evaluate Immune Biomarker Modulation in Response to Motolimod and Nivolumab in Patients with Squamous Cell Carcinoma of the Head and Neck (SCCHN)

Author

Adkins, D., primary, Cohen, E., additional, Nabell, L., additional, Zandberg, D., additional, Old, M., additional, Cognetti, D., additional, Blair, D., additional, Wei, X., additional, Wells, A., additional, Patel, A., additional, Foy, T., additional, Hege, K., additional, and Ferris, R.L., additional

Published
2020
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13. A phase 1b trial of prexasertib in combination with chemoradiation in patients with locally advanced head and neck squamous cell carcinoma (HNSCC)

Author

Yang, E.S., primary, Deutsch, E., additional, Mehmet, A., additional, Fayette, J., additional, Nabell, L., additional, Spencer, S.A., additional, Dobelbower, M.C., additional, Willey, C.D., additional, Bonner, J.A., additional, Wang, X., additional, Lin, A., additional, and William, W.N., additional

Published
2020
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15. Phase Ib/II, open label, multicenter study of intratumoral SD-101 in combination with pembrolizumab in anti-PD-1 treatment naïve patients with recurrent or metastatic head and neck squamous cell carcinoma (HNSCC)

Author

Cohen, E.E.W., primary, Algazi, A., additional, Laux, D., additional, Wong, D.J., additional, Amin, A., additional, Nabell, L., additional, Chisamore, M., additional, Gamelin, E., additional, Janssen, R., additional, and Bishnoi, S., additional

Published
2018
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16. A Randomized, Open-Label, Multicenter, Global Phase 2 Study of Durvalumab (D), Tremelimumab (T), or D Plus T, in Patients With PD-L1 Low/Negative Recurrent or Metastatic Head and Neck Squamous Cell Carcinoma: CONDOR

Author

Siu, L., primary, Even, C., additional, Mesía, R., additional, Daste, A., additional, Krauss, J., additional, Saba, N.F., additional, Nabell, L., additional, Ready, N.E., additional, Garcia, I.Brana, additional, Kotecki, N., additional, Zandberg, D.P., additional, Gilbert, J., additional, Mehanna, H., additional, Jarkowski, A., additional, Melillo, G., additional, Armstrong, J.M., additional, and Fayette, J., additional

Published
2018
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17. A phase II study of medroxyprogesterone acetate in patients with hormone receptor negative metastatic breast cancer: translational breast cancer research consortium trial 007

Author

Kimmick, G., Merino, M.J., Nabell, L., Rugo, H, Miller, K.D., Carey, L., Jones, D.R., Steeg, P.S., and Althouse, S.K.

Abstract

Preclinical data suggest that medroxyprogesterone acetate (MPA) has both anti-metastatic and anti-angiogenic activity in the absence of hormone receptors (HR). This phase II trial assessed the activity of MPA alone or in combination with low-dose chemotherapy in patients with metastatic HR-negative breast cancer. Postmenopausal women with HR-negative disease were eligible if they had not received more than 3 chemotherapy regimens for metastatic disease. All patients were treated with MPA 1,000���1,500 mg/day orally; patients in cohort two also received low-dose oral cyclophosphamide and methotrexate (ldCM, 50 mg/day and 2.5 mg twice daily on Days 1 and 2 each week). Tissue and circulating biomarkers were assessed serially. The primary endpoint was clinical benefit response defined as objective response or stable disease >6 months. Thirty patients were enrolled (14 MPA monotherapy; 16 MPA + ldCM); median age was 55 (35���80); nearly all had visceral involvement. Despite dose escalation in 90 % of patients, only 17 (57 %) patients ever achieved MPA trough concentrations >50 ng/ml. One patient developed grade 4 renal failure in the setting of rapid disease progression and dehydration. There were no objective responses. One patient in each cohort (~7 %) had stable disease for > 6 months. Skin Nm23 expression increased after 4 weeks of MPA + ldCM, but there were no significant changes in TSP-1, PAI-1 antigen, or PAI-1 activity. MPA had limited activity and does not warrant further development in patients with HR-negative advanced breast cancer. Poor bioavailability limited exposure despite dose escalation.

Published
2014
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19. Abstract P1-15-02: Long term follow-up of the neo-adjuvant pilot trial evaluating activity of letrozole in combination with bevacizumab in post-menopausal women with newly diagnosed estrogen and/or progesterone receptor positive primary breast cancer

Author

Forero, A, primary, DeLos Santos, J, additional, Bowen, K, additional, Jones, C, additional, Varley, KE, additional, Nabell, L, additional, Carpenter, JT, additional, Falkson, CI, additional, Krontiras, H, additional, Caterinicchia, V, additional, O'Malley, J, additional, Li, Y, additional, LoBuglio, AF, additional, Myers, R, additional, and Saleh, MN, additional

Published
2013
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20. Abstract P6-05-02: Endocrine biomarkers in response to AR-inhibition with bicalutamide for the treatment of AR(+), ER/PR(−) metastatic breast cancer (MBC) (TBCRC011)

Author

Gucalp, A, primary, Tolaney, S, additional, Isakoff, SJ, additional, Ingle, J, additional, Liu, MC, additional, Carey, L, additional, Blackwell, KL, additional, Rugo, H, additional, Nabell, L, additional, Forero, A, additional, Stearns, V, additional, Momen, L, additional, Gonzalez, J, additional, Akhtar, A, additional, Giri, DD, additional, Patil, S, additional, Feigin, KN, additional, Hudis, CA, additional, and Traina, TA, additional

Published
2012
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24. Abstract P1-12-04: Long Term Follow-Up of a Pilot Trial of Pre-Operative (Neoadjuvant) Letrozole in Combination with Bevacizumab in Post-Menopausal Women with Newly Diagnosed Estrogen and/or Progesterone Receptor Positive Breast Cancer

Author

Forero, A, primary, Saleh, M, additional, Galleshaw, J, additional, Jones, C, additional, Nabell, L, additional, Carpenter, J, additional, Falkson, C, additional, Krontiras, H, additional, Urist, M, additional, Bland, K, additional, De Los Santos, J, additional, Meredith, R, additional, Caterinicchia, V, additional, Bernreuter, W, additional, O'Malley, J, additional, Yufeng, L, additional, and LoBuglio, A., additional

Published
2010
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27. A Pilot Trial of Pre-Operative (Neoadjuvant) Letrozole in Combination with Bevacizumab in Post-Menopausal Women with Newly Diagnosed Estrogen and/or Progesterone Receptor Positive Breast Cancer.

Author

Forero, A., primary, Saleh, M., additional, Galleshaw, J., additional, Jones, C., additional, Shah, J., additional, Percent, I., additional, Nabell, L., additional, Carpenter, J., additional, Falkson, C., additional, Krontiras, H., additional, Urist, M., additional, Bland, K., additional, De Los Santos, J., additional, Meredith, R., additional, Caterinicchia, V., additional, Bernreuter, W., additional, O'Malley, J., additional, Li, Y., additional, and LoBuglio, A., additional

Published
2009
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32. A pilot open-label trial of preoperative (neoadjuvant) letrozole in combination with bevacizumab in postmenopausal women with newly diagnosed operable breast cancer

Author

Forero-Torres, A., primary, Galleshaw, J., additional, Jones, C., additional, Percent, I., additional, Nabell, L., additional, Carpenter, J., additional, Falkson, C., additional, Krontiras, H., additional, Bland, K., additional, De Los Santos, J., additional, and Saleh, M. N., additional

Published
2008
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35. Results of Radiation Therapy Oncology Group 97-03—A Randomized Phase II Trial of Concurrent Radiation and Chemotherapy for Advanced Squamous Cell Carcinomas of the Head and Neck: Long-term Results and Late Toxicities

Author

Garden, A.S., primary, Harris, J., additional, Vokes, E.E., additional, Forastiere, A.A., additional, Ridge, J.A., additional, Jones, C.U., additional, Horowitz, E.M., additional, Glisson, B.S., additional, Nabell, L., additional, and Cooper, J.S., additional

Published
2007
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45. Signal transduction by a CD16/CD7/Jak2 fusion protein.

Author

Sakai, I, Nabell, L, and Kraft, A S

Abstract

The addition of interleukin-3 (IL-3) and granulocyte-macrophage colony-stimulating factor (GM-CSF) to hormone-dependent cells induces tyrosine phosphorylation of Janus protein kinase 2 (Jak2) and activates its in vitro kinase activity. To explore the role of Jak2 in IL-3/GM-CSF-mediated signal transduction, we constructed a CD16/CD7/Jak2 (CD16/Jak2) fusion gene containing the external domain of CD16 and the entire Jak2 molecule and expressed this fusion protein using a recombinant vaccinia virus. The clustering of CD16/Jak2 fusion protein by cross-linking with an anti-CD16 antibody induced autophosphorylation of the fusion protein but did not induce the phosphorylation of either the endogenous Jak2 or the beta chain. Cross-linking of CD16/Jak2 stimulates the tyrosine phosphorylation of a large group of proteins that are also phosphorylated after the addition of IL-3 or GM-CSF and include proteins of 145, 97, 67, 52, and 42 kDa. Closer analysis demonstrated that the CD16/Jak2 phosphorylates Shc, a 52-kDa protein, and the 145-kDa protein associated tightly with Shc, as well as mitogen-associated protein kinase (pp42). Electrophoretic mobility shift assays demonstrate that CD16/Jak2 activates the ability of signal transduction and activation of transcription (STAT) proteins to bind to an interferon-gamma-activated sequence oligonucleotide in a manner similar to that seen after IL-3 treatment. Cross-linking of the CD16/Jak2 protein stimulated increases in c-fos and junB similar to IL-3 but did not cause major changes in the levels of the c-myc message, which normally increases after IL-3 treatment. Thus, a transmembrane CD16/Jak2 fusion is capable of activating protein phosphorylation and mRNA transcription in a manner similar but not identical to hematopoietic growth factors.

Published
1995

46. 17 beta-estradiol acts directly on the clonal osteoblastic cell line UMR106.

Author

Gray, T K, Flynn, T C, Gray, K M, and Nabell, L M

Abstract

We studied the effect of 17 beta-estradiol (E) on the proliferation and alkaline phosphatase activity of cultured UMR106 cells, a clonal osteoblastic cell line. Growth rates were reduced and alkaline phosphatase activity was increased in cells incubated for 2 days in medium containing E (10(-8) M). In contrast, E had no effect on the growth rates or alkaline phosphatase of a human fibroblastic cell line, S90E. The effect of E was not observed with low cell density or at confluence. 1,25-Dihydroxyvitamin D3 antagonized the response to E. Preincubation of the cells with dexamethasone, a potent inducer of differentiation, reversed the effect of E or 1,25-dihydroxyvitamin D3. These results indicate that cellular and/or extracellular factors such as cell density, the phase of the cell cycle, the state of differentiation, and the presence or absence of other steroids influenced the response of UMR106 cells to E. Serum was removed from the culture medium to minimize the effect of the steroids, growth factors, and nutrients present in serum. A striking stimulation of alkaline phosphatase by E occurred with serum-free conditions. This stimulation was biphasic over an E concentration from 10(-12) to 10(-8) M, with the peak response at 10(-10) M. The action of E on UMR106 cells was metabolite-specific, since the isomer 17 alpha-estradiol produced no effect on proliferation rates or alkaline phosphatase activity. The cyclic AMP response to parathyroid hormone (residues 1-34) was not altered by E treatment of these cells. In contrast, dexamethasone exposure did increase the cyclic AMP response to parathyroid hormone. These results demonstrate a direct effect of E on an osteoblastic cell line. They also raise the possibility that similar or identical actions of E occur in cultured normal osteoblasts.

Published
1987
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47. Breast cancer: Clinical practice guidelines in oncology

Author

Carlson, R. W., Anderson, B. O., Burstein, H. J., Cox, C. E., Edge, S. B., Farrar, W. B., Goldstein, L. J., Gradishar, W. J., Hayes, D. F., Hudis, C., Jahanzeb, M., Ljung, B. M., Marks, L. B., Beryl Mc Cormick, Nabell, L. M., Pierce, L. J., Reed, E. C., Silver, S. M., Smith, M. L., Somlo, G., Theriault, R. L., Ward, J. H., Winer, E. P., and Wolff, A. C.

48. NCCN Practice Guidelines for breast cancer

Author

Carlson, R. W., Anderson, B. O., Bensinger, W., Cox, C. E., Davidson, N. E., Edge, S. B., Farrar, W. B., Goldstein, L. J., Gradishar, W. J., Lichter, A. S., Mccormick, B., Nabell, L. M., Reed, E. C., Silver, S. M., Smith, M. L., Somlo, G., Theriault, R., Ward, J. H., Winer, E. P., and Antonio Wolff

49. Endocrine biomarkers in response to AR-inhibition with bicalutamide for the treatment of AR(+), ER/PR(-) metastatic breast cancer (MBC) (TBCRC011).

Author

Gucalp, A., Tolaney, S., Isakoff, S. J., Ingle, J., Liu, M. C., Carey, L., Blackwell, K. L., Rugo, H., Nabell, L., Forero, A., Stearns, V., Momen, L., Gonzalez, J., Akhtar, A., Giri, D. D., Patil, S., Feigin, K. N., Hudis, C. A., and Traina, T. A.

Subjects
*BREAST cancer research, *ESTROGEN receptors, *ANDROGEN receptors, *CANCER, *BIOMARKERS
Abstract

Background: Our group and others have identified a subset of ER/PR(-) breast cancers characterized by expression of the androgen receptor (AR) and androgen-dependent growth (Doane 2006). We conducted a proof-of-concept multicenter phase II study to test the efficacy of the AR-antagonist, bicalutamide for the treatment of AR(+) ER/PR(-) MBC (NCT00468715 ). Results of the primary endpoint, clinical benefit rate (CBR), were presented at ASCO (Gucalp 2012). Data for the impact of bicalutamide on circulating hormone levels in women are limited. Elevations in serum testosterone (T) and estradiol (E) have been observed for men treated with bicalutamide. We hypothesized comparable patterns of change in circulating endocrine markers in response to bicalutamide for women with MBC. Methods: Patients (pts) with AR(+) (IHC ≥10%), ER/PR(-) (IHC <10%) MBC were eligible for treatment (tx) if ECOG performance status ≥2 and normal organ function regardless of menopausal status. There was no limit to prior tx except prior trastuzumab required if HER2 (+). Tx consisted of bicalutamide 150mg orally daily in 28-day cycles (C). Toxicity assessed q4 weeks, response q12wks. Primary endpoint was CBR. Peripheral blood was collected for total and free T, E and sex hormone binding globulin (SHBG) at baseline, start of C2 (C2) and at end of study (EOS). Standard institutional assays were used. A Wlcoxon signed-rank test was done to compare baseline to C2 and EOS values. Results: 26 patients with AR(+) ER/PR(-) MBC were treated on study. Evaluable number (n) of pts at baseline, C2 and EOS are 26, 26 and 19 respectively. Two pts remain on study. Menopausal status: pre=2, post=24. Baseline median total and free T and estradiol were consistent with expected norms, however a wide range was observed (Table). There were no significant differences observed for median free T, total T, E or SHBG between baseline and C2 or baseline and EOS. Changes in hormone levels could not be stratified by menopausal status or response to bicalutamide given small sample size. Given the wide range of baseline values, we examined the percent change for each endocrine biomarker from baseline to C2 and EOS. As shown in the Table, there was no difference in median percent change observed across time points for each biomarker. Conclusions: No discernible patterns of change in T, E or SHBG were observed in response to bicalutamide therapy when given to women for the treatment of AR(+), ER/PR (-) MBC. These circulating hormones require further evaluation for use as a pharmacodynamic marker. [ABSTRACT FROM AUTHOR]

Published
2012
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50. Palbociclib in Patients With Head and Neck Cancer and Other Tumors With CDKN2A Alterations: Results From the Targeted Agent and Profiling Utilization Registry Study.

Author

Worden FP, Pisick E, Rothe M, Mangat PK, Garrett-Mayer E, Khalil MF, Carrizosa DR, Bauman JR, Leidner RS, Duvivier HL, Fu S, Park MS, Yost KJ, Calfa CJ, Marr AS, Balmanoukian AS, Behl D, Cannon TL, Nabell L, Powell SF, Thota R, Hinshaw DC, Gregory A, Grantham GN, Halabi S, and Schilsky RL

Subjects
Humans, Female, Male, Middle Aged, Aged, Adult, Aged, 80 and over, Mutation, Pyridines therapeutic use, Piperazines therapeutic use, Head and Neck Neoplasms drug therapy, Head and Neck Neoplasms genetics, Cyclin-Dependent Kinase Inhibitor p16 genetics, Registries
Abstract

Purpose: Targeted Agent and Profiling Utilization Registry is a phase II basket trial evaluating the antitumor activity of commercially available targeted agents in patients with advanced cancer and targetable genomic alterations. Two cohorts of patients with cyclin-dependent kinase inhibitor 2A ( CDKN2A )-mutated tumors treated with palbociclib are reported: one with head and neck cancer (HNC) with both squamous and nonsquamous cell histologies, and one with histology-pooled (HP) cancers., Methods: Eligible patients had measurable disease, Eastern Cooperative Oncology Group performance status 0-2, adequate organ function, and no standard treatment options. The primary end point was disease control (DC), defined as objective response (OR) or stable disease (SD) of at least 16+ weeks duration. For the HNC cohort, Simon's two-stage design with a null DC rate of 15% versus 35% (power = 0.85; α = .10) was used. For the HP cohort, the null hypothesis of a DC rate of 15% was rejected if the lower limit of a one-sided 90% CI was >15%. Secondary end points included OR, safety, progression-free survival, overall survival, duration of response, and duration of SD., Results: Seventy patients with HNC (N = 28) or HP cancers (N = 42) were treated with palbociclib. For the HNC cohort, DC and OR rates were 40% (one-sided 90% CI, 27 to 100) and 4% (95% CI, <1 to 18), respectively. The null hypothesis was rejected ( P = .002). For the HP cohort, DC and OR rates were 13% (one-sided 90% CI, 6 to 100) and 5% (95% CI, <1 to 17), respectively. The null hypothesis was not rejected. Thirty-one of 70 patients experienced treatment-related grade 3 to 4 adverse events (AEs) or serious AEs, the most common including neutropenia, thrombocytopenia, and leukopenia., Conclusion: Palbociclib met prespecified criteria to declare a signal of activity in patients with HNC with CDKN2A alterations, but not in the HP cohort.

Published
2024
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