Academic literature on the topic 'Brookmeyer'

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Journal articles on the topic "Brookmeyer"

1

Dagenais, Marcel. "Comment on Zeger and Brookmeyer." Journal of the American Statistical Association 86, no. 413 (March 1991): 255. http://dx.doi.org/10.1080/01621459.1991.10475025.

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2

Gale, Catharine R. "Dietary Antioxidants and Dementia." International Psychogeriatrics 13, no. 3 (September 2001): 259–62. http://dx.doi.org/10.1017/s1041610201007645.

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As the populations of the developed world continue to age, the number of people who develop Alzheimer's disease (AD) or other forms of dementia is set to rise. In the United States, for example, the prevalence of AD is projected to quadruple over the next 50 years (Brookmeyer & Gray, 2000). The search for factors that might help to prevent or treat these conditions has therefore assumed a particular relevance.
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3

Pencheon, D. "Monitoring the Health of Populations: Statistical Principles and Methods for Public Health Surveillance. Brookmeyer and Stroup, Oxford University Press, 2004." Journal of Public Health 27, no. 1 (March 1, 2005): 128. http://dx.doi.org/10.1093/pubmed/fdh209.

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4

Barnes, Josephine, and Nick C. Fox. "The search for early markers of AD: hippocampal atrophy and memory deficits." International Psychogeriatrics 26, no. 7 (May 30, 2014): 1065–66. http://dx.doi.org/10.1017/s1041610214000623.

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There is increasing interest in finding markers of Alzheimer's disease (AD) that are discriminative even at an early, pre-dementia stage. This interest is driven partly by a desire to improve clinical diagnosis in more mildly affected individuals, and also by the recent paradigm shift in thinking about clinical trials for AD. This shift is a result of concern that the recent failures of high-profile clinical trials conducted in patients with mild to moderate AD may have been because therapy was “too little, too late.” The implication being that if only treatments had been trialled earlier they would have had a greater chance of success. Certainly, lessons from other aspects of medicine have shown that treatments may be most, or in some cases only, effective if given early in disease. If we did have therapies that could slow disease progression at a very early stage that would increase the interest in early markers of disease. Ideally, such therapies would be given when the minimum of functional decline and irreversible neuronal loss had already occurred. From economic and public health standpoints, delaying symptom onset would be very important: a delay of five years has been estimated to reduce projections for prevalence of symptomatic AD by about 50% (Brookmeyer et al., 1998).
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5

Kudo, Masatoshi, Shukui Qin, Fabio Piscaglia, Arndt Vogel, T. R. Jeffry Evans, Jennifer J. Knox, Carlos López López, et al. "Characterization of tumor responses in patients (pts) with unresectable hepatocellular carcinoma (uHCC) treated with lenvatinib in REFLECT." Journal of Clinical Oncology 40, no. 16_suppl (June 1, 2022): 4078. http://dx.doi.org/10.1200/jco.2022.40.16_suppl.4078.

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4078 Background: In REFLECT, lenvatinib was noninferior to sorafenib based on overall survival in pts with uHCC (median 13.6 vs 12.3 mos; hazard ratio [HR] 0.92, 95% CI 0.79–1.06). The objective response rate (ORR) with lenvatinib was 18.8% by blinded independent imaging review (IIR) per RECIST v1.1; ORR was 40.6% by blinded IIR per mRECIST. Here we further characterize the tumor responses in pts with uHCC who were treated with lenvatinib in REFLECT. Methods: Assessments of ORR included all pts randomly assigned to lenvatinib treatment (12 mg/day for bodyweight ≥60 kg or 8 mg/day for bodyweight <60 kg). Time to first objective response (TTR) and duration of response (DOR) were calculated among pts who achieved a partial or complete tumor response. Tumors were assessed by IIR per RECIST v1.1 or mRECIST. Median DOR was estimated with the Kaplan-Meier product-limit method; 95% CI was estimated with a generalized Brookmeyer and Crowley method. Results: 478 Pts were randomly assigned to receive lenvatinib. Among the 90 pts (18.8%) who achieved an objective response by IIR per RECIST v1.1, median TTR was 2.8 mos (range 1–29) and median DOR was 7.4 mos (95% CI 5.6–9.2). Of the 194 pts who had an objective response by IIR per mRECIST, median TTR was 1.9 mos (range 1–15) and median DOR was 7.3 mos (95% CI 5.6–7.4). ORRs by selected baseline characteristics are reported in the Table. Notably, among responders by IIR per RECIST v1.1 (n=90), median overall survival (by Simon-Makuch method) was 23.4 mos (95% CI 17.6–26.3), median duration of treatment was 10.3 mos, and 65.6% of pts experienced grade ≥3 treatment-related adverse events. Conclusions: Pts with uHCC treated with lenvatinib achieved objective responses with a similar frequency to those seen with single-agent immune checkpoint inhibitors. These responses occurred irrespective of baseline characteristics. Tumor responses occurred early and were durable. Clinical trial information: NCT01761266. [Table: see text]
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Verzoni, Elena, Alessandra Bearz, Ugo De Giorgi, Franco Nole, Camillo Porta, Raffaele Ratta, Melanie Claps, et al. "A phase II open-label study of cabozantinib in patients with advanced or unresectable renal cell carcinoma pretreated with one immune-checkpoint inhibitor: The BREAKPOINT trial." Journal of Clinical Oncology 37, no. 7_suppl (March 1, 2019): TPS685. http://dx.doi.org/10.1200/jco.2019.37.7_suppl.tps685.

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TPS685 Background: First-line treatment landscape of metastatic renal cell carcinoma (mRCC) is evolving with strong evidence in favour of PD-1/PD-L1 combinations over tyrosine kinase inhibitors (TKIs). No prospective data about efficacy of TKIs post immune-checkpoint inhibitor (CPI) combinations are available. Among TKIs, cabozantinib has demonstrated progression-free survival (PFS) and overall survival (OS) benefit over everolimus in pre-treated mRCC patients (pts). Methods: Overall 49 mRCC pts who received a previous CPI (anti PD-1/PD-L1) will be treated with cabozantinib. Pts will be stratified according to Heng prognostic group, duration of first-line and type of previous therapy received (CPI+CPI or CPI+TKI or CPI+anti-VEGF or CPI monotherapy). Key inclusion criteria include: one previous treatment with a PD-1/PD-L1 inhibitor in first-line and histological diagnosis of clear-cell RCC. The primary endpoint is to assess the efficacy of cabozantinib based on PFS. Secondary endpoints include evaluation of OS, objective response rate and safety profile of the drug. Exploratory endpoints include evaluation of PD-L1 levels by immunohistochemistry in tumor samples; the analysis of the immunological signature/profile of tumor cells; the state of circulating immune cells, as well as the modulating activity of cabozantinib on systemic tumor immunity; the evaluation of bone formation and reabsorption markers in pts with or without bone involvement. Cabozantinib will be administered orally at a dose of 60 mg/day continuously until evidence of disease progression or onset of unacceptable toxicity. Statistical design: By the methodology of Brookmeyer and Crowley, assuming an accrual period of 18 months and a minimum follow-up of 10 months (mos), 49 pts are necessary to detect an increment of the median PFS time from 3.8 mos to 7.4 mos with a power of 90% and one-sided alpha of 5%. The large sample critical value detecting the increment of the PFS median survival time will be 5.54 mos. To date, 2 pts have been enrolled. Clinical trial information: NCT03463681.
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7

Molina, Ana M., Jingbo Zhang, Xun Lin, Liviu Niculescu, Beata Korytowsky, Ewa Matczak, Robin Wiltshire, and Robert John Motzer. "Sunitinib objective response (OR) in metastatic renal cell carcinoma (mRCC): Analysis of 1,059 patients treated on clinical trials." Journal of Clinical Oncology 30, no. 15_suppl (May 20, 2012): 4542. http://dx.doi.org/10.1200/jco.2012.30.15_suppl.4542.

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4542 Background: Sunitinib achieves robust OR and improved progression-free survival (PFS) in mRCC patients (N Engl J Med 2007;356:115). A retrospective analysis was performed to characterize the OR rate with sunitinib treatment (Tx) and OR-associated patient features and survival. Methods: Data from six phase II and III trials were pooled from 1,059 patients who received sunitinib on the approved 50 mg/d 4-week-on/2-week-off schedule (n=689; 65%) or at 37.5 mg continuous once-daily dosing (n=370; 35%), in both the 1st- (n=783; 74%) and 2nd-line (n=276; 26%) Tx settings. Median PFS and overall survival (OS) were estimated by the Brookmeyer and Crowley method, and compared between responders and nonresponders, and early and late responders (response ≤ and >12 weeks, respectively), by a log-rank test. Baseline characteristics were compared by Fisher-exact Test, T-Test, or Wilcoxon Rank-sum Test. Results: Of 1,059 patients, 398 (38%) had a confirmed investigator-assessed OR by RECIST (including 12 with a complete response), of whom 105 (26%), 243 (61%), 314 (79%), and 342 (86%) had a response by 6, 12, 18, and 24 weeks, respectively. Median (range) time to tumor response (TTR) in all patients was 10.6 (2.7–94.4) weeks, which was similar in the 1st- and 2nd-line Tx settings. Responders had better baseline ECOG scores, more favorable risk factor classification based on published MSKCC data, a longer interval since initial diagnosis, more prior nephrectomy, and less presence of baseline bone metastases (all p<0.05). Early responders had more lung metastases (p<0.01). Median PFS (16.3 vs. 5.3 months) and OS (40.1 vs. 14.5 months) were significantly longer in responders vs. nonresponders (both p<0.001), with similar results regardless of 1st- or 2nd-line Tx setting. Median OS did not differ between early and late responders (p=0.1438). Conclusions: OR was achieved in 38% of 1,059 mRCC patients treated with sunitinib and was predicted by favorable pretreatment prognostic factors. Patients with OR had longer PFS and OS. Median TTR was 10.6 weeks, and characteristics and outcome of early and late responders were similar, except for higher frequency of lung metastases among early responders.
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8

Singh, Gunjesh Kumar, Hollis D'souza, Sujay Srinivas, Dilip Harindran Vallathol, Mounika Boppana, Annu Rajpurohit, Abhishek Mahajan, et al. "Safety and efficacy of bevacizumab biosimilar in glioma." Journal of Clinical Oncology 38, no. 15_suppl (May 20, 2020): e14541-e14541. http://dx.doi.org/10.1200/jco.2020.38.15_suppl.e14541.

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e14541 Background: Anti-VEGF antibody Bevacizumab (Avastin: Roche Pharma AG) is the recommended drug for recurrent glioma. Multiple low-cost bio-similars of this drug are now available however their clinical efficacy has never been compared against the original molecule. The aim of the current analysis is to compare the overall survival (OS) between recurrent glioma patients with bio-similar and innovator molecule. Methods: Adult recurrent glioma patients treated with bevacizumab from 1st July 2015 to 30th July 2019 were identified from the Neuro-Medical Oncology database. These patients were either offered Avastin or Bevacizumab biosimilar (BevaciRel: Reliance Life sciences or Bryta: Zydus Oncosciences) depending upon the financial affordability. The primary endpoint of the study was OS. It was defined as the time in months from the start of bevacizumab to death. Progression-free survival (PFS) was defined as the time in months from the start of bevacizumab to progression or death. The time to event variables was estimated using Kaplan Meier method. The median with its 95% confidence interval (CI) was calculated using Brookmeyer and Crowley method. The estimates were compared between the original and bio-similar bevacizumab cohort using the log-rank test. The hazard ratio was calculated using COX regression analysis. Results: There were 82 patients, out of which 57 received innovator and 25 received bio-similar bevacizumab. At median follow up of 26 months, 76 patients had an event for progression. The median PFS was 3.66 (95% CI 2.08 to 5.25) and 3.3 months (95% CI 2.38 to 4.21) in innovator and bio-similar arm respectively (Log-rank test P-value = 0.072). The hazard ratio for progression was 0.61 (95% CI 0.35 to 1.05; P-value = 0.075). At the time of data cutoff, there were 69 deaths. The median OS was 5.53 (95% CI, 5.07 to 5.99) vs 7.33 months (95% CI, 5.63 to 9.03) in innovator and bio-similar arm respectively (Log-rank test P-value = 0.51). The hazard ratio for death was 1.21 (95% CI, 0.67 to 2.17; p-value = 0.51). Conclusions: In the brain tumor patients, both innovator and bio-similar bevacizumab seem to have similar clinical efficacy.
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9

Von Drygalski, A., T. B. Tran, K. Messer, M. Pu, S. Corringham, C. Nelson, E. D. Ball, and E. D. Ball. "Predictors of survival in patients with metastatic breast cancer (MBC) treated with high-dose chemotherapy and autologous stem cell transplantation (HD-ASCT)." Journal of Clinical Oncology 27, no. 15_suppl (May 20, 2009): e22086-e22086. http://dx.doi.org/10.1200/jco.2009.27.15_suppl.e22086.

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e22086 Background: Individualized care in MBC requires predictors of survival for tailored treatment. Although HD-ASCT has not resulted in improved overall survival (OS), retrospective analyses may identify patients who benefited. We reviewed records of all patients (n=96) in the bone marrow transplant registry at UCSD treated with HD-ASCT for MBC between 1989 and 2000. Methods: Age, race, stage at diagnosis, histology, estrogen receptor (ER) and menopausal status, body mass index (BMI) in kg/m2, time to transplant and death, sites of metastasis, disease status prior to and after transplant, and days in hospital were extracted. Brookmeyer & Crowley's 95% confidence intervals, Cox models for predictors of a time-to-event variable and Schoenfeld tests for proportional hazard assumptions were applied. Results: Median OS was 5.6 ys (CI 4.1–7.4) after initial diagnosis and 1.7 ys (CI 1.36–2.07) after transplant. OS after HD-ASCT at 12 ys was 8.2% and, although not statistically significant, 18.5% in ER- and 2.6% in ER+ patients, respectively. Stratified by ER status, stage at diagnosis was an independent predictor of OS. Patients with stage I at diagnosis were at lowest risk of death when compared to stage II-IV patients with HRs of 2.7 (II vs I CI 1.4–5.2), 4.6 (III vs I CI 2.1–10) and 17 (IV vs I CI 6.1- 47.8). Death risk was increased with BMI ≥ 30 (HR 3.1; CI 1.8–5.4), infiltrating lobular carcinoma (HR 2.5; CI 1.1–5.38) and visceral metastasis (HR 2.3; CI 1.3–4.1). Conclusions: The study highlights that ∼10% of patients experience ≥10 ys survival with HD- ASCT. Obesity, late stage at diagnosis, lobular infiltrating histology and visceral metastasis were independent negative predictors of OS. Surprisingly, ER- patients tended to live longer. Although survival was influenced by various disease characteristics, obesity was the only significant patient derived factor. How obesity negatively affects outcomes - whether affecting cancer growth or through associated morbidity - needs further study. These data may be useful stratification tools for future trials employing HD-ASCT as treatment modality in MBC. No significant financial relationships to disclose.
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Puri, Akshjot, Charisma Mylavarapu, Joe E. Ensor, Parveen Parveen, Ivo Tremont-Lukats, Jenny Chee Ning Chang, and Polly Ann Niravath. "Systemic chemotherapy in patients with brain only metastatic breast cancer: A retrospective analysis." Journal of Clinical Oncology 39, no. 15_suppl (May 20, 2021): 1093. http://dx.doi.org/10.1200/jco.2021.39.15_suppl.1093.

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1093 Background: The treatment of patients with brain only metastatic breast cancer (BO-MBC) remains very challenging. There is also very limited literature informing on appropriate treatment or natural history of this entity. Systemic chemotherapy in addition to targeted therapy and/or anti-estrogen treatment is often used, but little is known if it adds to the overall or disease free survival. In this retrospective study, we examine this, as well as other factors which may be associated with increased risk of CNS or systemic recurrence in these patients. Methods: A database search at a single institution identified 178 patients with brain metastases (BM) from breast cancer out of which 45 patients had BO-MBC between 2007-2020. We collected demographic, clinical, radiographic and other treatment data. Leptomeningeal disease (LMD) was diagnosed by cerebrospinal fluid (CSF) cytology, neuroimaging, or both. We used the Brookmeyer and Crowley method. Results: The patients were followed for a median of 17.9 months; 36 out of 45 patients (80%) received local treatment for BM (surgery/radiation/both) and HER2 directed antibodies or tyrosine kinase inhibitors and/or anti-estrogen treatment, whereas 9 out of 45 patients (20%) received systemic chemotherapy in addition. There were 22 out of 45 (49%) HER2 +, 5 out of 45 (11%) HR + and 18 out of 45 (40%) triple negative breast cancer (TNBC) patients. There were 17 out of 45 patients (38%) who were deemed to have low burden of BM (defined as one to three BM and largest being ≤3 cm) whereas there were 24 out of 45 patients (53%) who had high burden of BM (defined as four or more BM or largest being > 3 cm). Conclusions: Patients with BO-MBC represent a distinct entity. Despite having better survival than patients with BM and extra CNS disease these patients have a high risk of developing LMD, CNS and systemic recurrences. The addition of chemotherapy to targeted therapy and/or anti-estrogens does not decrease the rates of systemic or CNS recurrence. The ER+ subset have a lower rate of development of systemic disease, as expected due to their relatively indolent biology. The CNS and systemic recurrence seem to be higher in patients with HER2+ cancers and counterintuitively even in those with low burden of BM; albeit these were statistically insignificant.[Table: see text]
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Books on the topic "Brookmeyer"

1

Hudson, Rob. Evolution (The Improvisational Style of Bob Brookmeyer For Trombone). Universal Edition, 2003.

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2

Retorno a Brookmere/Return to Brookmere (Dungeons & Dragons Endless Quest Books). Timun Mas, 1985.

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Book chapters on the topic "Brookmeyer"

1

Martin, Williams. "Giuffre/Brookmeyer Reunion." In Jazz Changes, 84–89. Oxford University Press, 1993. http://dx.doi.org/10.1093/acprof:oso/9780195083491.003.0011.

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Martin, Williams. "Brookmeyer, Mulligan, and the Concert Jazz Band." In Jazz Changes, 26–29. Oxford University Press, 1993. http://dx.doi.org/10.1093/acprof:oso/9780195083491.003.0004.

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