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Article: Optimizing Neurology Inpatient Documentation: A Pilot Study of a Novel Discharge Documentation EHR Tool.

Fu, Katherine A / Kerbel, Russell / Obrien, Rylan J / Li, Joshua S / Jackson, Nicholas J / Keselman, Inna / Reider-Demer, Melissa

The Neurohospitalist

2023 Volume 14, Issue 1, Page(s) 5–12

Abstract: Background and purpose: Clinical documentation of patient acuity is a major determinant of payer reimbursement. This project aimed to improve case mix index (CMI) by incorporating a novel electronic health record (EHR) discharge documentation tool into ... ...

Abstract	Background and purpose: Clinical documentation of patient acuity is a major determinant of payer reimbursement. This project aimed to improve case mix index (CMI) by incorporating a novel electronic health record (EHR) discharge documentation tool into the inpatient general neurology service at the University of California, Los Angeles (UCLA) Medical Center. Methods: We used data from Vizient AMC Hospital: Risk Model Summary for Clinical Data Base (CBD) 2017 to create a discharge diagnosis documentation tool consisting of dropdown menus to better capture relevant secondary diagnoses and comorbidities. After implementation of this tool, we compared pre- (July 2017-June 2019) and post-intervention (July 2019-June 2021) time periods on mean expected length of stay (LOS) and mean CMI with two sample T-tests and the percentage of encounters classified as having Major Complications/Comorbidities (MCC), with Complication/Comorbidity (CC), and without CC/MCC with tests of proportions. Results: Mean CMI increased significantly from 1.2 pre-intervention to 1.4 post-intervention implementation ( Conclusions: This pilot study describes the creation of an innovative EHR discharge diagnosis documentation tool in collaboration with neurology healthcare providers, the clinical documentation improvement team, and neuro-informaticists. This novel discharge diagnosis documentation tool demonstrates promise in increasing CMI, shifting diagnosis related groups to a greater proportion of those with MCC, and improving the quality of clinical documentation.
Language	English
Publishing date	2023-08-04
Publishing country	United States
Document type	Journal Article
ZDB-ID	2629083-2
ISSN	1941-8752 ; 1941-8744
ISSN (online)	1941-8752
ISSN	1941-8744
DOI	10.1177/19418744231194680
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Article ; Online: Mesenchymal stem cells induce an immunosuppressive microenvironment in pituitary tumors.

Marrero-Rodriguez, Daniel / Cortes-Morales, Victor A / Cano-Zaragoza, Amayrani / Martinez-Mendoza, Florencia / Kerbel-Suton, Jacobo / Vela-Patiño, Sandra / Chavez-Santoscoy, Alejandra / Hinojosa-Alvarez, Silvia / Hernandez-Perez, Jesus / Gomez-Apo, Erick / Fajardo-Orduña, Guadalupe R / Taniguchi-Ponciano, Keiko / Montesinos, Juan Jose / Mercado, Moises

The Journal of clinical endocrinology and metabolism

2024

Abstract: Background: The tumor microenvironment (TME) includes diverse cellular components such as mesenchymal stem cells (MSC) and immune cells among others. MSC have been isolated from different tumors and they favor tumor cell growth, however, their role in ... ...

Abstract	Background: The tumor microenvironment (TME) includes diverse cellular components such as mesenchymal stem cells (MSC) and immune cells among others. MSC have been isolated from different tumors and they favor tumor cell growth, however, their role in pituitary tumors (PT) remains unknown. Herein we report the presence of MSCs in 2 ACTH-secreting PT causing Cushing disease (MCU), 2 nonfunctioning adenomas of gonadotrope differentiation (MNF) and 2 non tumoral pituitary glands (MS). Methods: We have analyzed their transcriptomic profiles by RNAseq and compared MSC in terms of their immunosuppressive effects against lymphoid T cell and macrophage populations by means of co-cultures and flow cytometry. Results: Our transcriptomic analysis revealed molecular differences between MSC derived from non-tumoral pituitaries and MSC derived from PT. Two distinct subpopulations of MSC, one displaying immunosuppressive properties and the other with increased pro-proliferative capabilities, regardless of their origin. MSC derived from ACTH- and nonfunctioning PT, but not those derived from non-tumoral glands significantly inhibited the proliferation of activated T cells, favored the generation of Tregs and promote M2 macrophage polarization. Such immunosuppressive effects were correlated with an upregulation of programmed death ligand 1 and intracellular expression of macrophage colony stimulating factor (M-CSF) and IL-10. Importantly, MSC derived from ACTH-PT showed a higher immunosuppressive potential than MSC isolated from nonfunctioning tumors. Conclusion: This study demonstrates the presence of at least two MSC subpopulations in the pituitary gland and suggests that immunosuppressive effects of MSC may have important implications in PT growth.
Language	English
Publishing date	2024-04-09
Publishing country	United States
Document type	Journal Article
ZDB-ID	3029-6
ISSN	1945-7197 ; 0021-972X
ISSN (online)	1945-7197
ISSN	0021-972X
DOI	10.1210/clinem/dgae212
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Article ; Online: Preoperative risk stratification minimizes 90-day complications in morbidly obese patients undergoing primary total knee arthroplasty.

Kerbel, Yehuda E / Johnson, Mitchell A / Barchick, Stephen R / Cohen, Jordan S / Stevenson, Kimberly Lola / Israelite, Craig L / Nelson, Charles L

The bone & joint journal

2021 Volume 103-B, Issue 6 Supple A, Page(s) 45–50

Abstract: Aims: It has been shown that the preoperative modification of risk factors associated with obesity may reduce complications after total knee arthroplasty (TKA). However, the optimal method of doing so remains unclear. The aim of this study was to ... ...

Abstract	Aims: It has been shown that the preoperative modification of risk factors associated with obesity may reduce complications after total knee arthroplasty (TKA). However, the optimal method of doing so remains unclear. The aim of this study was to investigate whether a preoperative Risk Stratification Tool (RST) devised in our institution could reduce unexpected intensive care unit (ICU) transfers and 90-day emergency department (ED) visits, readmissions, and reoperations after TKA in obese patients. Methods: We retrospectively reviewed 1,614 consecutive patients undergoing primary unilateral TKA. Their mean age was 65.1 years (17.9 to 87.7) and the mean BMI was 34.2 kg/m Results: Obese patients had a significantly increased rate of discharge to a rehabilitation facility compared with non-obese patients (38.7% (426/1,102) vs 26.0% (133/512), respectively; p < 0.001). When stratified by BMI, discharge to a rehabilitation facility remained significantly higher compared with non-obese (26.0% (133)) in both obese (34.2% (256), odds ratio (OR) 1.6) and morbidly obese (48.0% (170), OR 3.1) patients (p < 0.001). However, there was no significant difference in unexpected ICU transfer (0.4% (two) non-obese vs 0.9% (seven) obese (OR 2.5) vs 1.7% (six) morbidly obese (OR 5.4); p = 0.054), visits to the ED (8.6% (44) vs 10.3% (77) (OR 1.3) vs 10.5% (37) (OR 1.2); p = 0.379), readmissions (4.5% (23) vs 4.0% (30) (OR 1.0) vs 5.1% (18) (OR 1.4); p = 0.322), or reoperations (2.5% (13) vs 3.3% (25) (OR 1.2) vs 3.1% (11) (OR 0.9); p = 0.939). Conclusion: With the use of a preoperative RST, morbidly obese patients had similar rates of short-term postoperative adverse outcomes after primary TKA as non-obese patients. This supports the assertion that morbidly obese patients can safely undergo TKA with appropriate perioperative optimization and monitoring. Cite this article:
MeSH term(s)	Adolescent ; Adult ; Aged ; Aged, 80 and over ; Arthroplasty, Replacement, Knee ; Emergency Service, Hospital/statistics & numerical data ; Female ; Humans ; Intensive Care Units/statistics & numerical data ; Male ; Middle Aged ; Obesity, Morbid/complications ; Patient Readmission/statistics & numerical data ; Pennsylvania ; Postoperative Complications/prevention & control ; Reoperation/statistics & numerical data ; Retrospective Studies ; Risk Assessment/methods ; Risk Factors
Language	English
Publishing date	2021-05-30
Publishing country	England
Document type	Journal Article
ZDB-ID	2697156-2
ISSN	2049-4408 ; 2049-4394
ISSN (online)	2049-4408
ISSN	2049-4394
DOI	10.1302/0301-620X.103B6.BJJ-2020-2409.R1
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Zs.A 6989: Show issues

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Article ; Online: Vessel co-option in cancer.

Kuczynski, Elizabeth A / Vermeulen, Peter B / Pezzella, Francesco / Kerbel, Robert S / Reynolds, Andrew R

Nature reviews. Clinical oncology

2019 Volume 16, Issue 8, Page(s) 469–493

Abstract: All solid tumours require a vascular supply in order to progress. Although the ability to induce angiogenesis (new blood vessel growth) has long been regarded as essential to this purpose, thus far, anti-angiogenic therapies have shown only modest ... ...

Abstract	All solid tumours require a vascular supply in order to progress. Although the ability to induce angiogenesis (new blood vessel growth) has long been regarded as essential to this purpose, thus far, anti-angiogenic therapies have shown only modest efficacy in patients. Importantly, overshadowed by the literature on tumour angiogenesis is a long-standing, but continually emerging, body of research indicating that tumours can grow instead by hijacking pre-existing blood vessels of the surrounding nonmalignant tissue. This process, termed vessel co-option, is a frequently overlooked mechanism of tumour vascularization that can influence disease progression, metastasis and response to treatment. In this Review, we describe the evidence that tumours located at numerous anatomical sites can exploit vessel co-option. We also discuss the proposed molecular mechanisms involved and the multifaceted implications of vessel co-option for patient outcomes.
MeSH term(s)	Animals ; Humans ; Neoplasms/pathology ; Neovascularization, Pathologic/pathology
Language	English
Publishing date	2019-03-01
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	2491410-1
ISSN	1759-4782 ; 1759-4774
ISSN (online)	1759-4782
ISSN	1759-4774
DOI	10.1038/s41571-019-0181-9
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Zs.A 6029: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 2021: Bestellungen von Artikeln über das Online-Bestellformular ab Jg. 2022: Lesesaal (EG)
Zs.MG 103: Show issues

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Article: Molecular and physiologic mechanisms of drug resistance in cancer: an overview.

Kerbel, R S

Cancer metastasis reviews

2002 Volume 20, Issue 1-2, Page(s) 1–2

MeSH term(s)	Antineoplastic Agents/therapeutic use ; Drug Resistance, Neoplasm/genetics ; Drug Resistance, Neoplasm/physiology ; Humans ; Neoplasms/drug therapy
Chemical Substances	Antineoplastic Agents
Language	English
Publishing date	2002-01-17
Publishing country	Netherlands
Document type	Editorial
ZDB-ID	604857-2
ISSN	1573-7233 ; 0167-7659
ISSN (online)	1573-7233
ISSN	0167-7659
DOI	10.1023/a:1013129128673
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Article ; Online: Nesfatin-1 suppresses energy intake, co-localises ghrelin in the brain and gut, and alters ghrelin, cholecystokinin and orexin mRNA expression in goldfish.

Kerbel, B / Unniappan, S

Journal of neuroendocrinology

2012 Volume 24, Issue 2, Page(s) 366–377

Abstract: ... and the expression of mRNAs encoding preproghrelin, ghrelin receptor (GHS-R 1a-1), CCK and NUCB2 ...

Abstract	Nesfatin-1 is a novel anorectic peptide encoded in the precursor protein nucleobindin-2 (NUCB2). We recently reported the presence and appetite suppressing effects of nesfatin-1 in goldfish. Nesfatin-1 has been co-localised with ghrelin in the stomach of rats. Whether nesfatin-1 influences other appetite regulatory peptides in goldfish remains unclear. The main objectives of the present study were to investigate whether nesfatin-1 co-localises ghrelin in goldfish, and to test whether exogenous nesfatin-1 influences endogenous ghrelin, cholecystokinin (CCK) and orexin A (OXA). We found co-localisation of nesfatin-1-like and ghrelin-like immunoreactivity in the enteroendocrine cells of the goldfish anterior intestine (J-loop). Furthermore, co-localisation of ghrelin and nesfatin-1 was also observed in the posterior nucleus lateralis tuberis of the goldfish hypothalamus, a brain region implicated in the regulation of food intake. These findings suggest a functional relationship between ghrelin and nesfatin-1 in goldfish. In support of this, i.c.v. administration of goldfish (gf) nesfatin-1 [25 ng/g body weight (BW)], suppressed food intake and the expression of mRNAs encoding preproghrelin, ghrelin receptor (GHS-R 1a-1), CCK and NUCB2 in the forebrain of fed fish, as well as ghrelin and NUCB2 mRNA in the hypothalamus of unfed fish, both at 1 h post-injection. Nesfatin-1 stimulated hypothalamic CCK mRNA expression at 30 min post-injection in fed fish, and inhibited OXA mRNA in the unfed fish hypothalamus 1 h post-injection. Similarly, i.c.v. injections of gfghrelin (1 ng/g BW), although stimulating food intake, suppressed NUCB2 and preproghrelin mRNAs, but not ghrelin receptor mRNA expression in the forebrain. It is also evident that exogenous ghrelin and nesfatin-1 mRNAs encoding these peptides. Our novel results indicate interactions between nesfatin-1 and ghrelin, CCK and orexin, and show that nesfatin-1 acts on other appetite regulatory peptides in a time- and feeding status-dependent, as well as tissue-specific, manner in goldfish.
MeSH term(s)	Amino Acid Sequence ; Animals ; Brain/drug effects ; Brain/metabolism ; Calcium-Binding Proteins/genetics ; Calcium-Binding Proteins/metabolism ; Calcium-Binding Proteins/pharmacology ; Cholecystokinin/genetics ; Cholecystokinin/metabolism ; DNA-Binding Proteins/genetics ; DNA-Binding Proteins/metabolism ; DNA-Binding Proteins/pharmacology ; Energy Intake/drug effects ; Energy Intake/genetics ; Gene Expression/drug effects ; Ghrelin/metabolism ; Goldfish/genetics ; Goldfish/metabolism ; Goldfish/physiology ; Intestines/drug effects ; Intestines/metabolism ; Intracellular Signaling Peptides and Proteins/genetics ; Intracellular Signaling Peptides and Proteins/metabolism ; Molecular Sequence Data ; Nerve Tissue Proteins/genetics ; Nerve Tissue Proteins/metabolism ; Nerve Tissue Proteins/pharmacology ; Neuropeptides/genetics ; Neuropeptides/metabolism ; Orexins ; RNA, Messenger/genetics ; RNA, Messenger/metabolism ; Rats ; Tissue Distribution
Chemical Substances	Calcium-Binding Proteins ; DNA-Binding Proteins ; Ghrelin ; Intracellular Signaling Peptides and Proteins ; Nerve Tissue Proteins ; Neuropeptides ; Orexins ; RNA, Messenger ; nucleobindin ; Cholecystokinin (9011-97-6)
Language	English
Publishing date	2012-02
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	1007517-3
ISSN	1365-2826 ; 0953-8194
ISSN (online)	1365-2826
ISSN	0953-8194
DOI	10.1111/j.1365-2826.2011.02246.x
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Zs.A 2634: Show issues

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Article: Clinical trials of antiangiogenic drugs: opportunities, problems, and assessment of initial results.

Kerbel, R S

Journal of clinical oncology : official journal of the American Society of Clinical Oncology

2001 Volume 19, Issue 18 Suppl, Page(s) 45S–51S

MeSH term(s)	Angiogenesis Inhibitors/pharmacology ; Clinical Trials as Topic ; Drug Resistance, Neoplasm ; Evidence-Based Medicine ; Humans ; Neoplasms/blood supply ; Neoplasms/drug therapy ; Neoplasms/physiopathology ; Neovascularization, Pathologic ; Treatment Outcome
Chemical Substances	Angiogenesis Inhibitors
Language	English
Publishing date	2001-09-15
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, P.H.S. ; Review
ZDB-ID	604914-x
ISSN	1527-7755 ; 0732-183X
ISSN (online)	1527-7755
ISSN	0732-183X
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Zs.A 1847: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (1.OG) ab Jg. 2022: Lesesaal (EG)
Zs.MO 650: Show issues

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Article: Tumor angiogenesis: past, present and the near future.

Kerbel, R S

Carcinogenesis

2000 Volume 21, Issue 3, Page(s) 505–515

Abstract: The concept of treating solid tumors by inhibiting tumor angiogenesis was first articulated almost 30 years ago. For the next 10 years it attracted little scientific interest. This situation changed, relatively slowly, over the succeeding decade with the ...

Abstract	The concept of treating solid tumors by inhibiting tumor angiogenesis was first articulated almost 30 years ago. For the next 10 years it attracted little scientific interest. This situation changed, relatively slowly, over the succeeding decade with the discovery of the first pro-angiogenic molecules such as basic fibroblast growth factor and vascular endothelial growth factor (VEGF), and the development of methods of successfully growing vascular endothelial cells in culture as well as in vivo assays of angiogenesis. However, the 1990s have witnessed a striking change in both attitude and interest in tumor angiogenesis and anti-angiogenic drug development, to the point where a remarkably diverse group of over 24 such drugs is currently undergoing evaluation in phase I, II or III clinical trials. In this review I will discuss the many reasons for this. These features, together with other recent discoveries have created intense interest in initiating and expanding anti-angiogenic drug discovery programs in both academia and industry, and the testing of such newly developed drugs, either alone, or in various combinations with conventional cytotoxic therapeutics. However, significant problems remain in the clinical application of angiogenesis inhibitors such as the need for surrogate markers to monitor the effects of such drugs when they do not cause tumor regressions, and the design of clinical trials. Also of concern is that the expected need to use anti-angiogenic drugs chronically will lead to delayed toxic side effects in humans, which do not appear in rodents, especially in short-term studies.
MeSH term(s)	Angiogenesis Inhibitors/therapeutic use ; Endothelial Growth Factors/therapeutic use ; Fibroblast Growth Factor 2/therapeutic use ; Humans ; Lymphokines/therapeutic use ; Neoplasms/blood supply ; Neoplasms/drug therapy ; Neovascularization, Pathologic/drug therapy ; Neovascularization, Pathologic/metabolism ; Vascular Endothelial Growth Factor A ; Vascular Endothelial Growth Factors
Chemical Substances	Angiogenesis Inhibitors ; Endothelial Growth Factors ; Lymphokines ; Vascular Endothelial Growth Factor A ; Vascular Endothelial Growth Factors ; Fibroblast Growth Factor 2 (103107-01-3)
Language	English
Publishing date	2000-03
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, P.H.S. ; Review
ZDB-ID	603134-1
ISSN	1460-2180 ; 0143-3334
ISSN (online)	1460-2180
ISSN	0143-3334
DOI	10.1093/carcin/21.3.505
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Article ; Online: The Cost-Effectiveness of Preoperative Staphylococcus aureus Screening and Decolonization in Total Joint Arthroplasty.

Kerbel, Yehuda E / Sunkerneni, Anisha R / Kirchner, Gregory J / Prodromo, John P / Moretti, Vincent M

The Journal of arthroplasty

2018 Volume 33, Issue 7S, Page(s) S191–S195

Abstract: ... the absolute risk reduction (ARR) in infection rate required for cost-effectiveness.: Results: S aureus nasal screening ... effective with ARRs of 0.15% (TKA) and 0.12% (THA).: Conclusion: Preoperative S aureus decolonization ...

Abstract	Background: This article presents a break-even analysis for preoperative Staphylococcus aureus colonization screening and decolonization protocols in total hip arthroplasty (THA) and total knee arthroplasty (TKA). Methods: Protocol costs, baseline infection rates after arthroplasty, and average revision costs were obtained from institutional records and the literature. The break-even analysis determined the absolute risk reduction (ARR) in infection rate required for cost-effectiveness. Results: S aureus nasal screening ($144.07) was cost effective when initial infection rates of TKA (1.10%) and THA (1.63%) had an ARR of 0.56% and 0.45%, respectively. The most inexpensive decolonization treatment ($5.09) was cost effective with an ARR of 0.02% for both TKA and THA. The most expensive decolonization option ($37.67) was cost effective with ARRs of 0.15% (TKA) and 0.12% (THA). Conclusion: Preoperative S aureus decolonization can be highly cost effective, whereas colonization screening requires excessively high reductions in infection rate.
MeSH term(s)	Arthroplasty, Replacement, Hip/adverse effects ; Arthroplasty, Replacement, Hip/economics ; Arthroplasty, Replacement, Knee/adverse effects ; Arthroplasty, Replacement, Knee/economics ; Cost-Benefit Analysis ; Humans ; Mass Screening/economics ; Models, Economic ; Mupirocin/administration & dosage ; Mupirocin/economics ; Staphylococcal Infections/diagnostic imaging ; Staphylococcal Infections/economics ; Staphylococcal Infections/prevention & control ; Staphylococcus aureus ; Surgical Wound Infection/economics ; Surgical Wound Infection/prevention & control
Chemical Substances	Mupirocin (D0GX863OA5)
Language	English
Publishing date	2018-01-31
Publishing country	United States
Document type	Journal Article
ZDB-ID	632770-9
ISSN	1532-8406 ; 0883-5403
ISSN (online)	1532-8406
ISSN	0883-5403
DOI	10.1016/j.arth.2018.01.032
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Article ; Online: Suppressive impact of metronomic chemotherapy using UFT and/or cyclophosphamide on mediators of breast cancer dissemination and invasion.

Muñoz, Raquel / Hileeto, Denise / Cruz-Muñoz, William / Wood, Geoffrey A / Xu, Ping / Man, Shan / Viloria-Petit, Alicia / Kerbel, Robert S

PloS one

2019 Volume 14, Issue 9, Page(s) e0222580

Abstract: Metronomic chemotherapy using the 5-FU prodrug uracil-tegafur (UFT) and cyclophosphamide (CTX) was previously shown to only modestly delay primary tumor growth, but nevertheless markedly suppressed the development of micro-metastasis in an orthotopic ... ...

Abstract	Metronomic chemotherapy using the 5-FU prodrug uracil-tegafur (UFT) and cyclophosphamide (CTX) was previously shown to only modestly delay primary tumor growth, but nevertheless markedly suppressed the development of micro-metastasis in an orthotopic breast cancer xenograft model, using the metastatic variant of the MDA-MB-231 cell line, 231/LM2-4. Furthermore, a remarkable prolongation of survival, with no toxicity, was observed in a model of postsurgical advanced metastatic disease. A question that has remained unanswered is the seemingly selective anti-metastatic mechanisms of action responsible for this treatment. We assessed the in vivo effect of metronomic UFT, CTX or their combination, on vascular density, collagen deposition and c-Met (cell mediators or modulators of tumor cell invasion or dissemination) via histochemistry/immunohistochemistry of primary tumor sections. We also assessed the effect of continuous exposure to low and non-toxic doses of active drug metabolites 5-fluorouracil (5-FU), 4-hydroperoxycyclophosphamide (4-HC) or their combination, on 231/LM2-4 cell invasiveness in vitro. In the in vivo studies, a significant reduction in vascular density and p-Met[Y1003] levels was associated with UFT+CTX treatment. All treatments reduced intratumoral collagen deposition. In the in vitro studies, a significant reduction of collagen IV invasion by all treatments was observed. The 3D structures formed by 231/LM2-4 on Matrigel showed a predominantly Mass phenotype under treated conditions and Stellate phenotype in untreated cultures. Taken together, the results suggest the low-dose metronomic chemotherapy regimens tested can suppress several mediators of tumor invasiveness highlighting a new perspective for the anti-metastatic efficacy of metronomic chemotherapy.
MeSH term(s)	Animals ; Antineoplastic Combined Chemotherapy Protocols/pharmacology ; Breast Neoplasms/drug therapy ; Cell Line, Tumor ; Cyclophosphamide/pharmacology ; Female ; Fluorouracil/pharmacology ; Humans ; Mice ; Mice, SCID ; Neoplasm Invasiveness/pathology ; Neovascularization, Pathologic/drug therapy ; Tegafur/pharmacology ; Uracil/pharmacology ; Xenograft Model Antitumor Assays/methods
Chemical Substances	Tegafur (1548R74NSZ) ; Uracil (56HH86ZVCT) ; Cyclophosphamide (8N3DW7272P) ; Fluorouracil (U3P01618RT)
Language	English
Publishing date	2019-09-19
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2267670-3
ISSN	1932-6203 ; 1932-6203
ISSN (online)	1932-6203
ISSN	1932-6203
DOI	10.1371/journal.pone.0222580
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