Walker Wharton

New Mexico Cancer Center

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W. J. Pledger

Tampa General Hospital

Richard Selinfreund

Southern Illinois University School of Medicine

Cheryl L. Willman

University of New Mexico

C. Jeffrey Brinker

University of New Mexico

Carlee E. Ashley

Sandia National Laboratories California

Eric Wakshull

Bioanalytical Systems (United States)

Edward B. Leof

Mayo Clinic

Pope L. Moseley

Novo Nordisk Foundation

David S. Peabody

University of New Mexico

Barry Goz

University of North Carolina at Chapel Hill

Cooperative Institutions

University of New Mexico

Molecular Oncology (United States)

Moffitt Cancer Center

Los Alamos National Laboratory

St. Jude Children's Research Hospital

New Mexico Cancer Center

University of North Carolina at Chapel Hill

University of South Florida

Sandia National Laboratories

UNM Comprehensive Cancer Center

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Rearrangement of CRLF2 is associated with mutation of JAK kinases, alteration of IKZF1, Hispanic/Latino ethnicity, and a poor outcome in pediatric B-progenitor acute lymphoblastic leukemia

Blood (2010)

Richard C. Harvey Charles G. Mullighan I‐Ming Chen Walker Wharton Fady M. Mikhail

10.1182/blood-2009-09-245944

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Citations (566)

Inhibition of BALB/c‐3T3 cells in late G₁: Commitment to DNA synthesis controlled by somatomedin C

Journal of Cellular Physiology (1981)

Walker Wharton Judson J. Van Wyk W. J. Pledger

Methylglyoxal bis-(guanylhydrazone) (mGBG) blocked the stimulation of DNA synthesis in quiescent, density-inhibited BALB/c-3T3 cells treated with platelet-derived growth factor (PDGF) and platelet-poor plasma (PPP). Competence formation produced by a transient exposure to PDGF was not effected by mGBG. In contrast, mGBG effectively inhibited the PPP-stimulated progression of competent cells through the G1 phase of the cell cycle, although maximal inhibition was observed when mGBG was present during both the exposure to PDGF- and PPP-supplemented media. When quiescent cells were treated with PDGF and PPP-supplemented media in the presence of mGBG for 12--18 hours and the mGBG was then removed, cells entered the S phase after a 4 hour lag. The rate of entry into the S phase, but not the time necessary for the cells to progress from the mGBG block into the S phase, was dependent on the concentration of PPP present after removal of the mGBG. Either somatomedin C or insulin, but not epidermal growth factor, fibroblast growth factor, or PDGF were able to substitute for PPP in allowing cells to enter the S phase after the cells were released from the mGBG block. A marked inhibition of (3H)-leucine incorporation in serum-stimulated cultures was produced at mGBG concentrations which caused no decrease in the amount of (3H)-uridine incorporated during a short (15 minute) pulse. The ability of hormones to allow cells to progress to the late G1 phase and become committed to DNA synthesis after a mGBG inhibition was not related to their ability to restore the normal rate of protein synthesis as determined by (3H)-leucine incorporation.

Somatomedin

Platelet-derived growth factor

3T3 cells

10.1002/jcp.1041070105

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Citations (38)

Targeted Delivery of Protein Toxins: Delivery of Ricin Toxin A‐Chain by Peptide‐Targeted Mesoporous Silica Nanoparticle‐Supported Lipid Bilayers (Adv. Healthcare Mater. 3/2012)

Advanced Healthcare Materials (2012)

Katharine E. Epler David P. Padilla Genevieve K Phillips Peter Crowder Robert Castillo

Mesoporous silica nanoparticle-supported lipid bilayers, or “protocells”, are loaded with ricin toxin A-chain (RTA) and targeted to hepatocellular carcinoma (HCC) with a peptide (SP94) that binds to unknown HCC surface antigen(s). RTA-loaded, SP94-targeted protocells are selectively internalized by HCC and release encapsulated RTA upon endosome acid-ification. An endosomolytic peptide (H5WYG), present on the protocell's supported lipid bilayer, disrupts endosomal membranes, releasing RTA into the cytosol of HCC cells. As described by Eric Carnes, Carlee Ashley, and co-workers on page 348, RTA-loaded, SP94-targeted protocells kill HCC at a RTA concentration of 30 pM without affecting the viability of non-cancerous cells. In the cover image, protocells modified with SP94 (red), H5WYG (blue), and PEG (green) are shown interacting with an HCC cell.

Protocell

Ricin

Cell-penetrating peptide

10.1002/adhm.201290013

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Citations (2)

Multistep change in epidermal growth factor receptors during spontaneous neoplastic progression in Chinese hamster embryo fibroblasts.

PubMed (1985)

Eric Wakshull Paul M. Kraemer Walker Wharton

Whole Chinese hamster embryo lineages have been shown to undergo multistep spontaneous neoplastic progression during serial passage in culture. We have studied the binding, internalization, and degradation of 125I-labeled epidermal growth factor at four different stages of transformation. The whole Chinese hamster embryo cells lost cell surface epidermal growth factor receptors gradually during the course of neoplastic progression until only 10% of the receptor number present in the early-passage cells (precrisis) were retained in the late-passage cells (tumorigenic). No differences in internalization rates, chloroquine sensitivity, or ability to degrade hormone between the various passage levels were seen. No evidence for the presence in conditioned medium of transforming growth factors which might mask or down-regulate epidermal growth factor receptor was obtained. These results suggest that a reduction in cell surface epidermal growth factor receptor might be an early event during spontaneous transformation in whole Chinese hamster embryo cells.

Internalization

Neoplastic transformation

Chinese hamster

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Citations (23)

Epidermal growth factor (EGF) and somatomedin C regulate G1 progression in competent BALB/c-3T3 cells

Experimental Cell Research (1982)

Edward B. Leof Walker Wharton Judson J. Van Wyk W. J. Pledger

Somatomedin

Traverse

3T3 cells

10.1016/0014-4827(82)90073-8

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Citations (318)

Mitogenic activity elaborated by macrophage-like cell lines acts as competence factor(s) for BALB/c 3T3 cells

Journal of Cellular Physiology (1982)

Walker Wharton G. Yancey Gillespie Stephen W. Russell W. J. Pledger

Abstract The culture medium from several murine macrophage‐like cell lines contained a mitogenic activity that functioned synergistically with platelet‐poor plasma to induce DNA synthesis in quiescent density‐inhibited BALB/c 3T3 fibroblasts. This mitogenic activity was generated by P388D 1 (and other established lines of) macrophage‐like cells that were cultured either in medium alone or in medium supplemented with platelet‐poor plasma. The amount of mitogenic activity produced was directly related to the length of time the macrophage‐like cells were maintained in the medium. Serum‐free medium conditioned by macrophage‐cells did not stimulate DNA synthesis in density‐inhibited 3T3 cells in the absence of plasma; however, a transient (4‐hr) exposure to serum‐free macrophage‐conditioned medium allowed quiescent cells to respond to plasma‐derived progression factors. The addition of plasma to 3T3 cells that had been treated with the macrophage‐conditioned medium brought about DNA synthesis after a 12‐hr lag. The mitogenic activity that was in macrophage‐conditioned medium bound to DEAE‐Sephadex and eluted in a single peak using a linear NaCl gradient. This macrophage‐derived competence factor was not mitogenic for lymphocytes and was clearly separated by DEAE‐Sephadex chromatography from the major peak of the previously described mitogenic monokine, Interleukin‐I (lymphocyte activating factor).

Monokine

3T3 cells

Sephadex

10.1002/jcp.1041100115

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Citations (47)

LPS-induced cytokine levels are repressed by elevated expression of HSP70 in rats: possible role of NF-κB

Cell Stress and Chaperones (2010)

Karol Dokladny Rebecca Lobb Walker Wharton Y. Thomas Pope L. Moseley

Heat shock protein (HSP)70 provides a spectrum of protection against any of a variety of stresses, preventing damage measured at the level of molecules, cells, as well as whole organism. We have previously reported that lipopolysaccharide (LPS)-induced lethality in rats is prevented by a previous exposure to a mild thermal stress and that a thermal stress sufficient to induce HSP70 expression in the liver is accompanied by an inhibition of endotoxin-mediated cytokines and modulation of febrile response. However, the effect of HSP70 upregulation on cytokine expression in animals is unknown. The aim of the present study was to demonstrate the effect of HSP70 overexpression with adenovirus administration on LPS-induced increase in cytokines levels in animals. In the present study, Sprague-Dawley rats were infected with either the control AdTrack or Ad70 virus that directs the expression of human HSP70. After a 5-day incubation, animals were injected with either saline alone or LPS (50 microg/kg). Four hours later, blood samples were drawn and plasma levels of interleukin (IL)-6 or tumor necrosis factor (TNF)-alpha were measured by enzyme-linked immunosorbent assay. Our data demonstrate for the first time that HSP70 overexpression with adenovirus injection prevented the LPS-induced increase in TNF-alpha and IL-6 levels in rats. Repression of LPS-induced cytokines expressions by HSP70 upregulation was associated with inhibited IkappaBalpha degradation and nuclear factor kappa-B (NF-kappaB) p65 nuclear translocation in liver, suggesting that HSP70 overexpression may regulate LPS-induced cytokines expression through NF-kappaB pathway. We conclude that the effects of heat stress-induced increase in HSP70 protein expression on LPS-induced cytokine elaboration in whole animals can be reproduced by the actions of a single gene product.

Proinflammatory cytokine

10.1007/s12192-009-0129-6

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Citations (106)

A method for staining 3T3 cell nuclei with propidium iodide in hypotonic solution

Cytometry (1983)

Emily Tate Mark E. Wilder L. Scott Cram Walker Wharton

Abstract A modification of the propidium‐iodide hypotonic sodium citrate method has been developed specifically for high‐resolution staining of mouse 3T3 cell nuclei for analysis by flow cytometry. The method employs a brief treatment of cells at 37°C with Triton X‐100 and RNAse in the presence of propidium iodide in hypotonic sodium citrate, followed by restoration to isotonicity with NaCl. The average CV obtained for the G 1 peak was 3.5%, and the samples were stable for 1–2 weeks at 4°C. Compared to this technique, previously described propidium iodide‐staining methods gave poor resolution with 3T3 cells.

Propidium iodide

Sodium iodide

Sodium citrate

10.1002/cyto.990040304

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Citations (68)

Gene expression classifiers for relapse-free survival and minimal residual disease improve risk classification and outcome prediction in pediatric B-precursor acute lymphoblastic leukemia

Blood (2009)

Huining Kang I‐Ming Chen Carla S. Wilson Edward J. Bedrick Richard C. Harvey

Minimal Residual Disease

10.1182/blood-2009-05-218560

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Citations (192)

Induction of alkaline phosphatase activity in HeLa cells by choline chloride.

PubMed (1978)

Walker Wharton Barry Goz

Choline chloride produced a dose-dependent induction of alkaline phosphatase activity in HeLa cells. At the highest concentration tested, 40 mM, there was a 5- to 7-fold increase in alkaline phosphatase activity, a significantly greater induction than that produced by equiosmolar additions of either NaCl or sucrose. Enzyme activity was higher than control values by 24 hr after the addition of the salt, although the largest increases in activity occurred between 36 and 72 hr. The induction of alkaline phosphatase activity by choline chloride could be inhibited in a dose-dependent manner by the simultaneous addition of either caffeine or theophylline. At comparable concentrations of inhibitor, the magnitude of the inhibition of the induction produced by choline chloride was greater than that observed when the xanthines were used to inhibit the induction by either 5-iodo-2'-deoxyuridine or NaCl. Choline chloride, like NaCl, produced a proportionately greater increase in the heat-stable rather than the heat-labile form of alkaline phosphatase activity.

Choline chloride

Choline

HeLa

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Citations (11)