Oncologists
7 years of experience

Accepting new patients
Virginia Urology Center
9105 Stony Point Dr
Richmond, VA 23235
804-287-6101
Locations and availability (6)

Education ?

Medical School Score Rankings
Virginia Commonwealth University (2003)
  • Currently 3 of 4 apples
Top 50%

Awards & Distinctions ?

Associations
American Society for Therapeutic Radiology and Oncology
American Board of Radiology

Affiliations ?

Dr. Wallace is affiliated with 10 hospitals.

Hospital Affilations

Score

Rankings

  • Bon Secours-Memorial Regional Medical
    Medical Oncology
    8260 Atlee Rd, Mechanicsville, VA 23116
    • Currently 4 of 4 crosses
    Top 25%
  • St. Mary's Hospital of Richmond
    Medical Oncology
    5801 Bremo Rd, Richmond, VA 23226
    • Currently 4 of 4 crosses
    Top 25%
  • Bon Secours Maryview Medical Center
    Medical Oncology
    3636 High St, Portsmouth, VA 23707
    • Currently 4 of 4 crosses
    Top 25%
  • Bon Secours Depaul Medical Center
    Medical Oncology
    150 Kingsley Ln, Norfolk, VA 23505
    • Currently 1 of 4 crosses
  • BON SECOURS St. Francis Medical Center
    13700 St Francis Blvd, Midlothian, VA 23114
    • Currently 1 of 4 crosses
  • Retreat Hospital
    2621 Grove Ave, Richmond, VA 23220
    • Currently 1 of 4 crosses
  • Bon Secours St. Mary`s Hospital
  • St Francis Medical Center
  • St. Francis
  • St. Mary's
  • Publications & Research

    Dr. Wallace has contributed to 10 publications.
    Title Grouped Comparisons of Sleep Quality for New and Personal Bedding Systems.
    Date April 2008
    Journal Applied Ergonomics
    Excerpt

    The purpose of this study was to compare sleep comfort and quality between personal and new bedding systems. A convenience sample (women, n=33; men, n=29) with no clinical history of disturbed sleep participated in the study. Subjects recorded back and shoulder pain, sleep quality, comfort, and efficiency for 28 days each in their personal beds (pre) and in new medium-firm bedding systems (post). Repeated measures ANOVAs revealed significant improvement between pre- and post-test means for all dependent variables. Furthermore, reduction of pain and stiffness and improvement of sleep comfort and quality became more prominent over time. No significant differences were found for the groupings of age, weight, height, or body mass index. It was found that for the cheapest category of beds, lower back pain was significantly (p<0.01) more prominent than for the medium and higher priced beds. Average bed age was 9.5yrs. It was concluded that new bedding systems can significantly improve selected sleep variables and that continuous sleep quality may be dependent on timely replacement of bedding systems.

    Title Hypoxia Inducible Factor-1: Regulation by Nitric Oxide in Posthypoxic Microvascular Endothelium.
    Date May 2006
    Journal Biochemistry and Cell Biology = Biochimie Et Biologie Cellulaire
    Excerpt

    Microvascular endothelial cells provide a critical regulatory interface between blood constituents and tissue. Hypoxia inducible factor-1 (HIF-1) is a key transcription factor required for expression of hypoxia-dependent genes. We employed a model of hypoxia and reoxygenation (H/R) using the dermal microvascular endothelial cell line HMEC-1 to examine the effects of altered oxygen concentrations on microvascular HIF-1 expression and nitric oxide (NO) formation. Hypoxia increased inducible NO synthase (iNOS) mRNA in a time-dependent manner in HMEC-1. However, endothelial NO synthase mRNA progressively declined during hypoxia. H/R promoted significant increases in cellular nitrite levels that were significantly abrogated by the specific iNOS inhibitor N6-(1-iminoethyl)-L-lysine, di hy drochloride. Exogenous NO promoted stabilization of the alpha subunit of HIF-1 and produced functional DNA binding. Exposure of HMEC-1 to H/R resulted in previously unrecognized biphasic HIF-1alpha stabilization during reoxygenation. When the iNOS gene was silenced through the use of iNOS-specific small interfering RNA, HIF-1alpha stabilization and HIF-1 activation were dramatically diminished, suggesting that inducible NOS-derived NO is a key factor sustaining HIF-1 activation during both hypoxia and reoxygenation.

    Title Hypoxia-inducible Factor-1-dependent Regulation of the Multidrug Resistance (mdr1) Gene.
    Date July 2002
    Journal Cancer Research
    Excerpt

    The microenvironment of rapidly growing tumors is associated with increased energy demand and diminished vascular supply, resulting in focal areas of prominent hypoxia. A number of hypoxia-responsive genes have been associated with growing tumors, and here we demonstrate that the multidrug resistance (MDR1) gene product P-glycoprotein, a Mr approximately 170,000 transmembrane protein associated with tumor resistance to chemotherapeutics, is induced by ambient hypoxia. Initial studies using quantitative microarray analysis of RNA revealed an approximately 7-fold increase in MDR in epithelial cells exposed to hypoxia (pO(2) 20 torr, 18 h). These findings were further confirmed at the mRNA and protein level. P-Glycoprotein function was studied by analysis of verapamil-inhibitable efflux of digoxin and rhodamine 123 in intact T84 cells and revealed that hypoxia enhances P-glycoprotein function by as much as 7 +/- 0.4-fold over normoxia. Subsequent studies confirmed hypoxia-elicited MDR1 gene induction and increased P-glycoprotein expression in nontransformed, primary cultures of human microvascular endothelial cells, and analysis of multicellular spheroids subjected to hypoxia revealed increased resistance to doxorubicin. Examination of the MDR1 gene identified a binding site for hypoxia inducible factor-1 (HIF-1), and inhibition of HIF-1 expression by antisense oligonucleotides resulted in significant inhibition of hypoxia-inducible MDR1 expression and a nearly complete loss of basal MDR1 expression. Studies using luciferase promoter constructs revealed a significant increase in activity in cells subjected to hypoxia, and such hypoxia inducibility was lost in truncated constructs lacking the HIF-1 site and in HIF-1 binding site mutants. Extensions of these studies also identified a role for Sp1 in this hypoxia response. Taken together, these data indicate that the MDR1 gene is hypoxia responsive, and such results may identify hypoxia-elicited P-glycoprotein expression as a pathway for resistance of some tumors to chemotherapeutics.

    Title Mutation of Residues 423 (met/ile), 444 (thr/met), and 506 (asn/ser) Confer Cholesteryl Esterase Activity on Rat Lung Carboxylesterase. Ser-506 is Required for Activation by Camp-dependent Protein Kinase.
    Date October 2001
    Journal The Journal of Biological Chemistry
    Excerpt

    Site-directed mutagenesis is used to identify amino acid residues that dictate reported differences in substrate specificity between rat hepatic neutral cytosolic cholesteryl ester hydrolase (hncCEH) and rat lung carboxylesterase (LCE), proteins differing by only 4 residues in their primary sequences. Beginning with LCE, the substitution Met(423) --> Ile(423) alone or in combination with other mutations increased activity with p-nitrophenylcaprylate (PNPC) relative to more hydrophilic p-nitrophenylacetate (PNPA), typical of hncCEH. The substitution Thr(444) --> Met(444) was necessary but not sufficient for expression of cholesteryl esterase activity in COS-7 cells. The substitution Asn(506) --> Ser(506), creating a potential phosphorylation site, uniformly increased activity with both PNPA and PNPC, was necessary but not sufficient for expression of cholesteryl esterase activity and conferred susceptibility to activation by cAMP-dependent protein kinase, a property of hncCEH. The 3 mutations in combination were necessary and sufficient for expression of cholesteryl esterase activity by the mutated LCE. The substitution Gln(186) --> Arg(186) selectively reduced esterase activity with PNPA and PNPC but was not required for cholesteryl esterase activity. Homology modeling from x-ray structures of acetylcholinesterases is used to propose three-dimensional models for hncCEH and LCE that provide insight into the effects of these mutations on substrate specificity.

    Title Nitric Oxide Regulates Interleukin-8 Gene Expression in Activated Endothelium by Inhibiting Nf-kappab Binding to Dna: Effects on Endothelial Function.
    Date October 1999
    Journal Biochemistry and Cell Biology = Biochimie Et Biologie Cellulaire
    Excerpt

    Nuclear factor-kappaB (NF-kappaB) binds to nucleotide sequences between -80 and -70 bp upstream of the transcriptional start site in the interleukin-8 (IL-8) promoter and is crucial for transcription of the IL-8 gene. We showed that exogenous nitric oxide in the form of a nitric oxide donor significantly reduced IL-8 mRNA in cytokine-activated ECV304. Similarly, nitric oxide significantly reduced migration of polymorphonuclear neutrophils through cytokine-activated ECV304 monolayers, an IL-8-dependent process. Using a luciferase reporter construct containing the NF-kappaB site of the IL-8 gene, we showed that exposing cytokine-activated ECV304 to exogenous nitric oxide resulted in significant reduction of NF-kappaB binding. Follow-up studies using a luciferase reporter construct possessing a mutated NF-kappaB site confirmed that the luciferase activity observed in the NF-kappaB reporter resulted from NF-kappaB binding. These studies demonstrate that nitric oxide, supplied exogenously into reactions containing activated endothelium, down-regulates pro-inflammatory activity, such as the secretion of chemokines, and functional activity, such as transendothelial migration of neutrophils.

    Title Molecular Cloning and Expression of Rat Lung Carboxylesterase and Its Potential Role in the Detoxification of Organophosphorus Compounds.
    Date July 1999
    Journal American Journal of Respiratory Cell and Molecular Biology
    Excerpt

    The 1,839-base pair complementary DNA (cDNA) for rat lung carboxylesterase was cloned by reverse transcriptase polymerase chain reaction from total rat lung RNA using specific primers derived from the 5' and 3' untranslated regions of rat hepatic cholesteryl ester hydrolase (CEH). The unique cDNA was sequenced and found to be similar to hepatic CEH, pI 6.1 esterase, and hydrolase A. In Northern blot analysis, the cDNA hybridized with a single band from lung messenger RNA (mRNA). The 1.7-kb coding sequence, predicting a 62-kD protein, was transfected into COS-7 cells and Chinese hamster ovary (CHO) cells. Expression in COS-7 and CHO cells was accompanied by 4- and 3.2-fold increases in carboxylesterase activity (hydrolysis of p-nitrophenyl acetate), respectively. Unlike the hepatic CEH, the expressed lung carboxylesterase described here did not hydrolyze cholesterol esters. In situ hybridization experiments localized the lung carboxylesterase mRNA to the airway epithelium. The organophosphorus compound phosphoric acid diethyl 4-nitrophenyl ester, paraoxon, completely inhibited this lung carboxylesterase, placing it in the family of B esterases by this criterion.

    Title Acute Myocardial Infarction: Home and Hospital Treatment.
    Date September 1971
    Journal British Medical Journal
    Excerpt

    This is a preliminary report of a co-operative study of 1,203 episodes of acute myocardial infarction in men under 70 years in four centres in the south west of England. The mortality at 28 days was 15%. A comparison is made between home care by the family doctor and hospital treatment initially in an intensive care unit: 343 cases were allocated at random. The randomized groups do not differ significantly in composition with respect to age; past history of angina, infarction, or hypertension; or hypotension when first examined. The mortality rates of the random groups are similar for home and hospital treatment. The group sent electively to hospital contained a higher proportion of initially hypotensive patients whose prognosis was bad wherever treated; those who were not hypotensive fared rather worse in hospital.For some patients with acute myocardial infarction seen by their general practitioner home care is ethically justified, and the need for general admission to hospital should be reconsidered.

    Title Anomalous Values for the Half-life of Radiothyroxine in Dyshormonogenetic Goiter.
    Date January 1967
    Journal The Journal of Clinical Endocrinology and Metabolism
    Title Oxidation of Functional Thiols by Sulphoxides.
    Date December 1966
    Journal Chemistry & Industry
    Title Toxic Diffuse Goitre in Monozygotic Twins.
    Date October 1966
    Journal Lancet

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