Browse Health


Education ?

Medical School Score Rankings
University of Miami (2001)
Top 50%

Awards & Distinctions ?

Castle Connolly's Top Doctors™ (2013)
Patients' Choice 5th Anniversary Award (2015)
Patients' Choice Award (2011 - 2015)
Compassionate Doctor Award - 5 Year Honoree (2015)
Compassionate Doctor Recognition (2011 - 2015)
Top 10 Doctor - Neighborhood (2014)
Hillcrest Forest
Obstetrician & Gynecologist
Society of Gynecologic Oncology
American Board of Obstetrics and Gynecology
American Society of Clinical Oncology

Affiliations ?

Dr. Heffernan is affiliated with 25 hospitals.

Hospital Affiliations



  • Medical City Dallas Hospital
    7777 Forest Ln, Dallas, TX 75230
    Top 25%
  • UT Southwestern University Hospital - St. Paul
    5909 Harry Hines Blvd, Dallas, TX 75235
    Top 25%
  • Texas Health Harris Methodist Hospital Southwest Fort Worth
    6100 Harris Pkwy, Fort Worth, TX 76132
    Top 25%
  • Texas Health Presbyterian Hospital Plano
    6200 W Parker Rd, Plano, TX 75093
    Top 25%
  • Harris Methodist H E B
    1600 Hospital Pkwy, Bedford, TX 76022
    Top 25%
  • Frisco Medical Center
    5601 Warren Pkwy, Frisco, TX 75034
    Top 25%
  • UT Southwestern University Hospital - Zale Lipshy
    5151 Harry Hines Blvd, Dallas, TX 75235
    Top 25%
  • Texas Health Harris Methodist Hospital Azle
    108 Denver Trl, Azle, TX 76020
    Top 50%
  • Medical Center Of Lewisville
    500 W Main St, Lewisville, TX 75057
    Top 50%
  • Texas Health Presbyterian Hospital Allen
    1105 Central Expy N, Allen, TX 75013
    Top 50%
  • Baylor Medical Center At Garland
    2300 Marie Curie Dr, Garland, TX 75042
    Top 50%
  • Medical Center Of Plano
    3901 W 15th St, Plano, TX 75075
  • Parkland Health & Hospital System
    5201 Harry Hines Blvd, Dallas, TX 75235
  • Texas Health Plano
  • Saint Paul
  • Texas Health Allen
  • Zale-Lipshy
  • Texas Health
  • Texas Health Flower Mound
  • Harris Methodist - Springwood
    1608 Hospital Pkwy, Bedford, TX 76022
  • Harris Continued Care Hospital
    1301 Pennsylvania Ave, Fort Worth, TX 76104
  • Presbyterian Plano Center For Diagnostics & Surger
    6020 W Parker Rd, Plano, TX 75093
  • Medical Center Of Mckinney
    4500 Medical Center Dr, McKinney, TX 75069
  • Forest Park Medical Center
    11990 N Central Expy, Dallas, TX 75243
  • North Central Medical Center - West Park Campus
    130 S Central Expy, McKinney, TX 75070
  • Publications & Research

    Dr. Heffernan has contributed to 11 publications.
    Title Proinvasion Metastasis Drivers in Early-stage Melanoma Are Oncogenes.
    Date September 2011
    Journal Cancer Cell

    Clinical and genomic evidence suggests that the metastatic potential of a primary tumor may be dictated by prometastatic events that have additional oncogenic capability. To test this "deterministic" hypothesis, we adopted a comparative oncogenomics-guided function-based strategy involving: (1) comparison of global transcriptomes of two genetically engineered mouse models with contrasting metastatic potential, (2) genomic and transcriptomic profiles of human melanoma, (3) functional genetic screen for enhancers of cell invasion, and (4) evidence of expression selection in human melanoma tissues. This integrated effort identified six genes that are potently proinvasive and oncogenic. Furthermore, we show that one such gene, ACP5, confers spontaneous metastasis in vivo, engages a key pathway governing metastasis, and is prognostic in human primary melanomas.

    Title Recurrent Phyllodes Tumor of the Vulva: a Case Report with Review of Diagnostic Criteria and Differential Diagnosis.
    Date July 2010
    Journal International Journal of Gynecological Pathology : Official Journal of the International Society of Gynecological Pathologists

    Phyllodes tumor of the vulva is extremely rare with only 6 cases reported in the literature. We report a case of recurrent phyllodes tumor of the vulva in a 39-year-old woman. The tumor showed biphasic morphology with a typical leaf-like pattern and a cellular stroma with rare mitosis. Expression of estrogen receptors, progesterone receptors mammoglobin, and BRST-2 was shown in the epithelial component. Review of literature with emphasis on diagnostic features and differential diagnosis are discussed.

    Title Secondary Cytoreductive Surgery for Recurrent Platinum-sensitive Ovarian Cancer.
    Date April 2010
    Journal International Journal of Gynaecology and Obstetrics: the Official Organ of the International Federation of Gynaecology and Obstetrics

    To determine the risks and benefits of secondary cytoreductive surgery for recurrent platinum-sensitive ovarian cancer.

    Title Atr-chk1 Pathway Inhibition Promotes Apoptosis After Uv Treatment in Primary Human Keratinocytes: Potential Basis for the Uv Protective Effects of Caffeine.
    Date July 2009
    Journal The Journal of Investigative Dermatology

    New approaches to prevent and reverse UV damage are needed to combat rising sunlight-induced skin cancer rates. Mouse studies have shown that oral or topical caffeine promotes elimination of UV-damaged keratinocytes through apoptosis and markedly inhibits subsequent skin cancer development. This potentially important therapeutic effect has not been studied in human skin cells. Here, we use primary human keratinocytes to examine which of several caffeine effects mediates this process. In these cells, caffeine more than doubled apoptosis after 75 mJ cm(-2) of ultraviolet light B (UVB). Selectively targeting two of caffeine's known effects did not alter UVB-induced apoptosis: inhibition of ataxia-telangiectasia mutated and augmentation of cyclic AMP levels. In contrast, siRNA against ataxia-telangiectasia and Rad3-related (ATR) doubled apoptosis after UV through a p53-independent mechanism. Caffeine did not further augment apoptosis after UVB in cells in which ATR had been specifically depleted, suggesting that a key target of caffeine in this effect is ATR. Inhibition of a central ATR target, checkpoint kinase 1 (Chk1), through siRNA or a new and highly specific inhibitor (PF610666) also augmented UVB-induced apoptosis. These data suggest that a relevant target of caffeine is the ATR-Chk1 pathway and that inhibiting ATR or Chk1 might have promise in preventing or reversing UV damage.

    Title Feedback Circuit Among Ink4 Tumor Suppressors Constrains Human Glioblastoma Development.
    Date April 2008
    Journal Cancer Cell

    We have developed a nonheuristic genome topography scan (GTS) algorithm to characterize the patterns of genomic alterations in human glioblastoma (GBM), identifying frequent p18(INK4C) and p16(INK4A) codeletion. Functional reconstitution of p18(INK4C) in GBM cells null for both p16(INK4A) and p18(INK4C) resulted in impaired cell-cycle progression and tumorigenic potential. Conversely, RNAi-mediated depletion of p18(INK4C) in p16(INK4A)-deficient primary astrocytes or established GBM cells enhanced tumorigenicity in vitro and in vivo. Furthermore, acute suppression of p16(INK4A) in primary astrocytes induced a concomitant increase in p18(INK4C). Together, these findings uncover a feedback regulatory circuit in the astrocytic lineage and demonstrate a bona fide tumor suppressor role for p18(INK4C) in human GBM wherein it functions cooperatively with other INK4 family members to constrain inappropriate proliferation.

    Title Cdc7-dbf4 and the Human S Checkpoint Response to Uvc.
    Date May 2007
    Journal The Journal of Biological Chemistry

    The S checkpoint response to ultraviolet radiation (UVC) that inhibits replicon initiation is dependent on the ATR and Chk1 kinases. Downstream effectors of this response, however, are not well characterized. Data reported here eliminated Cdc25A degradation and inhibition of Cdk2-cyclin E as intrinsic components of the UVC-induced pathway of inhibition of replicon initiation in human cells. A sublethal dose of UVC (1 J/m(2)), which selectively inhibits replicon initiation by 50%, failed to reduce the amount of Cdc25A protein or decrease Cdk2-cyclin E kinase activity. Cdc25A degradation was observed after irradiation with cytotoxic fluences of UVC, suggesting that severe inhibition of DNA chain elongation and activation of the replication checkpoint might be responsible for the UVC-induced degradation of Cdc25A. Another proposed effector of the S checkpoint is the Cdc7-Dbf4 complex. Dbf4 interacted weakly with Chk1 in vivo but was recognized as a substrate for Chk1-dependent phosphorylation in vitro. FLAG-Dbf4 formed complexes with endogenous Cdc7, and this interaction was stable in UVC-irradiated HeLa cells. Overexpression of FLAG- or Myc-tagged Dbf4 abrogated the S checkpoint response to UVC but not ionizing radiation. These findings implicate a Dbf4-dependent kinase as a possible target of the ATR- and Chk1-dependent S checkpoint response to UVC.

    Title Checkpoint Regulation of Replication Dynamics in Uv-irradiated Human Cells.
    Date November 2006
    Journal Cell Cycle (georgetown, Tex.)

    At any moment during S phase, regions of genomic DNA are in various stages of replication (i.e., initiation, chain elongation, and termination). These stages may be differentially inhibited after treatment with various carcinogens that damage DNA such as UV. We used visualization of active replication units in combed DNA fibers, in combination with quantitative analyses of the size distributions of nascent DNA, to evaluate the role of S-checkpoint proteins in UV-induced inhibition of DNA replication. When HeLa cells were exposed to a low fluence (1 J/m(2)) of 254 nm UV light (UVC), new initiation events were severely inhibited (5-6-fold reduction). A larger fluence of UVC (10 J/m(2)) resulted in stronger inhibition of the overall rate of DNA synthesis without decreasing further the frequency of replicon initiation events. Incubation of HeLa cells with caffeine and knockdown of ATR or Chk1 kinases reversed the UVC-induced inhibition of initiation of new replicons. These findings illustrate the concordance of data derived from different experimental approaches, thus strengthening the evidence that the activation of the intra-S checkpoint by UVC is dependent on the ATR and Chk1 kinases.

    Title Telomerase Expression is Sufficient for Chromosomal Integrity in Cells Lacking P53 Dependent G1 Checkpoint Function.
    Date October 2005
    Journal Journal of Carcinogenesis

    Secondary cultures of human fibroblasts display a finite lifespan ending at senescence. Loss of p53 function by mutation or viral oncogene expression bypasses senescence, allowing cell division to continue for an additional 10-20 doublings. During this time chromosomal aberrations seen in mitotic cells increase while DNA damage and decatenation checkpoint functions in G2 cells decrease.

    Title The Effectiveness of Extrication Collars Tested During the Execution of Spine-board Transfer Techniques.
    Date January 2005
    Journal The Spine Journal : Official Journal of the North American Spine Society

    In the prehospital stages of emergency care, cervical collars are (supposedly) used to aid rescuers in maintaining in-line stabilization of the spinal column as patients with potential or actual injuries are shifted onto a spine board to achieve full spinal immobilization. Unfortunately, not a single study has examined the effectiveness of cervical collars to control motion during the execution of spine-board transfer techniques.

    Title Caffeine and Human Dna Metabolism: the Magic and the Mystery.
    Date January 2004
    Journal Mutation Research

    The ability of caffeine to reverse cell cycle checkpoint function and enhance genotoxicity after DNA damage was examined in telomerase-expressing human fibroblasts. Caffeine reversed the ATM-dependent S and G2 checkpoint responses to DNA damage induced by ionizing radiation (IR), as well as the ATR- and Chk1-dependent S checkpoint response to ultraviolet radiation (UVC). Remarkably, under conditions in which IR-induced G2 delay was reversed by caffeine, IR-induced G1 arrest was not. Incubation in caffeine did not increase the percentage of cells entering the S phase 6-8h after irradiation; ATM-dependent phosphorylation of p53 and transactivation of p21(Cip1/Waf1) post-IR were resistant to caffeine. Caffeine alone induced a concentration- and time-dependent inhibition of DNA synthesis. It inhibited the entry of human fibroblasts into S phase by 70-80% regardless of the presence or absence of wildtype ATM or p53. Caffeine also enhanced the inhibition of cell proliferation induced by UVC in XP variant fibroblasts. This effect was reversed by expression of DNA polymerase eta, indicating that translesion synthesis of UVC-induced pyrimidine dimers by DNA pol eta protects human fibroblasts against UVC genotoxic effects even when other DNA repair functions are compromised by caffeine.

    Title An Atr- and Chk1-dependent S Checkpoint Inhibits Replicon Initiation Following Uvc-induced Dna Damage.
    Date January 2003
    Journal Molecular and Cellular Biology

    Inhibition of replicon initiation is a stereotypic DNA damage response mediated through S checkpoint mechanisms not yet fully understood. Studies were undertaken to elucidate the function of checkpoint proteins in the inhibition of replicon initiation following irradiation with 254 nm UV light (UVC) of diploid human fibroblasts immortalized by the ectopic expression of telomerase. Velocity sedimentation analysis of nascent DNA molecules revealed a 50% inhibition of replicon initiation when normal human fibroblasts were treated with a low dose of UVC (1 J/m(2)). Ataxia telangiectasia (AT), Nijmegen breakage syndrome (NBS), and AT-like disorder fibroblasts, which lack an S checkpoint response when exposed to ionizing radiation, responded normally when exposed to UVC and inhibited replicon initiation. Pretreatment of normal and AT fibroblasts with caffeine or UCN-01, inhibitors of ATR (AT mutated and Rad3 related) and Chk1, respectively, abolished the S checkpoint response to UVC. Moreover, overexpression of kinase-inactive ATR in U2OS cells severely attenuated UVC-induced Chk1 phosphorylation and reversed the UVC-induced inhibition of replicon initiation, as did overexpression of kinase-inactive Chk1. Taken together, these data suggest that the UVC-induced S checkpoint response of inhibition of replicon initiation is mediated by ATR signaling through Chk-1 and is independent of ATM, Nbs1, and Mre11.

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