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Lisa M DiFrancesco

Publications and source records attributed to Lisa M DiFrancesco.

7 recordsLinked to original sources
PubMed2006

Extra-axial chordoma.

Chordomas are low-grade malignant tumors of bone that occur almost exclusively in the axial skeleton. Other neoplasms with a similar histologic picture but an extra-axial location have been described, including parachordoma, myxoid chondrosarcoma, and extra-axial chordoma. We herein present another case of the rare extra-axial chordoma. A 41-year-old woman developed an 8.3 cm mass in the pubic bone. The gross, microscopic, and immunohistochemical findings were identical to those of a classic chordoma. Parachordoma and myxoid chondrosarcoma were excluded from the differential diagnosis. Five previously reported cases of extra-axial chordoma were reviewed and found also to demonstrate clinical and pathologic features specific to chordoma, despite arising in an extra-axial location. Although rare, extra-axial chordoma does exist and should be recognized and managed in a similar fashion to its well-described counterpart. It must be differentiated from other histologic mimics, because the treatment and prognosis can differ significantly.

Adult↗
PubMed2005

Evaluation of conventional subciliary incision used in blepharoplasty: preoperative and postoperative videography and electromyography findings.

BACKGROUND: The purpose of this study was to evaluate the innervation and function of the orbicularis oculi area clinically, with video imaging, and electrically, with electromyography, before and after lower-eyelid blepharoplasty using a conventional subciliary incision. METHODS: Nine patients (18 eyes) were studied before and 4 to 12 weeks after lower-eyelid blepharoplasty. Video imaging documented clinical changes in involuntary (blink) and voluntary (squeeze and squint) eyelid function as well as resting lid position and tone. Electromyography was performed using concentric needle electrodes (25 mm in length, 0.03 mm in diameter) placed in the lateral and medial subciliary orbicularis oculi. A total of 36 sites in nine patients (four sites per patient) were studied. Acute denervation was identified by the presence of fasciculation; fibrillation potentials; insertional activity; sharp waves; and grade based on standard electromyography techniques. All patients underwent lower-eyelid blepharoplasty with a subciliary incision, skin-muscle flap and canthal anchoring with canthopexy or cantholysis, and canthoplasty. RESULTS: Video imaging of the lower eyelid before and after blepharoplasty showed evidence of eyelid malposition or abnormal voluntary or involuntary orbicularis oculi muscle function. There was no evidence of acute denervation in 34 of 36 sites (94 percent). Two patients had abnormal fasciculation in the left lateral position on two of 36 sites (6 percent). Thirty-three weeks postoperatively, one patient was retested and a normal electromyography result was obtained. CONCLUSIONS: This study demonstrated that lower-lid malposition or abnormal function after lower-lid blepharoplasty cannot be explained by denervation of the zygomatic branch of the facial nerve. Any acute or residual denervation seen in the subciliary orbicularis is not clinically significant. The importance of lower-lid support and canthal anchoring cannot be emphasized enough in preventing lower-lid malposition. Blepharoplasty is a challenging procedure that requires careful preoperative planning, intraoperative reassessment, and meticulous surgical technique to optimize facial rejuvenation and patient safety.

Adult↗
PubMed2004

Upper eyelid reconstruction.

There are several options available for upper eyelid reconstruction that depend on the extent of involvement of the anterior and posterior lamella. Knowledge of the anatomy will ensure that in addition to the creation of an aesthetically acceptable eyelid reconstruction, a functional upper lid will be restored. The purpose of this article is to outline the anatomy of the eyelid, to analyze the components of eyelid defects, and to provide options for lid reconstruction.

Algorithms↗
PubMed2003

A cutaneous manifestation of antiphospholipid antibody syndrome.

Antiphospholipid antibody syndrome is a disease defined by the presence of a hypercoagulable clinical state in association with antiphospholipid antibodies. This syndrome can involve large-vessel thrombosis or thrombotic microangiopathy. Approximately 40% of patients will present with a cutaneous manifestation as the first indication of this disease, with a marked number of patients concurrently developing multiorgan involvement. The authors present a patient with extensive cutaneous necrosis-a devastating sequela of antiphospholipid antibody syndrome. Additionally, multiorgan involvement developed, requiring systemic anticoagulation and supportive care. When medically stable, plastic surgical intervention was necessary to treat extensive areas of cutaneous necrosis. Widespread cutaneous necrosis is a rare but known sequela of this syndrome. Studies have demonstrated that prophylaxis for thrombosis is not effective. However, long-term medical management with oral anticoagulants has been shown to reduce the risk of recurrent thrombosis. Occasionally, plastic surgical intervention is needed to treat the sequelae of this disease. Therefore, knowledge of the presentation and manifestations of this disease is critical in the early detection and prompt treatment of patients to prevent life-threatening consequences of this catastrophic disease process.

Adult↗
PubMed2002

Reovirus oncolysis of human breast cancer.

We have previously shown that human reovirus replication is restricted to cells with an activated Ras pathway, and that reovirus could be used as an effective oncolytic agent against human glioblastoma xenografts. This study examines in more detail the feasibility of reovirus as a therapeutic for breast cancer, a subset of cancer in which direct activating mutations in the ras proto-oncogene are rare, and yet where unregulated stimulation of Ras signaling pathways is important in the pathogenesis of the disease. We demonstrate herein the efficient lysis of breast tumor-derived cell lines by the virus, whereas normal breast cells resist infection in vitro. In vivo studies of reovirus breast cancer therapy reveal that viral administration could cause tumor regression in an MDA-MB-435S mammary fat pad model in severe combined immunodeficient mice. Reovirus could also effect regression of tumors remote from the injection site in an MDA-MB-468 bilateral tumor model, raising the possibility of systemic therapy of breast cancer by the oncolytic agent. Finally, the ability of reovirus to act against primary breast tumor samples not propagated as cell lines was evaluated; we found that reovirus could indeed replicate in ex vivo surgical specimens. Overall, reovirus shows promise as a potential breast cancer therapeutic.

Animals↗
PubMed2002

Loss of heterozygosity associated with uniparental disomy in breast carcinoma.

Loss of heterozygosity is commonly assumed to be due to deletion of the appropriate genomic region in one chromosome within a neoplastic cell but may be due to other mechanisms such as mitotic non-disjunction or somatic recombination leading to uniparental heterodisomy. We chose to study the genomic regions surrounding the p53 and RB1 tumor suppressor genes in breast carcinoma to evaluate the different mechanisms that could mediate loss of heterozygosity. A microsatellite analysis of polymorphic markers in 50 breast cancer samples showed loss of heterozygosity for at least 1 of the 10 markers analyzed in 50% of the tumors studied, and an overall 8.47% of the informative loci showed loss of heterozygosity. All of the cases with loss of heterozygosity were further analyzed for gene copy number of the tumor suppressor genes RB1 and p53 by fluorescence in situ hybridization of either tumor touch preparations or microdissected tumor nuclei with specific genomic probes. Surprisingly, all samples showed the presence of both copies of tumor suppressor genes, including 4/50 cases showing loss of heterozygosity of tumor suppressor gene-spanning markers. One of the 4 cases showed loss of heterozygosity of markers spanning a distance of 6 cM over the RB1 gene, with normal copy numbers of the gene. Three other cases showed loss of heterozygosity of markers within the tumor suppressor gene (RBI or p53) and at least one other spanning marker. No cases showed a simultaneous reduction to homozygosity of markers both near the tumor suppressor gene and distal loci. We suggest that the presence of both copies of the tumor suppressor gene in the cases with loss of heterozygosity of spanning markers and internal markers for that tumor suppressor gene could be explained by somatic recombination resulting in uniparental disomy, but not mitotic nondisjunction or deletion. As the mechanism for physical deletion of a chromosome may be different from those mediating somatic recombination, study of this phenomenon may identify different pathways of genomic instability that may be of diagnostic or treatment significance in breast or other cancers, particularly in those treatments based upon DNA-altering agents.

Breast Neoplasms↗