Faculty Bibliography

Objective: The efficacy and safety of use of the transvaginal ultrasound probe for percutaneous abdominal oocyte retrieval in patients with limited vaginal access has been established in prior studies,^1-2 but the technique has not been demonstrated widely. Methodology: This video uses a patient case to explain and demonstrate the technique of percutaneous transabdominal oocyte retrieval with the transvaginal ultrasound probe in a patient without vaginal access to her ovaries. Patient consent was obtained prior to creation of the video.
Conclusion(s): Abdominal oocyte aspiration using a high frequency transvaginal ultrasound probe should be considered in patients with ovaries inaccessible vaginally. It is safe, effective and an easily skill to acquire. References: 1. Baldini D, Lavopa C, Vizziello G, Sciancalepore AG, Malvasi A. The safe use of transvaginal ultrasound probe for transabdominal oocyte retrieval in patients with vaginally inaccessible ovaries. Front Womens Healt. 2018; 3(2):1-3. 2. Sekhon L, Said T, Del Valle A. Percutaneous transabdominal oocyte retrieval using vaginal ultrasound probe: A novel, effective and safe method for oocyte retrieval in patients with vaginally inaccessible ovaries. Fertil Steril. 2014; 101(2) Supplement.
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Basal-like breast cancers (BBCs) are enriched for increased EGFR expression and decreased expression of PTEN. We found that treatment with metformin and erlotinib synergistically induced apoptosis in a subset of BBC cell lines. The drug combination led to enhanced reduction of EGFR, AKT, S6 and 4EBP1 phosphorylation, as well as prevented colony formation and inhibited mammosphere outgrowth. Our data with other compounds suggested that biguanides combined with EGFR inhibitors have the potential to outperform other targeted drug combinations and could be employed in other breast cancer subtypes, as well as other tumor types, with activated EGFR and PI3K signaling. Analysis of BBC cell line alterations led to the hypothesis that loss of PTEN sensitized cells to the drug combination which was confirmed using isogenic cell line models with and without PTEN expression. Combined metformin and erlotinib led to partial regression of PTEN-null and EGFR-amplified xenografted MDA-MB-468 BBC tumors with evidence of significant apoptosis, reduction of EGFR and AKT signaling, and lack of altered plasma insulin levels. Combined treatment also inhibited xenografted PTEN null HCC-70 BBC cells. Measurement of trough plasma drug levels in xenografted mice and a separately performed pharmacokinetics modeling study support possible clinical translation.

Phosphatase and tensin homolog on chromosome ten (PTEN) is a tumor suppressor and an antagonist of the phosphoinositide-3 kinase (PI3K) pathway. We identified a 576-amino acid translational variant of PTEN, termed PTEN-Long, that arises from an alternative translation start site 519 base pairs upstream of the ATG initiation sequence, adding 173 N-terminal amino acids to the normal PTEN open reading frame. PTEN-Long is a membrane-permeable lipid phosphatase that is secreted from cells and can enter other cells. As an exogenous agent, PTEN-Long antagonized PI3K signaling and induced tumor cell death in vitro and in vivo. By providing a means to restore a functional tumor-suppressor protein to tumor cells, PTEN-Long may have therapeutic uses.