raise awareness of unconscious bias at future ASTRO meetings.

Male introducers were significantly less likely to introduce any speaker, regardless of gender, by their professional title, and overall use of professional introductions decreased from 2017 to 2019. Furthermore, no difference in professional introduction use by speaker gender was identified at the recent ASTRO meetings. Implementing speaker guidelines could increase the use of professional introductions and raise awareness of unconscious bias at future ASTRO meetings.

Because of the COVID-19 pandemic, the Radiation Oncology Education Collaborative Study Group (ROECSG) hosted its annual international symposium using a virtual format in May 2020. This report details the experience of hosting a virtual meeting and presents attendee feedback on the platform.

The ROECSG symposium was hosted virtually on May 15, 2020. A postsymposium survey was distributed electronically to assess attendee demographics, participation, and experience. Attendee preference and experience were queried using 3-point and 5-point Likert-type scales, respectively. Symplur LLC was used to generate analytics for the conference hashtag (#ROECSG).

The survey was distributed to all 286 registrants, with a response rate of 67% (191 responses). Seventeen nonattendee responses were omitted from this analysis, for a total of 174 included respondents. Eighty-two attendees (47%) were present for the entire symposium. A preference for a virtual symposium was expressed by 78 respondents (45%), whereas 44 (25%)received and can serve as a framework for future virtual meetings. Although the virtual setting may facilitate sharing research, networking aspects are more limited. Effort is needed to develop hybrid virtual and in-person meetings that meet the needs of participants in both settings. Social media is a significant avenue for dissemination and discussion of information and may be valuable in the virtual setting.

Human papillomavirus (HPV)-related squamous cell carcinoma of the oropharynx (OPSCC) is extremely radiosensitive. Radiation therapy plus high-dose cisplatin remains the standard of care but causes long-term toxicity. Treatment deintensification approaches that reduce toxicity while maintaining survival are desirable for HPV-related OPSCC.

We conducted a single-arm, multicenter, phase 2 trial. Patients with newly diagnosed, biopsy-proven, American Joint Committee on Cancer (seventh edition) stage III or IV OPSCC positive for both p16 and HPV DNA were eligible. Patients with T4, N3, or T1N1 disease were excluded. DLin-KC2-DMA Smoking history was not included in eligibility criteria. Patients received intensity modulated radiation therapy (IMRT) of 70 Gy in 35 fractions or 70.4 Gy in 32 fractions without chemotherapy. The primary endpoint was complete response or complete metabolic response 10 weeks after IMRT completion.

Between September 13, 2013, and November 15, 2016, 39 patients were enrolled according to a 2-stagnted.

IMRT alone is associated with excellent response as well as reduced toxicity and could be a treatment option for carefully selected patients with locally advanced “true” HPV-related OPSCC. Further studies are warranted.

The oncogenic EWSFli1 fusion protein is a key transcriptional mediator of Ewing sarcoma initiation, progression, and therapeutic resistance. Mithramycin A (MithA) is a potent and specific inhibitor of transcription mediated by the EWSFli1. We tested the hypothesis that pretreatment with MithA could selectively radiosensitize EWSFli1

tumor cells by altering the transcriptional response to radiation injury.

A panel of 4 EWSFli1

and 3 EWSFli1

Ewing sarcoma cell lines and 1 nontumor cell line were subjected to MithA dose-response viability assays to determine the relative potency of MithA in cells possessing or lacking the EWSFli1 fusion. Radiosensitization by MithA was evaluated by clonogenic survival assays invitro and in a murine xenograft model. DNA damage was evaluated by comet assay and γ-H2Ax flow cytometry. Immunoblotting, flow cytometry, and reverse-transcription, polymerase chain reaction were used to evaluate DNA damage-induced signaling and repair processes and apoptosis.

We found that MithA alone could potently and selectively inhibit the growth of EWSFli1

tumor cells, but not cells lacking this fusion. Pretreatment with MithA for 24 hours before irradiation significantly reduced clonogenic survival invitro and delayed tumor regrowth invivo, prolonging survival of EWSFli1

tumor-bearing mice. Although MithA did not increase the level of DNA double-strand breaks, mechanistic studies revealed that MithA pretreatment selectively inhibited DNA double-strand break repair through downregulation of EWSFli1-mediated transcription, leading to tumor cell death by apoptosis.

Our data indicate that MithA is an effective radiosensitizer of EWSFli1

tumors and may achieve better local control at lower doses of radiation.

Our data indicate that MithA is an effective radiosensitizer of EWSFli1+ tumors and may achieve better local control at lower doses of radiation.

Transforming growth factor-β (TGF-β) mediated super-activation of urethra fibroblasts contributes to the progression of traumatic urethral stricture (TUS), and the Rho-associated kinase inhibitors, Fasudil, might be a novel therapeutic agent for TUS, but the underlying mechanisms had not been studied.

The primary urethral fibroblasts (PUFs) were isolated from rabbit urethral scar tissues and cultured in vitro, and the PUFs were subsequently treated with TGF-β (10μg/L) to simulate the realistic conditions of TUS pathogenesis. Next, the PUFs were exposed to Fasudil (50μM) and autophagy inhibitor 3-methyladenine (3-MA) treatment. Genes expression was examined by Western Blot and immunofluorescence staining, and cellular functions were determined by MTT assay and Transwell assay.

TGF-β promoted cell proliferation, migration, autophagy, and secretion of extracellular matrix (ECM), including collagen I and collagen III, which were reversed by co-treating cells with both Fasudil and 3-MA. In addition, TGF-β treatment decreased the expression levels of phosphorylated Akt (p-Akt) and mTOR (p-mTOR) to inactivate the Akt/mTOR pathway in the PUFs, which could be re-activated by Fasudil.