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OBJECTIVE Internal carotid artery (ICA) injury is a rare but severe complication of endonasal surgery. The authors describe their endovascular experience managing ICA injuries after transsphenoidal surgery; they review and summarize the current literature regarding endovascular techniques; and they propose a treatment algorithm based on the available evidence. METHODS A retrospective review of 576 transsphenoidal pituitary adenoma resections was performed. Cases of ICA injury occurring at our institution and transfers from other hospitals were evaluated. Endovascular treatments for ICA injury reported in the literature were also reviewed and summarized. RESULTS Seven cases were identified from the institutional cohort (mean age 46.3 years, mean follow-up 43.4 months [1–107 months]) that received endovascular treatment for ICA injury. Five injuries occurred at our institution (5 [0.9%] of 576), and 2 injuries occurred at outside hospitals. Three patients underwent ICA sacrifice by coil placement, 2 underwent lesion embolization (coil or stent-assisted coil placement), and 2 underwent endoluminal reconstruction (both with flow diversion devices). Review of the literature identified 98 cases of ICA injury treated with endovascular methods. Of the 105 total cases, 46 patients underwent ICA sacrifice, 28 underwent lesion embolization, and 31 underwent endoluminal reconstruction. Sacrifice of the ICA proved a durable solution in all cases; however, the rate of persistent neurological complications was relatively high (10 [21.7%] of 46). Lesion embolization was primarily performed by coil embolization without stenting (16 cases) and stent-assisted coiling (9 cases). Both techniques had a relatively high rate of at least some technical complication (6 [37.5%] of 16 and 5 [55.6%] of 9, respectively) and major technical complications (i.e., injury, new neurological deficit, or ICA sacrifice) (5 [31.3%] of 16 and 2 [22.2%] of 9, respectively). Endoluminal reconstruction was performed by covered stent (24 cases) and flow diverter (5 cases) placement. Covered stents showed a reasonably high rate of technical complications (10 [41.7%] of 24); however, 8 of these problems were resolved, leaving a small percentage with major technical complications (2 [8.3%] of 24). Flow diverter placement was also well tolerated, with only 1 minor technical complication. CONCLUSIONS Endovascular treatments including vessel sacrifice, coil embolization (with or without stent assistance), and endoluminal reconstruction offer a tailored approach to ICA injury management after endonasal surgery. Vessel sacrifice remains the definitive treatment for acute, uncontrolled bleeding; however, vessel preservation techniques should be considered carefully in select patients. Multiple factors including vascular anatomy, injury characteristics, and risk of dual antiplatelet therapy should guide best treatment, but more study is needed (particularly with flow diverters) to refine this decision-making process. Ideally, all endovascular treatment options should be available at institutions performing endonasal surgery.

6071Background: Prognosis in smokers with LASCCHN remains poor. Activating mutations of PI3K are linked to poor outcome and PI3K activation in response to RT is implicated in resistance to CRT. Met...

Introduction: Internal carotid artery (ICA) injury is a rare, but severe complication of transsphenoidal pituitary surgery. Several endovascular techniques are available for the treatment of these injuries, including many that spare the injured vessel. The aim of this study was to review a single institutions experience with endovascular treatment of ICA injuries, highlighting cases that illustrate the advantages and constraints of the different techniques. Methods: A retrospective review was performed of 576 transsphenoidal pituitary adenoma resection to identify baseline demographic, operative, and endovascular treatment characteristics of cases in which there was intraoperative ICA injury, and evaluate postendovascular treatment outcomes. Patients transferred to our institution for management of ICA injury were also evaluated for postendovascular treatment outcomes. Results: A total of 20 cases were identified (mean age, 46.3 years; mean follow-up, 43.4 months [range, 1–107 months]) who received endovascular treatment for ICA injury. Five ICA injuries occurred at our institution (5/576; 0.9%), while two had surgery at other institutions. Four cases had ICA injury noted at the time of surgery, while three were diagnosed in a delayed fashion. Emergent ICA sacrifice was performed in three patients who suffered acute ICA injury during surgery and demonstrated good collateral circulation on balloon test occlusion. Two of these patients suffered no permanent neurological sequela from the ICA occlusion, while one patient experienced a small permanent visual field defect. Vessel sparing endovascular repair was performed in four patients. One patient received coiling without stent-assistance for an 18 mm, narrow necked pseudoaneurysms discovered 2 months after surgery, which later required stent-assisted coiling and Onyx embolization for recurrence before ultimately having complete ipsilateral ICA occlusion without neurological deficit at 36 months after initial endovascular treatment. One patient with significant intracranial atherosclerosis and compromised collateral circulation received stent-assisted coiling for a 5 mm pseudoaneurysm discovered intraoperatively. In this case, endovascular treatment was deferred for 3 days because of the risk of antiplatelet/anticoagulation therapy in the postoperative period; however, the patient had significant baseline comorbidities which contributed to expiration from cerebral infarction 22 days after stenting. The Pipelinetm Embolization Device was for two patients, one who received delayed treatment 15 days after ICA injury and a second patient 20 years after ICA injury and pseudoaneurysm coiling. Neither patient developed neurovascular complications associated with the ICA injury or endovascular treatment within the available follow-up (16 and 9 months, respectively). Conclusion: Endovascular treatments including vessel sacrifice, coiling (with or without stent assistance), and flow diversion allow for a tailored approach to ICA injury management after transsphenoidal surgery. If the injury is acute and collateral flow is good, vessel sacrifice is well-tolerated and effective. Decision making for patients with acute bleeding and poor collateral flow is more challenging, and may require delayed vessel preservation and/or covered stenting when the anatomy allows. Flow diversion may be the procedure of choice for patients with pseudoaneurysms that present in a delayed fashion. Multiple factors such as vascular anatomical features, injury characteristics, baseline comorbidity, and risk of antiplatelet/anticoagulation therapy should also be used to guide selection of the most appropriate treatment.

In the absence of adaptive immunity, NK cells polarize M1 macrophages to facilitate cancer immunoediting., Cancer immunoediting is the process whereby immune cells protect against cancer formation by sculpting the immunogenicity of developing tumors. Although the full process depends on innate and adaptive immunity, it remains unclear whether innate immunity alone is capable of immunoediting. To determine whether the innate immune system can edit tumor cells in the absence of adaptive immunity, we compared the incidence and immunogenicity of 3′methylcholanthrene-induced sarcomas in syngeneic wild-type, RAG2−/−, and RAG2−/−x γc−/− mice. We found that innate immune cells could manifest cancer immunoediting activity in the absence of adaptive immunity. This activity required natural killer (NK) cells and interferon γ (IFN-γ), which mediated the induction of M1 macrophages. M1 macrophages could be elicited by administration of CD40 agonists, thereby restoring editing activity in RAG2−/−x γc−/− mice. Our results suggest that in the absence of adaptive immunity, NK cell production of IFN-γ induces M1 macrophages, which act as important effectors during cancer immunoediting.

6042 Background: Cetuximab (C) improved overall survival (OS) in patients (pts) with HNSCC when added to definitive RT or to palliative chemotherapy; however, the role of cetuximab in induction che...

e17076 Background: The genetic landscape of HNSCC is heterogeneous. However, only one targeted therapy (an EGFR inhibitor) has shown efficacy, albeit modest. We hypothesized that a TCCG set of 40 c...

Over the last 12 yr, we have shown that interferon-gamma and lymphocytes collaborate to regulate tumor development in mice. Specifically, we found that the immune system not only prevents the growth of primary (carcinogen-induced and spontaneous) and transplanted tumors but also sculpts the immunogenicity of tumors that form. These observations led us to refine the old and controversial "cancer immunosurveillance" hypothesis of Burnet and Thomas into one that we termed cancer immunoediting that better emphasizes the paradoxical host-protective and tumor-sculpting roles of immunity on developing tumors. Our current work focuses on defining the molecular mechanisms that underlie cancer immunoediting and exploring the implications of this process for cancer immunotherapy.

6013 Background: Achievement of a favorable (> PR) response (particularly CR) at the PTS to IC predicts a higher likelihood of long-term disease control after definitive chemoradiotherapy (CRT) in ...

Cancer immunoediting is the process whereby immune cells protect against cancer formation and sculpt the immunogenicity of developing tumors. The complete process of immunoediting requires both innate and adaptive immunity, but it remains unclear to what extent innate immunity alone is capable of immunoediting. To determine whether the innate immune system can edit tumor cells in the absence of adaptive immunity, we compared the incidence and immunogenicity of 3’methylcholanthrene-induced sarcomas in syngeneic wild-type, RAG2-/-, and RAG2-/-x γc-/- mice. We found that innate immune cells could indeed manifest cancer immunoediting activity in the absence of adaptive immunity. This activity required γc and IFNγ, which mediated the induction of M1 macrophages. M1 macrophages could be elicited by administration of CD40 agonists, thereby restoring editing activity in RAG2-/-x γc-/- mice. Our results suggest that in the absence of adaptive immunity, natural killer cell production of IFNγ induces M1 macrophages, which act as important effectors during cancer immunoediting.