Добірка наукової літератури з теми "621.382 043.744(043.3)"

The syntheses and room-temperature single-crystal X-ray structural characterization of 1 : 3 adducts formed between silver(I) (pseudo-) halides, AgX, and triphenylstibine, SbPh3, are described for X = Cl, I, SCN, NCS, CN, NO3 (1)-(6). The chloride, as its methanol solvate (1a), is isomorphous with the arsine analogue: triclinic, P-1, a 13·373(4), b 14·48(6), c 14·702(3) Å, α 83·49(3), β 87·76(2), γ 76·45(3)°; Z = 2, conventional R on F being 0·046 for No 5514 independent ‘observed’ reflections (I > 3σ(I )). A new form (1b) of the chloride has also been authenticated: monoclinic, P 21/c, a 12·832(2), b 54·24(1), c 18·519(8) Å, β 129·68(3)°; Z = 8 (R 0·065 for No 5672). No bromide has been obtained; the iodide (2) is described as monoclinic, P 21/n, a 19·611(4), b 14·473(6), c 17·74(1) Å, β 98·28(3)°; Z = 4 (R 0·036 for No 6769). The thiocyanate crystallizes from acetonitrile or pyridine as an S-bonded form (3) isomorphous with the arsine analogue: monoclinic, P 21/n, a 19·143(7), b 14·288(5), c 18·694(6) Å, β 98·81(2)°; Z = 4 (R 0·037 for No 4482). From 2-methylpyridine, remarkably, a solvate is obtained in which the thiocyanate is N-bonded (4): triclinic, P-1, a 27·261(5), b 14·767(3), c 13·319(1) Å, α 91·53(1), β 101·58(1), γ 92·29(2)°; Z = 4 (R 0·045 for No 6900). The cyanide is also monoclinic, P 21/n, a 19·442(7), b 14·267(3), c 17·741(6) Å, β 97·63(3)°, z = 4; R 0·057 for No 2487. The unsolvated 1 : 3 nitrate complex (6a) is monoclinic, P 21/n, a 19·602(5), b 14·455(1), c 17·727(2) Å, β 97·19(2)°, Z = 4; R was 0·034 for No 6522. The complex is isomorphous with the arsenic and phosphorus analogues, being mononuclear [(Ph3Sb)3Ag(O2NO)]. The ethanol solvate (6b) is triclinic, P-1, a 13·352(5), b 14·548(9), c 14·701(4) Å, α 81·64(4), β 84·45(3), γ 75·32(4)°, Z = 2; R was 0·058 for No 4702. Ag-Sb range between 2·6980(8) and 2·843(3) Å in the precise determinations; Ag-X are 2·481(4) and 2·52(1) Å (the two chlorides), 2·757(1) (I), 2·533(3) (SCN), 2·21(1) (NCS), 2· 09(3) (CN), 2·377(7) Å (unidentate ONO2)

Abstract Background: Obesity is associated with an increased risk of breast cancer recurrence and poor survival. Obesity rate in adults in the city of Philadelphia is high, with non-Hispanic blacks and Hispanics having the highest rates. We sought to evaluate changes in body mass index (BMI) in breast cancer survivors within the first 2 years from initial encounter for a breast cancer (BC) diagnosis (dx), and investigate factors that may correlate with a change in BMI. Methods: We identified 5,423 BC patients (pts) in our electronic medical record, (1/2015-present), using ICD-10 code C50.X. We then selected pts with BMI values at the three-time points: baseline, 1 year and 2 year intervals from baseline. The closest BMI value before the 1st encounter within 6 months prior to BC dx was considered as the baseline BMI. BMI at 1 year +/- 3 months after the BC dx was considered 1-year interval BMI. BMI at 2 years +/- 6 months after the BC dx was considered 2-year interval BMI. Subjects needed baseline BMI and at least 1 year or 2 year follow-up BMI for inclusion. After all BMI exclusions, 630 pts were included in the study cohort. We used a mixed effects model to predict BMI changes as a linear function of association with time, sex, race and ethnicity, age at BC dx, baseline BMI, treatments (i.e., chemotherapy [CT], endocrine therapy [ET], or immunotherapy [IO] and the interaction of race and ethnicity and treatment in estimating mean change of BMI. The significance level of all tests was set a priori to the 0.05 level. Results: The mean age at BC dx was 61 years; pts identified were mostly white, non-Hispanic/Caucasian (55%), or Black/African American (AA) (34%). By BMI category, we did not observe any substantial difference in the mean age at BC dx and gender distribution (p = 0.81 for age and p = 0.86 for gender). However, the distributions of race and ethnicity differed among BMI categories (p < .01) where the percentage of Black/AA pts was high in the BMI ≥ 30 category. Black/AA pts receiving IO were likely to have BMI change (decrease) compare to white non-Hispanic pts with similar conditions. Black/AA pts receiving no treatment or non IO-treatment were more likely to change BMI (increased, 95% CI: 0.22, 1.03) after BC dx compared to white, non-Hispanic pts. Interestingly, Black/AA pts receiving IO tended to change BMI (decreased) compared to Black/AA pts not receiving IO. Conclusion: We observed the interaction effect of race/ethnicity and treatment on BMI change in BC survivors within 2 years after a BC dx, with Black/AA pts more likely to have an increase in BMI. Table 1.Descriptive Statistics Summary, n = 630.VariableALL (n=630)BMI ≤ 24.9 (n=160, 25%)25 ≤ BMI ≤ 29.9 (n=180, 29%)BMI ≥ 30 (n=290, 46%)p-valueAge at 1st Encounter with BC dx, mean (SD)61.8 (11.8)62.1 (12.5)62.1 (12.1)61.5 (11.2)0.808Sex, n (%)Female625 (99.2)159 (99.4)178 (98.9)288 (99.3)0.857Male5 (0.8)1 (0.6)2 (1.1)2 (0.7)Race & Ethnicity, n (%)White/Caucasian348 (55.2)103 (64.4)106 (58.9)139 (47.9)<.001Black/AA215 (34.1)35 (21.9)48 (26.7)132 (45.5)Hispanic/Latino20 (3.2)5 (3.1)5 (2.8)10 (3.4)Asian/Pacific Islander39 (6.2)17 (10.6)18 (10.0)4 (1.4)American Indian/Alaskan Native2 (0.3)0 (0.0)0 (0.0)2 (0.7)Unknown6 (1.0)0 (0.0)3 (1.7)3 (1.0)BMI (baseline), mean (SD)29.9 (7.1)22.2 (2.0)27.1 (1.4)35.9 (5.7)<.001Treatment (Yes) , n (%)HistoricalCT2 (0.3)1 (0.6)1 (0.6)0 (0.0)0.294ET35 (5.6)7 (4.4)12 (6.7)16 (5.5)0.663IO4 (0.6)2 (1.3)1 (0.6)1 (0.3)0.487BaselineCT20 (3.2)4 (2.5)7 (3.9)9 (3.1)0.815ET54 (8.6)16 (10.0)15 (8.3)23 (7.9)0.742IO11 (1.7)5 (3.1)2 (1.1)4 (1.4)0.3111 yearCT154 (24.4)41 (25.6)42 (23.3)71 (24.5)0.886ET309 (49.0)73 (45.6)93 (51.7)143 (49.3)0.535IO29 (4.6)10 (6.3)8 (4.4)11 (3.8)0.4892 yearsCT71 (11.3)20 (12.5)15 (8.3)36 (12.4)0.337ET231 (36.7)50 (31.3)73 (40.6)108 (37.2)0.198IO32 (5.1)7 (4.4)4 (2.2)21 (7.2)0.051 Citation Format: Maysa Abu-Khalaf, Fnu Nikita, Ayako Shimada, Hannah Hackbart, Dina Alnabulsi, Scott Keith, Ana Maria Lopez, Meghan Butryn. Change in body mass index in breast cancer survivors [abstract]. In: Proceedings of the 2021 San Antonio Breast Cancer Symposium; 2021 Dec 7-10; San Antonio, TX. Philadelphia (PA): AACR; Cancer Res 2022;82(4 Suppl):Abstract nr P4-11-32.

Abstract Background: BC remains the most commonly diagnosed cancer for women. TNBC is an aggressive form with a poorer prognosis compared with other subtypes. Neoadjuvant therapy (NAT) is the standard-of-care approach to shrink tumors in the breast and axilla and to improve patient outcomes. Few RW studies exist of US patients with early BC (eBC); this study aimed to describe clinical parameters by receipt of systemic therapy and to assess overall survival (OS) and progression-free survival (PFS) after NAT and adjuvant therapy (AT) in women with early HR+/HER2− or TNBC using RW evidence in the US. Methods: This retrospective observational study used the Flatiron Health nationwide electronic health record-derived de-identified database, including women ([pts], age ≥18 years) diagnosed with early HR+/HER2− BC or TNBC between 01/01/2011 and 05/31/2018. The primary outcome was to describe pt demographics, clinical characteristics, and treatment patterns. Secondary outcomes included OS and PFS. Results: Of the pts identified for inclusion (N = 5,299), 13.3% (n = 707) were diagnosed with early TNBC and 86.7% (n = 4,592) with HR+/HER2− eBC, of whom 34.7% (n = 245) and 10.9% (n = 502), respectively, did not receive systemic therapy (Table). Systemically treated pts with TNBC vs HR+/HER2− tended to be younger (59.0 years vs 64.0 years); were represented by a higher proportion of Black women (18.0% vs 7.2%); had a greater proportion presenting with invasive ductal carcinoma (IDC) (91.6% vs 78.2%); had a higher proportion with progression to metastasis (19.0% vs 5.7%) and presented with a more aggressive disease (Grade 3) at diagnosis (79.0% vs 18.4%). Most pts (98.4%) received surgery, predominantly breast-conserving surgery (BCS; unilateral lumpectomy: 62.8%); however, 17.8% received bilateral mastectomies. Overall, 9.1% of pts received NAT. More pts with TNBC vs HR+/HER2− received NAT (34.0% vs 7.9%) and achieved a pathologic complete response (pCR; 36.3% vs 6.2%). Consistent with treatment guidelines, pts with TNBC were treated with chemotherapy (CT)-doublet or single-agent regimens and pts with HR+/HER2− received hormone and CT-based regimens. Duration of NAT was similar for both subtypes (3.3 months) but was shorter for AT in pts with TNBC vs HR+/HER2− (3.4 vs 38.2 months). From initial diagnosis, the 36-month survival probability [standard error] was lower for systemically treated pts with TNBC vs HR+/HER2− (85.7% [1.8%] vs 95.6% [0.3%]) and from start of therapy by line setting (NAT: 80.6% [3.5%] vs 91.9% [1.7%]; AT: 84.7% [2.2%] vs 95.8% [0.4%]). Similarly, the 36-month PFS probability was lower for pts with TNBC vs HR+/HER2− from diagnosis (77.9% [2.1%] vs 93.3% [0.4%]) and from start of therapy by line setting (NAT: 68.7% [4.1%] vs 85.2% [2.1%]; AT: 79.5% [2.5%] vs 93.5% [0.4%]). Conclusion: This analysis of US RWE further confirms early TNBC to be a particularly aggressive form of BC, with poorer survival compared with pts with HR+/HER2− eBC. While these RW data indicate BCS is becoming more routine, almost one-fifth of pts still receive bilateral mastectomies. Overall, these data confirm there remains a high unmet need to reduce the need for aggressive treatments while further improving outcomes in pts with early TNBC and HR+/HER2− BC. Table: Patient demographics, clinical characteristics, OS and PFSPatient selection criteriaNumber of patients, n (%)SubgroupsEarly HR+/HER2− BC4,592 (86.7)Patients who received systemic therapy4,090 (89.1)Early TNBC707 (13.3)Patients who received systemic therapy462 (65.3)All patients [1] (N = 5,299), n (%)Systemically treated patients with early HR+/HER2− BC (n = 4,090), n (%)Systemically treated patients with early TNBC (n = 462), n (%)Patient demographicsMedian age (years)64.064.059.0RaceBlack or African American449 (8.5)294 (7.2)83 (18.0)White3,602 (68.0)2,835 (69.3)283 (61.3)Asian139 (2.6)111 (2.7)9 (1.9)Hispanic or Latino15 (0.3)12 (0.3)1 (0.2)Clinical characteristicsHistology at initial diagnosisIDC4,222 (79.7)3,197 (78.2)423 (91.6)ILC684 (12.9)612 (15.0)7 (1.5)Infiltrating ductal mixed and infiltrating lobular mixed132 (2.5)108 (2.6)3 (0.6)Mucinous adenocarcinoma97 (1.8)88 (2.2)0 (0.0)Other [2]122 (2.3)63 (1.5)26 (5.6)Unknown/ND42 (0.8)22 (0.5)3 (0.6)Tumor grade at initial diagnosisGrade 11,350 (25.5)1,161 (28.4)5 (1.1)Grade 22,462 (46.5)2,098 (51.3)88 (19.0)Grade 31,374 (25.9)752 (18.4)365 (79.0)Unknown/ND113 (2.1)79 (1.9)4 (0.9)Surgery at initial diagnosisYes5,215 (98.4)4,032 (98.6)450 (97.4)Surgery type [3]Unilateral lumpectomy3,277 (62.8)2,568 (63.7)241 (53.6)Unilateral mastectomy1,168 (22.4)883 (21.9)128 (28.4)Bilateral lumpectomy75 (1.4)61 (1.5)5 (1.1)Bilateral mastectomy927 (17.8)713 (17.7)89 (19.8)Treatment line settingNumber of patients who received NAT481 (9.1)324 (7.9)157 (34.0)Number of patients who received AT4,263 (80.4)3,949 (96.6)314 (68.0)pCR to NATAchieved pCR77 (16.0)20 (6.2)57 (36.3)OSFrom initial diagnosis: survival probability at Month 36, % (SE)94.0 (0.4)95.6 (0.3)85.7 (1.8)From NAT: survival probability at Month 36, % (SE)88.3 (1.6)91.9 (1.7)80.6 (3.5)From AT: survival probability at Month 36, % (SE)94.9 (0.4)95.8 (0.4)84.7 (2.2)PFSFrom initial diagnosis: progression-free probability at Month 36, % (SE)91.3 (0.4)93.3 (0.4)77.9 (2.1)From NAT: progression-free probability at Month 36, % (SE)79.9 (2.0)85.2 (2.1)68.7 (4.1)From AT: progression-free probability at Month 36, % (SE)92.5 (0.4)93.5 (0.4)79.5 (2.5)Duration of treatment, Months (n)Median duration of NAT3.3 (481)3.3 (324)3.3 (157)Median duration of AT35.3 (4263)38.2 (3,949)3.4 (314)[1] All patients includes both patients systemically treated and systemically untreated. [2] Other includes Inflammatory, Papillary, Metaplastic, Medullary and Tubular histologies. [3] Patient may have received more than one surgery. AT, adjuvant therapy; IDC, invasive ductal carcinoma; NAT, neoadjuvant therapy; ND, not documented; SE, standard error. Citation Format: Anagha Gogate, Amanda Crosbie, Trong Kim Le, Ying Zhang, Rolee Das, Catherine Davis. Clinical characteristics, treatment patterns, and survival outcomes in women with early triple-negative (TN) or hormone receptor-positive/human epidermal growth factor receptor-2 negative (HR+/HER2−) breast cancer (BC) in the real-world (RW) setting [abstract]. In: Proceedings of the 2021 San Antonio Breast Cancer Symposium; 2021 Dec 7-10; San Antonio, TX. Philadelphia (PA): AACR; Cancer Res 2022;82(4 Suppl):Abstract nr P3-12-15.

Abstract Background Intrathecal morphine is commonly and effectively used for analgesia after joint arthroplasty, but has been associated with delayed respiratory depression. Patients with obstructive sleep apnea may be at higher risk of postoperative pulmonary complications. However, data is limited regarding the safety of intrathecal morphine in this population undergoing arthroplasty. Methods This retrospective cohort study aimed to determine the safety of intrathecal morphine in 1,326 patients with documented or suspected obstructive sleep apnea undergoing hip or knee arthroplasty. Chart review was performed to determine clinical characteristics, perioperative events, and postoperative outcomes. All patients received neuraxial anesthesia with low-dose (100 μg) intrathecal morphine (exposure) or without opioids (control). The primary outcome was any postoperative pulmonary complication including: (1) respiratory depression requiring naloxone; (2) pneumonia; (3) acute respiratory event requiring consultation with the critical care response team; (4) respiratory failure requiring intubation/mechanical ventilation; (5) unplanned admission to the intensive care unit for respiratory support; and (6) death from a respiratory cause. The authors hypothesized that intrathecal morphine would be associated with increased postoperative complications. Results In 1,326 patients, 1,042 (78.6%) received intrathecal morphine. The mean age of patients was 65 ± 9 yr and body mass index was 34.7 ± 7.0 kg/m2. Of 1,326 patients, 622 (46.9%) had suspected obstructive sleep apnea (Snoring, Tired, Observed, Pressure, Body Mass Index, Age, Neck size, Gender [STOP-Bang] score greater than 3), while 704 of 1,326 (53.1%) had documented polysomnographic diagnosis. Postoperatively, 20 of 1,322 (1.5%) patients experienced pulmonary complications, including 14 of 1,039 (1.3%) in the exposed and 6 of 283 (2.1%) in the control group (P = 0.345). Overall, there were 6 of 1 322 (0.5%) cases of respiratory depression, 18 of 1,322 (1.4%) respiratory events requiring critical care team consultation, and 4 of 1,322 (0.3%) unplanned intensive care unit admissions; these rates were similar between both groups. After adjustment for confounding, intrathecal morphine was not significantly associated with postoperative pulmonary complication (adjusted odds ratio, 0.60 [95% CI, 0.24 to 1.67]; P = 0.308). Conclusions Low-dose intrathecal morphine, in conjunction with multimodal analgesia, was not reliably associated with postoperative pulmonary complications in patients with obstructive sleep apnea undergoing joint arthroplasty. Editor’s Perspective What We Already Know about This Topic What This Article Tells Us That Is New

Abstract Background: Total lymphocyte count (TLC) has been shown to correlate with outcomes in patients (pts) with acute leukemia. The clinical correlation to TLC in pts with chronic myeloid leukemia in chronic phase (CML-CP) who were treated with a tyrosine-kinase inhibitor (TKI) is unclear. Methods: Lymphocyte data in pts with newly diagnosed CML-CP who were enrolled in consecutive or parallel clinical trials with front-line imatinib (IM), nilotinib (Nilo), or dasatinib (Dasa) were collected at the time of diagnosis, and 3 and 6 months (M) after the start of TKI. Relative lymphocytrosis (RLC) was defined as lymphocyte >150% at 3 or 6M compared with baseline at diagnosis. Absolute lymphocytosis (ALC) was defined as lymphocyte > 4,000 /µL at 3 or 6M after the start of TKI. Pts were assessed for response, overall survival (OS), event-free survival (EFS), transformation-free survival (TFS), and failure-free survival (FFS) based on ALC and RLC. The Kaplan-Meier method was used to calculate OS, EFS, TFS, and FFS. A log-rank test and Cox regression were used for univariate (UVA) and multivariate analysis (MVA), respectively. Results: A total of 483 pts were enrolled in this study: 271 in IM, 105 in Nilo, and 107 in Dasa. Patient characteristics and outcomes are summarized in Table 1. Median age at diagnosis was 48 years, and median follow-up was 85M and ongoing (5-154+). Time from diagnosis to start of TKI, Sokal risk score, and ALC at baseline between groups did not differ clinically. Of 481 pts, 93 (19%) developed RLC at 3 or 6M; IM, 38 (14%); Nilo, 23 (22%); Dasa, 32 (30%) (p= .001). ALC at 3 or 6M was observed in 15 (3%); IM, 3 (1%); Nilo, 1 (1%); Dasa, 11 (10%) (p<.001). Overall, cumulative incidence of complete cytogenetic response (CCyR) at 6M, major molecular response (MMR) at 12M, molecular response with 4.5 log reduction by IS (MR4.5) at 24M did not differ significantly between RLC and non-RLC (3 or 6M), or between ALC and non-ALC (3 or 6M). 5-y TFS, EFS and OS in ALC group were significantly worse than those in non-ALC group (p= .002, p=.016, p=.008, respectively). By UVA and MVA related to OS, age [p <.001; Hazard ratio (HR), 1.062; 95% confidence interval (95%CI), 1.036-1.089], presence of ALC at 3 or 6M [p = .028; HR, 10.948; 95%CI, 1.297-92.415], absence of MMR at 24M [p=.016; HR, 2.263; 95%CI, 1.165-4.393] were identified as adverse prognostic factors for OS. Conclusion: The presence of ALC ≥4,000/µL at 3 or 6M of TKI therapies is rare but is adversely associated with overall survival. Table 1. Patient Characteristics and Outcomes (N=483)a Overall [n= 481] IM [n= 271] Nilo [n= 105] Dasa [n= 107] Age, (year) 48 (15-85) 48 (15-85) 49 (17-82) 48 (16-83) Sokal Risk, No. (%) Low 334 (69) 175 (65) 79 (75) 80 (75) Intermediate 114 (24) 74 (27) 18 (17) 22 (21) High 32 (7) 20 (7) 8 (8) 4 (4) Time from diagnosis to start of TKI, (M) 0.9 (0-12.6) 1.0 (0-12.6) 0.5 (0-5.6) 0.7 (0.1-7.8) ALC at baseline, (/109L) 2.5 (0-86.6) 2.4 (0-16.7) 2.6 (0.4-9.2) 2.7 (0.3-86.6) Incidence of Relative Lymphocytosis, No. (%) At 3M 65 (14) 25 (9) 16 (15) 24 (22) At 6M 76 (16) 32 (12) 20 (19) 24 (22) Overall 93 (19) 38 (14) 23 (22) 32 (30) Incidence of Absolute Lymphocytosis, No. (%) At 3M 8 (2) 1 (0) 0 7 (7) At 6M 11 (2) 3 (1) 1 (1) 7 (7) Overall 15 (3) 3 (1) 1 (1) 11 (10) Outcomes of RLC and ALC at any time in each group, +/- (%/%) (p) <10% BCR-ABL/ABL at 3M RLC 36/40 (.596) 22/44 (.213) 50/37 (.280) 31/38 (.537) ALC 38/39 (.952) 0/42 (.394) 100/39 (.214) 36/35 (.952) Cumulative CCyR at 6M RLC 75/75 (.288) 50/66 (.063) 96/90 (.413) 90/87 (.628) ALC 67/75 (.711) 33/64 (.276) 0/92 (.001) 82/89 (.599) Cumulative MMR at 12M RLC 67/74 (.406) 53/70 (.030) 83/82 (.921) 72/74 (.903) ALC 60/73 (.488) 33/68 (.197) 0/83 (.033) 73/74 (.745) Cumulative MR4.5 at 24M RLC 46/52 (.564) 37/50 (.139) 57/55 (.889) 50/57 (.729) ALC 33/52 (.332) 33/48 (.610) 0/56 (.264) 36/57 (.252) 5-y FFS RLC 61/71 (.133) 56/69 (.167) 62/70 (.710) 61/74 (.285) ALC 50/69 (.076) 0/68 (<.001) 0/70 (<.001) 71/70 (.974) 5-y TFS RLC 90/93 (.369) 88/93 (.597) 91/88 (.115) 91/99 (.213) ALC 72/93 (.002) 67/93 (.014) 0/90 (<.001) 80/97 (.121) 5-y EFS RLC 80/86 (.213) 71/83 (.154) 84/87 (.450) 86/93 (.486) ALC 64/85 (.016) 33/82 (<.001) 0/87 (<.001) 80/92 (.574) 5-y OS RLC 89/93 (.068) 81/94 (.007) 100/84 (.126) 96/99 (.207) ALC 82/93 (.008) 67/93 (.001) 100/88 (.847) 83/99 (.040) a Two in IM and 1 in Dasa were not evaluable due to lack of differential data at 3 and 6M. Figure 1. OS in Pts with ALC Figure 1. OS in Pts with ALC Disclosures O'Brien: Amgen, Celgene, GSK: Consultancy; CLL Global Research Foundation: Membership on an entity's Board of Directors or advisory committees; Emergent, Genentech, Gilead, Infinity, Pharmacyclics, Spectrum: Consultancy, Research Funding; MorphoSys, Acerta, TG Therapeutics: Research Funding.

BackgroundDelta-like ligand 3 (DLL3) is an inhibitory Notch ligand that is highly expressed in small cell lung cancer (SCLC) and minimally expressed in normal tissues.1 AMG 757, a half-life extended BiTE® immune therapy, binds to DLL3 on tumor cells and CD3 on T cells, resulting in T cell-dependent killing of tumor cells. We report initial safety and efficacy from the ongoing phase 1 study of AMG 757 in patients with SCLC.MethodsAMG 757 was administered intravenously every two weeks (with/without step dose) at doses of 0.003–3.0 mg. Eligible patients had SCLC that progressed or recurred following ≥1 platinum-based regimen. Antitumor activity was assessed using modified RECIST 1.1. The study was approved by the Ethics Board at participating institutions.ResultsAs of 1 June 2020, safety and efficacy data are available for 31 patients enrolled at the first seven dose levels (DL) with median age, 63 (44–74) years; ECOG PS: 0–1, n=30 (96.8%); median prior lines, 2.0 (1–6); and previous PD-1/PD-L1 treatment: n=12 (38.7%). Median treatment duration was 6.1 (0.1–59.4) weeks. Treatment-emergent adverse events (AEs) were reported for 30 (96.8%) patients. AMG 757-related AEs occurred in 25 (80.6%) patients, including 5 (16.1%) that were grade ≥3 and one (3.2%) grade 5 (pneumonitis in DL5 [0.3 mg]). Three AEs (dyspnea, pneumonitis, fatigue) led to treatment discontinuation. The most common AE was cytokine release syndrome (CRS), which was reported in 11 (35.5%) patients. CRS AEs were grade 1–2, consisted mainly of fever with/without hypotension, and occurred mostly within 24 hours of the first or second dose of AMG 757. CRS events were reversible, did not lead to treatment interruption or discontinuation, and were managed with supportive care, corticosteroids, and/or anti-IL 6 therapy. The MTD for AMG 757 has not yet been reached. AMG 757 exhibited dose proportional increase in exposures. Response to AMG 757 is shown (figure 1). Confirmed partial response was reported in 5 (16.1%) patients (1/12 [8.3%] in DL5, 1/8 [12.5%] in DL6, 3/7 [42.9%] in DL7), and stable disease in 8 (25.8%) of all treated patients. Most responses occurred after 8 weeks on treatment. All responders remain on treatment with duration of response ranging from 2.0+ to 7.4 months+.Abstract 359 Figure 1Tumor shrinkage over time in response to AMG 757ConclusionsAMG 757 administered at a dose of up to 3 mg every two weeks has an acceptable safety profile and shows anti-tumor activity in patients with relapsed/refractory SCLC. Further dose escalation is ongoing.Trial RegistrationNCT03319940Ethics ApprovalThe study was approved by the Ethics Board at participating institutions.ConsentN/AReferenceLeonetti A, Facchinetti F, Minari R, Cortellini A, Rolfo CD, Giovannetti E, Tiseo M. Cell Oncol (Dordr). 2019;42:261–273.

Abstract Introduction: PIK3CA mutations (mut) occur in ~40% of patients (pts) with HR+, HER2- ABC, and lead to phosphatidylinositol 3-kinase (PI3K) pathway hyperactivation, endocrine resistance, and poor survival in advanced disease. Alpelisib, an α-selective PI3K inhibitor and degrader, demonstrated efficacy in combination with fulvestrant in the Phase III SOLAR-1 trial in pts with PIK3CA-mut HR+, HER2- ABC. Notably, treatment benefit was not seen in pts without PIK3CA-mut tumors. Expert guidelines now recommend testing for PIK3CA mut at advanced diagnosis; however, data on PIK3CA mut prevalence in a broader population outside of clinical trials are limited. This real-world study snapshot describes the global prevalence of PIK3CA mut across geographic areas in HR+, HER2- ABC. Methods: This noninterventional, retrospective cohort study of ~2,000 adults (≥18 years) in ~20 countries from Europe, Asia, Middle East (ME), and Latin America (LA) is assessing the frequency of PIK3CA mut in HR+, HER2- ABC. Key inclusion criteria are histologically/cytologically confirmed estrogen/progesterone receptor-positive and HER2- ABC with available fresh or archival tumor tissue. The primary endpoint is the percentage of pts with PIK3CA-mut tumors, specifying each hotspot. Key secondary endpoints include the percentage of pts with PIK3CA-mut tumors by geographic region, demographics by PIK3CA status, clinical characteristics, number of lines of treatment in the advanced setting, and time to subsequent treatment by PIK3CA status. Tumor tissue samples are assessed at a local laboratory, at a minimum, for PIK3CA mut in C420R, E542K, E545A/D/G/K, Q546E/R, and H1047L/R/Y. All statistical analyses are descriptive, and the prognostic role of PIK3CA mut will be evaluated in the final analysis. Results: As of data cut-off (03 May 2021), 1,361 pts were enrolled in the Full Analysis Set, 574 (42.2%) of whom have tumors harboring a PIK3CA mut. Table 1 summarizes demographics and baseline characteristics in the mut and non-mut cohorts. Polymerase chain reaction and next-generation sequencing were the common methods used to assess PIK3CA mut in 570 (41.9%) and 625 (45.9%) of pts, respectively. PIK3CA mut rates are generally consistent across regions (30.7-44.0%, Table 2). Table 2 shows sample types and most common biomarker muts. Conclusions: In this study, PIK3CA mut rates, 43.0% in Asia, 44.0% in Europe, 40.9% in LA, and 30.7% in ME, were consistent across regions and closely followed previous reports, supporting the prevalence of this mut outside the trial setting and in a more diverse real-world pt population. The most common PIK3CA muts found in this study were H1047R, E545K, and E542K, consistent with SOLAR-1. PIK3CA mut rates were comparable in primary vs metastatic samples, supporting the existing body of evidence that PIK3CA mut are truncal and can be tested on any available tissue. Further analysis, including treatment-related information, will be presented. Table 1.Demographics, baseline characteristics, and disease history (Full Analysis Set)Mutant PIK3CANon-mutant PIK3CAAll patientsn=574n=787N=1,361Median age (range) at early disease diagnosisa50.0 (28.0-85.0)51.0 (23.0-83.0)51.0 (23.0-85.0)Median age (range) at advanced disease diagnosis57.0 (26.0-89.0)55.5 (23.0-87.0)56.0 (23.0-89.0)Median age (range) at enrollment59.5 (27.0-89.0)59.0 (23.0-87.0)59.0 (23.0-89.0)Sex, n (%)Female566 (98.6)778 (98.9)1,344 (98.8)Male8 (1.4)8 (1.0)16 (1.2)Unknown01 (0.1)1 (0.1)Race, n (%)White294 (51.2)418 (53.1)712 (52.3)Asian183 (31.9)239 (30.4)422 (31.0)Black or African American5 (0.9)13 (1.7)18 (1.3)Multiple1 (0.2)0 (0.0)1 (0.1)Unknown91 (15.9)117 (14.9)208 (15.3)Menopausal status at advanced disease diagnosis, n (%)bMutant PIK3CANon-mutant PIK3CAAll patientsn=566n=778N=1,344Postmenopausal410 (72.4)554 (71.2)964 (71.7)Premenopausal146 (25.8)214 (27.5)360 (26.8)Stage at initial diagnosis, n (%)Mutant PIK3CANon-mutant PIK3CAAll patientsn=574n=787N=1,361Recurrent breast cancerc299 (52.1)414 (52.6)713 (52.4)De novo advanced breast cancerd265 (46.2)357 (45.4)622 (45.7)Unknown10 (1.7)16 (2.0)26 (1.9)Time from early diagnosis to advanced disease, n (%)&lt;1 year32 (5.6)33 (4.2)65 (4.8)1 to &lt;2 years25 (4.4)25 (3.2)50 (3.7)2 to &lt;3 years29 (5.1)40 (5.1)69 (5.1)≥ 3 years149 (26.0)214 (27.2)363 (26.7)Extent of metastatic disease, n (%)Bone390 (67.9)456 (57.9)846 (62.2)Liver141 (24.6)204 (25.9)345 (25.3)Lung171 (29.8)245 (31.1)416 (30.6)Other127 (22.1)155 (19.7)282 (20.7)Number of metastatic sites, n (%)013 (2.3)21 (2.7)34 (2.5)1229 (39.9)324 (41.2)553 (40.6)&gt;1332 (57.8)442 (56.2)774 (56.9)aCensored patients initially diagnosed as de novo advanced breast cancer.bMenopausal status is applicable only to female patients. Sites are provided the option to choose from 1) Able to bear children, 2) Post-menopausal, or 3) Sterile - of childbearing age.cStage 0-IIIA at initial diagnosis.dStage IIIB, IIIC, or IV at initial diagnosis. Table 2.PIK3CA mutation status by region and sample typeFrequency of mutant PIK3CA by regionMutant/Number of patients% (95% CI)All patients574/1,36142.2 (39.5-44.9)Asia193/44943.0 (38.4-47.7)Europe312/70944.0 (40.3-47.8)Latin America27/6640.9 (29.0-53.7)Middle East42/13730.7 (23.1-39.1)Mutant PIK3CANon-mutant PIK3CAAll patientsn=574n=787N=1,361Region, n (%)Asia193 (33.6)256 (32.5)449 (33.0)Europe312 (54.4)397 (50.4)709 (52.1)Latin America27 (4.7)39 (5.0)66 (4.8)Middle East42 (7.3)95 (12.1)137 (10.1)Tumor tissue type, n (%)Archival tumor536 (93.4)754 (95.8)1,290 (94.8)Newly obtained tumor sample38 (6.6)33 (4.2)71 (5.2)Source of tumor biopsy, n (%)Primary372 (64.8)496 (63.0)868 (63.8)Metastatic202 (35.2)291 (37.0)493 (36.2)Most common PIK3CA mutationsa, n (%); 95% CIbH1047R197 (34.3); 95% CI (30.4-38.4)0197 (14.5); 95% CI (12.6-16.5)E545K100 (17.4); 95% CI (14.4-20.8)0100 (7.3); 95% CI (6.0-8.9)E542K66 (11.5); 95% CI (9.0-14.4)066 (4.8); 95% CI (3.8-6.1)aIncludes patients with double or multiple mutations.b95% Confidence Interval (CI) is calculated using exact binomial method. Citation Format: Pathmanathan Rajadurai, Tatiana Semiglazova, Alinta Hegmane, Fadi El Karak, Joanne W Chiu, Sudeep Gupta, Hamdy A Azim, Josef JEM Kitzen, Antoine Arnaud, Sina Haftchenary, Jiwen Wu, Lakshmi Menon-Singh, LaTonya Smith, Lyudmila Zhukova. PIK3CA registry: A noninterventional, descriptive, retrospective cohort study of PIK3CA mutations in patients with hormone receptor-positive (HR+), human epidermal growth factor receptor 2-negative (HER2-) advanced breast cancer (ABC) [abstract]. In: Proceedings of the 2021 San Antonio Breast Cancer Symposium; 2021 Dec 7-10; San Antonio, TX. Philadelphia (PA): AACR; Cancer Res 2022;82(4 Suppl):Abstract nr P5-13-25.

Fertility among cattle breeds can vary. The Swedish Red and White dairy breed (SRB) has been systematically bred for good reproductive traits since 1970 and might therefore have retained a better oocyte quality than other dairy breeds. The aim of this study was to determine if the breed of oocyte donor affects the development of embryos using IVM, IVF, and IVC. Oocyte developmental competence in vitro was compared between the SRB (n = 77 animals), the Swedish Holstein breed (SLB, n = 49), and beef breeds (mixed breeds, n = 97). The oocytes (n = 1380, 18 batches) were aspirated from abattoir-derived ovaries from healthy animals with known identity. Statistical analyses were performed using Student’s t-tests and generalized linear mixed models with random effects. The time of collection in relation to slaughter and time of day, as well as aspiration and the following in vitro procedures, were consistent throughout the experiment. The oocytes were matured, fertilized (frozen semen), and cultured according to conventional protocols without serum. Data are presented as mean ± SEM. The SRB and SLB groups were comparable in age [SRB: 66% cows (over 3 years of age), 27% young cows (calved at least once but not over 3 years of age), and 7% heifers; SLB: 63% cows, 20% young cows, and 17% heifers], carcass classification (scale 1-15, where 15 = highest amount of muscle; SRB: 3.8 ± 0.2, SLB 3.5 ± 0.3), body fat (scale 1-15, where 15 =highest amount of fat; SRB: 8.4 ± 0.4, SLB 8.8 ± 0.5) and kilograms of carcass weight (SRB: 297.3±7.4, SLB: 311.6 ± 9.0). The beef group had a significantly higher mean carcass classification (6.2 ± 0.2) and a different age distribution with a higher proportion of heifers (38% cows, 12% young cows, and 50% heifers), but was comparable in body fat content (8.5 ± 0.4) and kilograms of carcass weight (310.9 ± 7.9). Cleavage rate, number of embryos developed beyond the 2-cell stage by 44 h post-fertilization, and the number of blastocysts developed by Days 7 and 8 were noted. All blastocysts were graded and stained with Hoechst 33 342 and the number of nuclei was determined. Cleavage rate was not different among the breeds (SRB: 71.9 ± 0.03%, SLB: 72.5 ± 0.02%, beef: 73.9 ± 0.03%). The percentage of embryos developed beyond 2-cells (from cleaved) did not differ between the beef and SRB (beef: 65.1 ± 6.1%; SRB: 70.4 ± 4.9%) but SLB was significantly greater than than the other breeds (75.4 ± 4.5%). The percentage of blastocysts developed by Day 8 was significantly higher in the beef (21.1 ± 2.7%) and SRB (23.3 ± 3.5%) breeds compared with the SLB (12.5 ± 2.4%). There was no significant difference in blastocyst grades among breeds (scale 1-4, where 1 = highest grade; SRB: 2.4 ± 0.1, SLB: 2.4 ± 0.2, beef: 2.1 ± 0.2), but the number of nuclei in Day 8 blastocysts was significantly lower in the SLB (SRB: 98.9 ± 7.7, SLB: 79.2 ± 8.7, beef: 101.4 ± 6.9). In conclusion, the breed of origin of the oocytes is an important factors affecting the development during in vitro embryo production in cattle. Funded by Formas.

Abstract Background: There is great interest in determining prognostic indicators in cancer as they enable more informed treatment decisions and patient counseling. Perineural invasion (PNI) has been established as a poor prognostic indicator in many types of cancer, however its significance in breast cancer is not clear. Research Objectives: The objective of this study was to explore the prognostic importance of PNI in breast cancer and identify clinicopathologic variables associated with PNI in breast cancer. Methods: A prospectively maintained database was used to identify patients treated at a single institution for stage I-III unilateral breast cancer from 2006-2014. PNI-positive cases included all patients whose tumors were reported to contain PNI in either the needle biopsy specimen or the surgical pathology, and each case was matched with two PNI-negative control patients on age, clinical stage, ER, PR, and HER2 status. A total of 492 patients were included in the analysis, including 164 PNI-positive patients and 328 control patients. Distributions of age, race, lymphovascular invasion, multifocality, clinical tumor size and pathologic tumor size were compared using Fisher’s exact test (categorical variables) or Wilcoxon rank-sum test (continuous variables). The method of Kaplan and Meier was used to estimate the distribution of overall survival, disease-free survival, and time to locoregional recurrence from the diagnosis date. All statistical tests used a significance level of 5%. No adjustments for multiple testing were made. Results: The median follow up was 6.26 years (6.3 years versus 6.2 years for PNI-positive and controls, respectively). The number of reported PNI-positive cases increased over the study period, with 76 cases reported during the 6-year period 2006-2011 and 88 cases reported during the last two years, 2013-2014. There was no statistical difference noted in overall survival, disease-free survival, or time to recurrence by clinical stage for PNI-positive patients compared to controls. It was noted that clinical stage 3 disease showed a trend toward poorer disease-free survival in PNI-positive patients although this did not reach statistical significance. Median pathologic tumor size was significantly higher in the PNI-positive patients compared to controls (2.2 cm versus 1.6 cm, respectively, p&lt;0.0001). In the subset of patients treated with neoadjuvant chemotherapy, median tumor size was also significantly higher in the PNI-positive patients compared to controls (2.8 cm versus 1.5 cm, p=0.0087). Pathologic node-positive status was more likely in the PNI-positive patients (47% versus 41%, p=0.019). Analysis of non-matched variables including race, lymphovascular invasion, multifocality and nuclear grade showed no statistically significant difference between the PNI and control groups.Conclusion: Perineural invasion was not found to be a statistically significant prognostic indicator of survival or locoregional recurrence. PNI is associated with larger pathologic tumor size, and this finding persists among patients treated with neoadjuvant chemotherapy. PNI is also associated with lymph node metastasis. This analysis is limited by small sample sizes and likely under reporting of PNI. Additional research is needed to evaluate the significance of PNI in breast cancer. Table 1.Patient CharacteristicsVariableLevelsPNI (%)Control (%)P-ValueAge≤ 5047 (28.7)94 (28.7)p = 1.00&gt; 50117 (71.3)234 (71.3)RaceAsian10 (6.1)24 (7.3)p = 0.22Black9 (5.5)30 (9.2)Hispanic22 (13.4)51 (15.6)White122 (74.4)214 (65.2)Lymphovascular invasionY53 (32.3)80 (24.4)p = 0.07Lymphovascular invasionN111 (67.7)248 (75.6)p = 0.07MultifocalityN123 (75.0)206 (69.8)p = 0.28Y41 (25.0)89 (30.2)Nuclear Grade129 (18.4))47 (14.8)p = 0.28288 (55.7)166 (52.4)341 (25.9)104 (32.8)Clinical StageIA55 (33.5)110 (33.5)p = 1.00IIA59 (36.0)118 (36.0)IIB23 (14.0)46 (14.0)IIIA6 (3.7)12 (3.7)IIIB14 (8.5)28 (8.5)IIIC7 (4.3)14 (4.3)Pathologic N StageNx2 (1.2)1 (0.3)p = 0.019N083 (51.5)193 (59.0)N149 (30.4)88 (26.9)N217 (10.6)22 (7.0)N310 (6.2)23 (7.0)ERNeg11 (6.7)22 (6.7)p = 1.00Pos153 (93.3)306 (93.30PRNeg19 (11.6)38 (11.6)p = 1.00Pos145 (88.4)290 (88.4)HER2Neg155 (94.5)310 (94.5)p = 1.00Pos9 (5.5)18 (5.5)Neoadjuvant ChemotherapyN121 (73.3)240 (73.2)p = 1.00Y44 (26.7)88 (26.8)Clinical tumor sizeRange (cm)0.15 - 9.800.50-10.00p = 0.0013Median (cm)2.453.00Pathologic tumor sizeRange (cm)0.02-15.000.00 - 20.00p &lt; 0.0001Median (cm)2.201.60Pathologic tumor size after neoadjuvant chemotherapyRange (cm)0.02-120.00-20p = 0.0087Median (cm)2.751.47 Citation Format: Solange Erlyn Cox, Roland Bassett, Min Yi, Aysegul Sahin, Mediget Teshome, Kelly Hunt, Catherine Akay. An exploratory case-control study of perineural invasion in breast cancer [abstract]. In: Proceedings of the 2021 San Antonio Breast Cancer Symposium; 2021 Dec 7-10; San Antonio, TX. Philadelphia (PA): AACR; Cancer Res 2022;82(4 Suppl):Abstract nr P4-07-13.

Background: Concussion injuries are synonymous with vestibular impairments and symptoms include dizziness, impaired balance, and problems with gaze stability (Covassin et al., 2014). Common ocular motor impairments after a concussion include convergence/accommodative insufficiencies and saccadic dysfunction (Mucha et al., 2014). Vestibular and ocular motor impairments have been linked to worse outcomes following concussion (Pearce et al., 2015), including prolonged recovery (Corwin et al., 2015). The purpose of the current study was to determine which VOMS impairments were linked with longer recovery. Methods: Pediatric patients diagnosed with concussion (n = 131) presenting to an outpatient concussion clinic within 7 days from their initial date of injury were administered a standardized version of the VOMS. Patients were administered the VOMS by certified athletic trainers educated and trained on administration. The VOMS consists of nine measures and was validated by the University of Pittsburgh (Mucha et al., 2014) as a symptom provocation measure with a symptom rating of 0-10 with convergence measured in centimeters, and scores of 6 cm or greater being indicative of abnormal. Demographic, acute injury, and baseline values were summarized using descriptive statistics. Point estimates and 95% confidence intervals were calculated for all end points. Results: 131 patients with a mean age of 13.5 + 2.4 completed the VOMS within 7 days (mean = 3.2 + 1.7) of a diagnosed concussion. The sample was evenly divided by gender (52.7% male, 47.3% female). Patients were grouped by recovery time: <14 days (n = 19, 14.5%) 15-28 days (n = 64, 48.9%), and 29-120 days (n = 48, 36.6%). In the <14 day recovery group, 5.2% (n = 2) reported a history of concussion, 15.8% (n = 3) reported a history of migraine, and 5.2% (n = 2) reported a history of psychiatric diagnosis. In the 15-28 day recovery group, 21.9% (n = 14) reported a history of concussion, 9.4% (n = 6) reported a history of migraine, and 6.5% (n = 4) reported a history of psychiatric diagnosis. In the 29-120 day recovery group, 25% (n = 12) reported a history of concussion, 25% (n = 12) reported a history of migraine, and 6.25% (n = 3) reported a history of psychiatric diagnosis. Descriptive statistics for baseline VOMS symptoms were recorded for the <14 day recovery group; headache (mean = 1 + 1.49, CI = 0.7 -1.3), dizziness (mean = 0.2 + 0.5, CI = 0.1-0.3), nausea (mean = 0 + 0, CI = 0-0), and fogginess (mean = 0.9 + 1.5, CI = 0.5 -1.3), for the 15-28 day recovery group; headache (mean = 3.3 + 2.4, CI = 3-3.6), dizziness (mean = 1.5 + 1.9, CI = 1.3 -1.7), nausea (mean = 0.8 + 1.7, CI = 0.6 -1), and fogginess (mean = 1.7 + 2.2, CI = 1.4-2), for the 29-120 day recovery group; headache (mean = 4.4 + 2.2, CI = 4.1-4.7), dizziness (mean = 1.9 + 2.2, CI = 1.6-2.2), nausea (mean = 1.4 + 2.2, CI = 1.1 -1.7), and fogginess (mean = 2.4 + 2.9, CI = 2-2.8). VOMS convergence in centimeters across trials for the <14 day recovery group; T1 (mean = 2.6 + 2.4, CI = 2.1-3.1), T2 (mean = 3.4 + 2.4, CI = 2.9-3.9), and T3 (mean = 3.8 + 2.5, CI = 3.2-4.4), for the 15-29 day recovery group; T1 (mean = 3.9 + 3.9, CI = 3.4-4.4), T2 (mean = 4.8 + 4.2, CI = 4.3-5.3), and T3 (mean = 5.3 + 5.1, CI = 4.7-5.9), for the 29-120 day recovery group; T1 (mean = 6.9 + 5.2, CI = 6.1-7.7), T2 (mean = 8.3 + 1.8, CI = 7.4-9.2), and T3 (mean = 9.6 + 2.1, CI = 8.6-10.6). VOMS symptom provocation increase of +2 and +3 from baseline were totaled for each recovery group. Abnormal convergence greater than 6 cm on any trial was totaled for each group. Percentages for all 3 recovery groups with symptom provocation of +2, +3, and abnormal convergence were calculated. In the <14 day recovery group, 21% had a +2 symptom provocation on at least one symptom, 16% had a +3 symptom increase on at least one symptom, and 16% had abnormal convergence greater than 6 cm on at least one convergence trial. 11% of the <14 day recovery group had a +2, +3, increase and abnormal convergence greater than 6 cm. In the 15-29 day recovery group, 69% had a +2 symptom provocation on at least one symptom, 34% had a +3 symptom increase on at least one symptom, and 38% had abnormal convergence greater than 6 cm on at least one convergence trial. 13% of the 15-29 day recovery group had a +2, +3, increase and abnormal convergence greater than 6 cm. In the 29-120 day recovery group, 85% had a +2 symptom provocation on at least one symptom, 60% had a +3 symptom increase on at least one symptom, and 58% had abnormal convergence greater than 6 cm on at least one convergence trial. 38% of the 29-120 day recovery group had a +2, +3, increase and abnormal convergence greater than 6 cm. Conclusion: The current study identified symptom provocation of +2 and +3 as well as abnormal convergence greater than 6 cm were the most synonymous with recovery across the three recovery groups. Clinicians should consider these findings in providing recommendations and discussing anticipated recovery with patients. Further research is needed to determine more definitive parameters when predicting recovery following concussion.

Ovarian cancers tend to recur in 15-70% cases. CA-125 - is a tumor marker used for monitoring therapeutic response, and in surveillance, for recurrent disease. However, it has a limited role as a persistent high level can signify either recurrence or persistence of residual tumor. Metastases from ovarian cancer primarily involve the peritoneum rather than parenchymal sites; thus, the presence of small-volume recurrence or metastatic deposits on the visceral surfaces poses a challenge for interpretation of CT and MR images. PET/CT utilizes its property of higher accumulation in malignant cells to provide both anatomic and functional information for diagnosing malignant tumors. Objectives: The objectives of the study were to find the correlation between PET/CT findings and final histopathological diagnosis after a secondary cytoreductive surgery in suspected ovarian cancer recurrences. Materials and Methods: PET/CT was done in cases with rising or above normal CA-125 and no radiological findings. These patients with abnormal PET/CT findings were taken up for a secondary cytoreductive surgery and histopathological proven were taken as the standard against which PET/CT positive findings was compared. Results: The mean age in our group of patients with suspected recurrence was 53 years (Range 39-74 years). Of the 52 patients with suspected recurrence, 40 patietnts with a PET-CT scan with findings suggestive of an avid uptake underwent surgery. 22 patients had serous histology, 12 mucinous and 8 had clear cell carcinoma. Stage-wise distribution at the time of primary surgery is as follows stage I-3, stage II-7, stage III-26, stage IV-4. Of the 40 patients who underwent a second look surgery 32 had histopathologically confirmed recurrence. PET-CT detected a total of 86 lesions in the 40 patients who underwent surgery. Of these, 38 were in the lymph nodes 28 in para-aortic and 10 in pelvic, 32 were peritoneal lesions and 14 were pelvic, 2 were metastatic in the parenchyma of liver. Detection of the lesion on PET-CT was size dependant, of the 9 lesions were missed on PET-CT, 7 were less than 0.5 cm. The mean diameter of the lesions detected was 2.2 cm (range 0.3-6.2 cm). PET-CT accurately identified 62 of 70 histopathologically proven lesions. The overall lesion-based sensitivity of PET-CT is 88.6%, specificity 56.2%, Positive predictive value being 72.1%, negative predictive value of 69.2%. Accuracy of detecting lesions greater than 1 cm is 78.6% (44 of 56 lesions). Conclusions: Corelation between PET/CT and histopathologicaldisease: k (cohen value) = 0.81 which suggests excellent correlation. For selected patients with ovarian cancer recurrence may benefit from a comprehensive radiographic imaging survey (PET-CT) at the time of even no or minimal CA-125 elevation in early detection and successful cytoreductive surgical resection and an increase in overall survival.