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Despite advances in surgery, chemotherapy, and radiation, there are limited treatment options for advanced head and neck squamous cell carcinoma (HNSCC) and survival remains very poor. Therefore, effective therapies are desperately needed. Recently, selective exploitation of DNA damage and replication stress responses has become a novel approach for cancer treatment. Wee1 kinase and Rad51 recombinase are two proteins involved in regulating replication stress and homologous recombination repair in cancer cells. In this study, we investigated the combined effect of Rad51 inhibitor (B02) and Wee1 inhibitor (AZD1775) in vitro and in vivo in various HNSCC cell lines. Clonogenic survival assays demonstrated that B02 synergized with AZD1775 in vitro in all HNSCC cell lines tested. The synergy between these drugs was associated with forced CDK1 activation and reduced Chk1 phosphorylation leading to induction of excessive DNA damage and replication stress, culminating in aberrant mitosis and apoptosis. Our results showed that elevated Rad51 mRNA expression correlated with worse survival in HNSCC patients with HPV-positive tumors. The combination of B02 and AZD1775 significantly inhibited tumor growth in vivo in mice bearing HPV-positive HNSCC tumors as compared to HPV-negative HNSCC. This differential sensitivity appears to be linked to HPV-positive tumors having more in vivo endogenous replication stress owing to transformation by E6 and E7 oncogenes. Furthermore, addition of B02 radiosensitized the HPV-negative HNSCC tumors in vitro and in vivo. In conclusion, our data implicate that a novel rational combination with Rad51 and Wee1 inhibitors holds promise as synthetic lethal therapy, particularly in high-risk HPV-positive HNSCC.

The rising incidence of pancreatic cancer is largely driven by the skyrocketing prevalence of obesity and type 2 diabetes (T2D). Hyperinsulinemia is a cardinal feature of both conditions, and is independently associated with increased cancer incidence and mortality. Our previous studies demonstrated that genetically reducing insulin production suppressed formation of pancreatic intraepithelial neoplasia (PanIN) pre-cancerous lesions in mice with mutant Kras. However, we found that hyperinsulinemia affected many cell types in the pancreatic microenvironment. Thus, it remained unclear whether hyperinsulinemia exerted its effects directly on the cells that give rise to PanINs or indirectly on the tumor microenvironment, and molecular mechanisms involved were unknown. Here, we tested whether insulin receptors (Insr) in KrasG12D-expressing pancreatic acinar cells are necessary for the effects of hyperinsulinemia on obesity-associated pancreatic cancer development. Loss of Insr in KrasG12D-expressing acinar cells did not prevent hyperinsulinemia or weight gain associated with high fat diet (HFD) consumption in mice. However, solely reducing Insr in KrasG12D-expressing acinar cells significantly reduced formation of PanIN and tumors, in a gene dose-dependent manner. Mechanistically, proteomic analyses showed that hyperinsulinemia acts through Insr to drive the excess production of digestive enzymes in acinar cells by modulating the activity of the spliceosome, ribosome, and secretory machinery. This resulted in increased inflammation, which was abrogated by acinar-specific Insr knockout. We confirmed that insulin increased the conversion of wild-type acinar cells into acinar-to-ductal metaplasia (ADM) in a trypsin-dependent manner. Collectively, these data demonstrate that hyperinsulinemia acting via acinar cells insulin receptors promotes inflammatory conditions that cooperate with Kras signaling to increase the risk of developing pancreatic cancer, mechanistically linking obesity and pancreatic cancer.

Treatment with immune checkpoint blockade (ICB) has resulted in durable responses for a subset of patients with cancer, with predictive biomarkers for ICB response originally identified largely in the context of hypermutated cancers. Although recent clinical data have demonstrated clinical responses to ICB in certain patients with non-hypermutated cancers, previously established ICB response biomarkers have failed to accurately identify which of these patients may benefit from ICB. Here, we demonstrate that a replication stress response (RSR) defect gene expression signature, but not other proposed biomarkers, is associated with ICB response in 12 independent non-hypermutated cohorts of patients with cancer across 7 tumor types, including those of the breast, prostate, kidney, and brain. Induction or suppression of RSR deficiencies was sufficient to modulate response to ICB in pre-clinical models of breast and renal cancers. Mechanistically, we find that despite robust activation of checkpoint kinase 1 (Chk1) signaling in RSR-deficient cancer cells, aberrant replication origin firing causes exhaustion of replication protein A, resulting in accumulation of immunostimulatory cytosolic DNA. We further found that deficient RSR coincided with increased intratumoral dendritic cells in both mouse cancer models and human tumors. Together, this work demonstrates the RSR defect gene signature can accurately identify patients who may benefit from ICB across numerous non-hypermutated tumor types, and pharmacological induction of RSR defects may further expand the benefits of ICB to more patients.

Velocities of irregular particles are difficult to measure and analyse owing to their irregular shapes. In this study, the method of spatial filtering velocimetry is used to measure the velocities at which the particles flow on a surface in the roll mode. The images of the particle flow show that the surface is not a straight line but mound exists due to the accumulation of particles at the middle of the drum which influence the velocity profile. The variation of the velocity distribution of irregular particles with drum speeds, particle sizes, and drum diameters is presented and discussed in the paper. The results indicate that there were two velocity peaks in the velocity profile of irregular glass sand at a relatively lower rotating speed. Furthermore, with the increase in the drum speed, the middle valley in the profile gradually moves to the upper right and merges with the second velocity peak, and consequently, there is only one peak in the velocity profile along streamwise direction of the bed surface which is consequently similar to spherical particles velocity profile.

In this study, we develop the spatial filtering velocimetry (SFV) technique to measure the velocity distribution of small spherical and irregular particle flows using a linear CCD camera. In addition, energy barycentre correction algorithm is used to enhance the measurement accuracy. A constantly running conveyor belt is used to test the accuracy of this SFV system. Furthermore, the velocity distributions of the spherical and irregular particle flows in a rotating drum are measured to demonstrate the usability of this method in a granular system. We further discuss the effect of the key system parameters on the results of the measurement, and the optimal thresholds of the parameters are given in this paper.

PURPOSE/OBJECTIVE(S) Cancer Associated Macrophage-Like cells (CAMLs) are a type of circulating stromal cell found in the blood of cancer patients (pts), described as of myeloid origin that represent the inflammatory state of the tumor microenvironment. We have previously reported that in non-small cell lung carcinoma (NSCLC), CAML PD-L1 expression is dynamic and trackable throughout chemoradiation (CRT). However, it is unknown if PD-L1 on CAMLs has clinical utility, particularly in immunotherapy (IMT) efficacy after CRT. We studied stage 3 unresectable NSCLC pts treated with (n = 80) or without (n = 55) IMT agents after CRT to evaluate CAML PD-L1 expression on progression free survival (PFS) & overall survival (OS). MATERIALS/METHODS We used 2 sets of IMT treated pts: first set from a single arm phase 2 trial treated with CRT and atezolizumab (atezo) (n = 34) and a second from a multi-year prospective study treated with standard of care CRT with consolidation durvalumab (durva) (n = 46). A control group of CRT alone pts (n = 55) were evaluated during the same period (majority before 2018). In all, 135 pts with pathologically confirmed unresectable stage 3 NSCLC were included. 15mL blood samples were taken at Baseline (BL) & ∼1 month after completion of CRT. Blood was filtered & CAMLs quantified for PD-L1 expression using a binary score (0/1 = low & 2/3 = high), to evaluate PFS & OS hazard ratios (HRs) by censored univariate & multivariate analysis at 24 months. RESULTS CAMLs were found in 92% of all samples, on average 5.2 CAMLs/15mL. From the available tumor biopsies, > 1% PD-L1 expression using DAKO 22c3 did not predict CRT+IMT (atezo/durva) response (PFS HR 1.4 P = 0.642 & OS HR 1.9 P = 0.293). At BL, high CAML PD-L1 was not associated with PFS in CRT alone (HR 1.5 P = 0.435), CRT+atezo (HR 1.0 P = 0.843), or CRT+durva (HR 1.6 P = 0.6180). After CRT, while high CAML PD-L1 did not predict PFS in CRT alone (HR 1.0 P = 0.925), it was associated with superior PFS in CRT+atezo (HR 2.8 P = 0.046), & CRT+durva (HR 5.2 P = 0.036). For OS, high CAML PD-L1 was not predictive of outcomes in CRT alone (HR 0.8 P = 0.929), but strongly predictive of superior OS for CRT+atezo (HR 4.3 P = 0.036) & CRT+durva (HR 5.9 P = 0.033) groups. Combined (atezo or durva, n = 80), 57% of pts had either maintained high PD-L1 before and after CRT (N = 25) or increased from BL (N = 21). Pts with high PD-L1 post CRT had better outcomes than pts with low expression, PFS HR = 4.1 P < 0.001 and OS HR = 4.7 P < 0.001. This pattern was not seen in pts treated with CRT alone (PFS HR = 1.2 P = 0.763 and OS HR = 0.9 P = 0.977). CONCLUSION Our data suggests that in unresectable stage 3 NSCLC, high PD-L1 expression on CAMLs after CRT completion is predictive of superior clinical outcomes in pts treated with IMT, but not in those treated with CRT alone. Prospective validation is needed to confirm these findings.

BackgroundWhile immune checkpoint blockade is regarded as standard of care for treatment of non-small cell lung cancer (NSCLC), up to 50% of patients with metastatic NSCLC do not achieve an optimal response.1–3 Previous work by our group and others in adoptive cell therapy (ACT) of metastatic melanoma (MM) has shown that infusion of a CD8+-rich TIL product significantly improved clinical outcomes, yet traditional IL-2 expansion methods have resulted in a predominantly CD4+ NSCLC TIL expansion product.7–12 This preclinical study explores the feasibility of producing a tumor-specific, CD8+-enriched NSCLC TIL product for ACT with an improved culture method.MethodsTIL from resected NSCLC tumors were cultured using 1) the traditional method using IL-2 alone in 24-well plates (TIL 1.0) or 2) IL-2 in combination with agonistic antibodies against CD3 and 4-1BB (Urelumab) in a G-Rex flask (TIL 3.0). Expanded TIL were phenotyped using flow cytometry for CD4 and CD8 subset assessment and the CDR3-beta variable region of the T-cell receptor (TCR) involved in antigen binding was sequenced to assess the T-cell repertoire.ResultsIn a shorter manufacturing time (median of 14 days vs 27.5 days), TIL 3.0 expanded on average 5.3-times more NSCLC TIL (95% CI= 4.3–6.2, pConclusionsThis study reports the feasibility of using the TIL 3.0 methodology to robustly expand a CD8+ T-cell repertoire which maintains the respective clonal hierarchy in NSCLC tumors and enriches for putative tumor-specific TIL clones. The robustness and speed of the new process may facilitate testing and implementing effective TIL ACT in NSCLC.ReferencesGaron EB, Rizvi NA, Hui R, Leighl N, Balmanoukian AS, Eder JP, et al. Pembrolizumab for the treatment of non-small-cell lung cancer. N Engl J Med 2015;372(21):2018–28.Borghaei H, Paz-Ares L, Horn L, Spigel DR, Steins M, Ready NE, et al. Nivolumab versus Docetaxel in Advanced Nonsquamous Non-Small-Cell Lung Cancer. N Engl J Med 2015;373(17):1627–39.Gettinger S, Horn L, Jackman D, Spigel D, Antonia S, Hellmann M, et al. Five-Year Follow-Up of Nivolumab in Previously Treated Advanced Non-Small-Cell Lung Cancer: Results from the CA209–003 Study. J Clin Oncol 2018;36(17):1675–84.Melioli G, Ratto G, Guastella M, Meta M, Biassoni R, Semino C, et al. Isolation and in vitro expansion of lymphocytes infiltrating non-small cell lung carcinoma: functional and molecular characterisation for their use in adoptive immunotherapy. Eur J Cancer 1994;30A(1):97–102.McGranahan N, Furness AJ, Rosenthal R, Ramskov S, Lyngaa R, Saini SK, et al. Clonal neoantigens elicit T cell immunoreactivity and sensitivity to immune checkpoint blockade. Science 2016;351(6280):1463–9.Rosenberg SA, Yang JC, Sherry RM, Kammula US, Hughes MS, Phan GQ, et al. Durable complete responses in heavily pretreated patients with metastatic melanoma using T-cell transfer immunotherapy. Clin Cancer Res 2011;17(13):4550–7.Besser MJ, Shapira-Frommer R, Treves AJ, Zippel D, Itzhaki O, Hershkovitz L, et al. Clinical responses in a phase II study using adoptive transfer of short-term cultured tumor infiltration lymphocytes in metastatic melanoma patients. Clin Cancer Res 2010;16(9):2646–55.Pilon-Thomas S, Kuhn L, Ellwanger S, Janssen W, Royster E, Marzban S, et al. Efficacy of adoptive cell transfer of tumor-infiltrating lymphocytes after lymphopenia induction for metastatic melanoma. J Immunother 2012;35(8):615–20.Radvanyi LG, Bernatchez C, Zhang M, Fox PS, Miller P, Chacon J, et al. Specific Lymphocyte Subsets Predict Response to Adoptive Cell Therapy Using Expanded Autologous Tumor-Infiltrating Lymphocytes in Metastatic Melanoma Patients. Clinical Cancer Research 2012;18(24):6758–70.Forget MA, Haymaker C, Hess KR, Meng YJ, Creasy C, Karpinets T, et al. Prospective Analysis of Adoptive TIL Therapy in Patients with Metastatic Melanoma: Response, Impact of Anti-CTLA4, and Biomarkers to Predict Clinical Outcome. Clin Cancer Res 2018;24(18):4416–28.Ben-Avi R, Farhi R, Ben-Nun A, Gorodner M, Greenberg E, Markel G, et al. Establishment of adoptive cell therapy with tumor infiltrating lymphocytes for non-small cell lung cancer patients. Cancer Immunol Immunother 2018;67(8):1221–30.Ma Y, Ou J, Lin T, Chen L, Wang J, Qiao D, et al. Phenotypic analysis of tumor-infiltrating lymphocytes from non-small cell lung cancer and their potential application for adoptive cell therapy. Immunopharmacol Immunotoxicol 2020;42(4):319–29Ethics ApprovalThis study was performed on NSCLC tumor tissue resected from 16 patients enrolled, following informed consent, in the ImmunogenomiC prOfiling of early-stage NSCLC (ICON) project. This study was approved by the University of Texas MD Anderson Cancer Center‘s Institutional Review Board (protocol number PA15-1112_MODCR001).

PURPOSE/OBJECTIVE(S) Systemic therapy is often held during radiation treatment for metastatic lesions due to the risk for toxicity. However, holding systemic therapy can result in increased risk of disease progression. In this study, we investigated whether continuing targeted therapy during lung stereotactic body radiation therapy (SBRT) leads to increased toxicity. MATERIALS/METHODS Using our institutional prospectively collected genome-marker database, we identified 67 patients who were treated with SBRT to the lung while receiving tyrosine kinase inhibitor (TKI) targeted therapies for stage IIIB/IV oncogene-driven lung cancers. We segregated patients based on whether they had continuation of TKI treatment during radiation or had TKI held until completion of radiation. We gathered demographic, treatment, toxicity, and outcome data and compared toxicity and local control between the two groups using multivariate regression analysis. RESULTS For our cohort, median age at radiation treatment was 61.3, 67% were females, and median follow up was 19.8 months. Karnofsky performance status of patients at the time of radiation ranged from 70-90 with the majority at 90. 94% of patients (n = 63) had adenocarcinoma histology. 6 patients had ALK translocation mutation, 1 patient had BRAF mutation, 57 patients had EGFR mutations, 1 patient had MET exon 14 skipping mutation, and 2 patients had ROS1 fusion. At the time of radiation, patients were on the following targeted therapies: afatinib (n = 10), alectinib (n = 1), brigatinib (n = 3), crizotinib (n = 5), dabrafenib/trametinib (n = 1), erlotinib (n = 20), gefitinib (n = 3), osimertinib (n = 23), and poziotinib (n = 1). 37 patients had continuation of TKI therapy during radiation, while 30 patients had TKI therapy held during radiation. The radiation regimens are shown in the table. No patients had grade 3 or higher toxicity. 2 patients in the concurrent group had grade 2 pneumonitis compared to 1 in the held group. Local control in the continuation group was 97% compared to 93% in the held group. On multivariate analysis including age, sex, KPS, fractionation, and type of TKI, holding TKI therapy was not a significant factor influencing the likelihood of grade 2 pneumonitis (P = 0.75) or local control (P = 0.87). CONCLUSION Our results suggest that continuing TKI therapy during lung SBRT does not result in increased pulmonary toxicity. Thus, patients may not necessarily require a break from TKI treatment while undergoing SBRT, but more work will be required to assess the toxicities of each TKI in combination with radiation.

Rectal preservation is gaining popularity in the surgical treatment of degenerated rectal polyps or early rectal cancer (1,2). Tis/T1 rectal lesions can be safely treated without chemoradiation (3). Treatment by transanal minimally invasive surgery (TAMIS) offers more advantages than endoscopic submucosal dissection (ESD) (4). The authors report a 60 year-old woman who underwent TAMIS for a large polyp located anteriorly in the middle 1/3 of the rectum, 7 cm from the dentate line and staged preoperatively as uTisN0M0. This article is protected by copyright. All rights reserved.

Introduction: Differences in the host immune environment are thought to mediate heterogeneous treatment responses in non-small cell lung cancer (NSCLC). Unlike individual platform analyses, integrative analysis of multi-platform profiling allows for the discovery of novel interactions that expand our understanding of the disease. Utilizing the ImmunogenomiC prOfiling of NSCLC patient cohort (ICON), a prospective multi-omics protocol of operable early-stage NSCLC tumors with integrated immune, genomic, and clinical data, we hypothesized that multi-platform analyses would identify differences in the immune-genomic landscape that are associated with disease recurrence. Methods: Tumor and tumor-adjacent uninvolved lung was collected at resection; blood was collected before and after surgery. Tissue samples underwent WES, RNAseq, TCR sequencing (TCRseq), multiplex immunofluorescence (mIF), and RPPA profiling; tissue and blood (PBMC) samples were analyzed by flow cytometry. An integrated, inter-modality network was built using Spearman correlations between measurement pairs from different data modalities. Multivariate analysis was performed to adjust for stage and histology. Results: A total of 89 treatment-naïve patients with Stage 1-3 resected NSCLC (Squamous: 19; Non-squamous: 70) and 24 months of follow-up were analyzed (recurrence N = 24; no recurrence N = 65). The data network includes over 4,000 measurements linked by over 50,000 correlations. InfoMap, a community detection approach, was used to extract sub-network modules, which were used to contextualize the results of multivariate analysis. Tumors from patients with recurrence demonstrated decreased immune cell infiltration and activation including decreased cytotoxic CD8 T-cells (CD8+PD1+; fold-change (FC) = 0.898, p = 0.018; flow cytometry), decreased T-cell clonality (FC = 0.954, p = 0.017; TCRseq), and decreased tumor-associated macrophages (CD68+PD-L1+; FC = 0.426, p = 0.011; mIF). Furthermore, circulating CD8+ICOS+ activated T cells were decreased in patients with recurrence suggesting an impaired systemic anti-tumor immune response (FC = 0.552, p = 0.042; PBMC Flow). Finally, tumor-adjacent uninvolved lungs showed distinct T-cell phenotypes with accumulation of inactive CD8 T-cells (CD8+PD1-TIM3-) in patients with recurrence and increased populations of activated CD8 T-cells (CD8+PD1+) in patients without recurrence. Conclusion: Integrative multi-omic analysis suggests preserved anti-tumor immune surveillance in patients who are disease-free after 2 years from surgical resection with curative intent for treatment of NSCLC relative to patients with disease recurrence. Further analysis is ongoing to interrogate genomic and immune variables that are associated with disease recurrence. Citation Format: Neal Akhave, Stephanie Schmidt, Alexandre Reuben, Tina Cascone, Jianhua Zhang, Jun Li, Junya Fujimoto, Lauren A. Byers, Beatriz Sanchez-Espiridion, Lixia Diao, Jing Wang, Lorenzo Federico, Marie-Andree Forget, Daniel J. McGrail, Annikka Weissferdt, Shiaw-Yih Lin, Younghee Lee, Carmen Behrens, Ignacio I. Wistuba, Andrew Futreal, Ara Vaporciyan, Boris Sepesi, John V. Heymach, Chantale Bernatchez, Cara Haymaker, Jianjun Zhang, Christopher A. Bristow, Marcelo V. Negrao, Don L. Gibbons. Integrated multi-platform profiling of early-stage non-small cell lung cancer identifies relationship between disease recurrence and decreased native immune response in treatment-naïve resected NSCLC [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2021; 2021 Apr 10-15 and May 17-21. Philadelphia (PA): AACR; Cancer Res 2021;81(13_Suppl):Abstract nr 619.

Alkali-heat treatment (AHT) is an effective surface treatment technology for improving the bioactivity of medical metal biomaterials. However, the effects of AHT on the biocompatibility of the original material are not yet fully clear. Accordingly, in the present study, tantalum (Ta) coatings are deposited on Ti6Al4V substrates using a vacuum plasma spraying (VPS) technique and the coatings are then processed using either alkali treatment (AT) or AHT using 0.5 M and 1.0 M NaOH aqueous solution. In vitro bioactivity tests are performed in simulated body fluid for 3~14 days. It is shown that the surface of the AHT sample treated with 0.5 M NaOH (0.5 M AHT) has excellent bioactivity, irrespective of whether or not ultrasonic cleaning (UC) is performed following the heat treatment process. The surface of the AHT sample processed with 1.0 M NaOH (1.0 M AHT) contains a large number of irregular block-shaped compounds, which hinder the bioactivity of the coating. However, following UC treatment, the block-shaped compounds are removed, and the bioactivity of the AHT-UC sample is similar to that of the 0.5 M AHT sample. In in vitro biocompatibility tests for 1–7 days, the Ta coating and 0.5 M AHT-UC coating exhibited significantly better cellular attachment, growth, spreading, and viability of osteoblast-like osteosarcoma MG-63 cells than the 1.0 M AHT-UC coating. It is speculated that this is due to the presence of excess amorphous sodium tantalate on the surface of the 1.0 M AHT-UC coating. Overall, the present results show that AHT treatment performed with an appropriate NaOH concentration yields a significant improvement in both the bioactivity and the biocompatibility of VPS Ta coatings.

In this paper, we demonstrate a novel Source Drain Extension (SDE) approach to enable NMOS device scaling along with improved performance. For the first time, SDE formation with epitaxially grown As doped Si (Si:As) has been examined and compared to the current state-of-the-art SDE formation in FinFET at 10nm logic ground rules. It is found that a Si:As layer based SDE provides a clear improvement in the short channel effect and a significant device performance increase. It is also shown that a careful co-optimization of the Si:As layer and Source / Drain (S/D) lateral recess is required to achieve the optimum device gain. This paves the way for the ultimate nSDE formation for current and next generation CMOS devices.

FinFET doping via implantation at room temperature could result in Fin damage within the Fin body and degrade Fin device performance. Heated implantation techniques are developed to address the detrimental effects on devices caused by the damage. The wafer can be maintained at specific temperature on the platen while the implantation is in progress. The wafer substrate temperature can affect the implant caused damage cascade by enhancing or retarding the interstitial and vacancy (IV) recombination process.In this paper, the heated implantation technique was applied to IO FinFET LDD formation. Since IO devices operate at relative high voltage and electrical field which could result in higher leakage, multiple implants were used to tailor the junction to mitigate so-called band to band tunneling (BTBT) leakage. A scaled FinFET with tight pitch demands higher implanted dose to form a suitable junction for leakage control. However, increased dose induces more damage to the Fin which leads to device degradation. Therefore, implant damage should be mitigated to achieve device performance gain by LDD implant. We will present bare wafer SIMS profile studies and device results along with TCAD simulations, comparing room temperature and heated temperature implants. 14nm FinFET device studies showed 3–5% device gain with heated implant and it demonstrated heated implant technique can bring device benefits for further scaled FinFET.

On 22 Aug 2003, an unknown disease was found on banana (Musa nana) leaves in the Guangxi Agro-Reclamation State-owned Jinguang Farm (22°48´37˝N, 107°58´51˝E), Nanning, China. The disease occurred only on the rainy …

In this investigation, the transmittance and electrical properties of NiFe thin films were measured under three conditions. NiFe thin films were sputtered on a glass substrate with a thickness ( t f ) from 300 A to 1500 A under the following conditions: (a) substrate temperature ( T s ) maintained at room temperature (RT), (b) post-annealing at T A =150 °C for 1 h, and (c) post-annealing at T A =250 °C for 1 h. Transmission electron microscopy (TEM) demonstrated that the NiFe film yielded a strong face-centered cubic (FCC) (1 1 1) selected-area-diffraction (SAD) pattern. A spectral analyzer was utilized to measure transmittance through various thicknesses. Post-annealing treatment promoted the growth of grains, yielding a large average grain size, and therefore a small transmittance. However, electrical measurements revealed that increasing the electron mobility reduces the resistivity ( ρ ) and sheet resistance ( R s ). At a thickness of 300 A with post-annealing 250 °C, the optimal maximum transmittance is 50%; the optimal ρ is 110 μΩ cm, and the optimal R s is 13 Ω/□. Accordingly, a 300 A-thick NiFe thin film with favorable electrical and optical properties can be utilized in the components of a magneto-optical recording medium.