tbuckley/cabot-search huggingface dataset:
Bacteria-Driven Particles: Patterned and Specific Attachment of Bacteria on Biohybrid Bacteria-Driven Microswimmers (Adv. Healthcare Mater. 18/2016)
Authors: Ajay Vikram Singh, Metin Sitti
Journal: Advanced Healthcare Materials (2016)

On page 2325, Ajay Vikram Singh and Metin Sitti propose a facile surface patterning technique and a specific, strong biotin–streptavidin bonding of bacteria on patterned surfaces to fabricate Janus particles that are propelled by the attached bacteria. Such bacteria-driven Janus microswimmers could be used for future medicine in targeted drug delivery and environmental remediation.
Dynamic GABAergic afferent modulation of AgRP neurons
Authors: Alastair S Garfield, Bhavik P Shah, Christian R Burgess, Monica M Li, Chia Li, Jennifer S Steger, Joseph C Madara, John N Campbell, Daniel Kroeger, Thomas E Scammell, Bakhos A Tannous, Martin G Myers, Mark L Andermann, Michael J Krashes, Bradford B Lowell
Journal: Nature Neuroscience (2016)
Number and type of TET2 mutations in chronic myelomonocytic leukemia and their clinical relevance
Authors: M M Patnaik, M F Zahid, T L Lasho, C Finke, R L Ketterling, N Gangat, K D Robertson, C A Hanson, A Tefferi
Journal: Blood Cancer Journal (2016)

TET2, located on chromosome 4q24, is frequently mutated (~60%) in patients with chronic myelomonocytic leukemia (CMML). 1,2TET2 has 11 exons, and variations, especially in exon 3 have been described as a part of age-related clonal hematopoiesis. 3 In a large population-based study (n = 17 182), somatic variations involving DNMT3A, TET2 and ASXL1 were seen in ~11% of the population 480 years of age, and in comparison with patients without clonal hematopoiesis, were associated with an increased risk of hematological malignancies (HR-11.1)and all-cause mortality (HR-3.7). 3 In CMML, thus far, clonal TET2 mutations in the absence of clonal ASXL1 mutations (ASXL1wt/TET2mt) have been associated with favorable outcomes. 1,4The exact mechanism behind this interaction remains to be elucidated, one potential explanation being better responses to hypomethylating agents. 4In the current larger CMML patient cohort (n = 261), we describe the number and type of TET2 mutations and examine their phenotypic and prognostic effects.Two hundred and sixty one patients with CMML were included in the study.All patients had bone marrow (BM) biopsies and cytogenetics performed at diagnosis.Targeted capture assays were carried out on BM DNA specimens obtained at diagnosis for the following genes: TET2, DNMT3A, IDH1, IDH2, ASXL1, EZH2, SUZ12, SRSF2, SF3B1, ZRSR2, U2AF1, PTPN11, Tp53, SH2B3, RUNX1, CBL, NRAS, KRAS, JAK2, CSF3R, FLT3, KIT, CALR, MPL, NPM1, CEBPA, IKZF and SETBP1, by previously described methods. 1 TET2 (NM_001127208.2) coverage extended from exons 3-11, with frame shift, nonsense and missense variations considered pathogenic.Previously annotated single nucleotide polymorphisms (http//www.hapmap.org)were considered non-pathogenic.The 2008 and 2016 World Health Organization (WHO) criteria were used for CMML diagnosis and classification. 5mong the 261 study patients, 65% were males and median age was 70 years (range, 28-91).One hundred and fifty four (59%), 64 (25%) and 43 (16%) patients were classified as CMML-0, 1 and 2, respectively.At a median follow-up of 23 months, 174 (67%) deaths and 37 (14%) leukemic transformations were documented.
Implementing genomically-guided trials in non-small cell lung carcinoma (NSCLC).
Authors: A. Potti, G. Vlahovic, F. Dunphy, W. Barry, M. B. Datto, T. A. D'Amico, J. Crawford, G. S. Ginsburg, J. R. Nevins, N. Ready
Journal: Journal of Clinical Oncology (2010)

e18003 Background: The incorporation of prognostic and predictive microarray-based biomarker assays in clinical trials or routine clinical practice is challenging. We report the methodology and design of prospective, phase II, gene expression based, directed chemotherapy trials in NSCLC. Methods: Using an Affymetrix platform, we developed genomic signatures of sensitivity to chemotherapy in NSCLC. Retrospective studies validated the sensitivity and specificity of these signatures. We initiated two prospective phase II clinical trials in NSCLC. TOP0703 is an adjuvant study that stratifies between cisplatin + pemetrexed or cisplatin + vinorelbine using genomic predictors of pemetrexed and vinorelbine in non-squamous histology. TOP602 is an advanced stage study stratifying by predicted sensitivity to cisplatin and histology: cisplatin sensitive (cisplatin + pemetrexed for non-squamous or cisplatin + gemcitabine for squamous) and cisplatin resistant (pemetrexed + gemcitabine for non-squamous or docetaxel + gemcitabine for squamous). Results: After investigating signature analytic performance in biologic replicates, we began applying them in the contexts of prospective, directed chemotherapy clinical trials designed to demonstrate feasibility of the approach and validate the predictors of chemosensitivity. 21 patients have been accrued to the adjuvant (TOP0703) NSCLC trial and 34 patients in the advanced (TOP0602) lung trial. In the advanced lung study, the real-time processing to direct therapy is 5-7 business days. In the adjuvant trial, 91% of resected tumors yielded high quality RNA for analysis. In the advanced stage NSCLC study, a core biopsy of 18G or larger and visceral biopsy sites (e.g. lymph node, liver) were more likely to yield high quality genomic data. Procedure-related adverse events and chemotherapy related toxicities were typical of routine clinical practice. Conclusions: Genome-wide microarray expression profiles are robust, and can be practically obtained in NSCLC and applied in prospective clinical trials. Ultimately, the data from these prospective trials will be invaluable in assessing the feasibility and validity of such an approach. Author Disclosure Employment or Leadership Position Consultant or Advisory Role Stock Ownership Honoraria Research Funding Expert Testimony Other Remuneration Exeression Analysis, Inc., Lilly Expression Analysis, Inc. Lilly Lilly
Response to Comment on the FLAT-SUGAR Trial Investigators. Glucose Variability in a 26-Week Randomized Comparison of Mealtime Treatment With Rapid-Acting Insulin Versus GLP-1 Agonist in Participants With Type 2 Diabetes at High Cardiovascular Risk. Diabetes Care 2016;39:973–981
Authors: Kevin D. O’Brien, Irl B. Hirsch, Matthew C. Riddle, Jeffrey L. Probstfield
Journal: Diabetes Care (2016)

We thank Monnier et al. (1) for both their interest in our trial (2) and their thoughtful comments. We appreciate their suggestion regarding a possible relationship between exogenous insulin dosage and the observed levels of urinary 8-iso-prostaglandin F2α, which we plan to address in the future in a more …
Case 46-1969
Authors: William H. Baker, Benjamin Castleman
Journal: New England Journal of Medicine (1969)

Presentation of CaseAn eighty-year-old woman was admitted to the hospital because of pain in the back.She had been well until four months previously, when there was the onset of gradually increasing pain in the lower portion of the back. X-ray films of the spine showed mild osteopenia consistent with her age. Analgesics, heat, bed rest and a corset did not afford relief, and the pain subsequently migrated to different areas of the thoracic and lumbar spine. There was no weakness or paresthesia. On the day before admission the pain was markedly aggravated by a sudden movement.There was . . .
Correlation of regulatory T-cell levels and overall survival in metastatic renal cancer patients treated with sunitinib-based therapy.
Authors: E. Tartour, O. Adotevi, H. Pere, B. Beuselinck, J. Ayllon, J. Medioni, S. Oudard
Journal: Journal of Clinical Oncology (2010)

4619 Background: Sunitinib, an anti-angiogenic drug, is one of the first-line treatment of care in patients with metastatic renal cell carcinoma (mRCC). However, it only benefits to a subgroup of patients and no predictive markers of sunitinib efficacy have been identified. Methods: Twenty eight mRCC were treated with sunitinib-based therapy and a subgroup of 7 primary renal cell cancer patients were also treated by sunitinib in a neoadjuvant trial (2 cycles of sunitinib prior to nephrectomy). Measurements of CD3+CD4+CD25hi Foxp3+ regulatory T cells, an immunosuppressive cell population, were performed before and after each cycle of treatment in blood and tumor. Results: We observed a decrease in the number of Foxp3+CD4+CD25hi regulatory T cells during each cycle of sunitinib-based therapy. The overall survival was significantly longer in patients showing a decrease in the number of Foxp3+ regulatory T cells after 2 or 3 cycles of treatment (p < 0.05). The decrease in the number of regulatory T cells after sunitinib-based therapy positively correlated with the number of regulatory T cells at baseline. The clinical relevance of these results was also supported by an intratumoral decrease of regulatory T cells in 5 out of 7 patients treated by sunitinib in the neoadjuvant trial. Conclusions: Our study represents the first work reporting that the measurement of immune parameters (regulatory T cells) may have a predictive value on anti-angiogenic response. Anti-angiogenic therapy also reversed some levels of immunosuppression in the tumor microenvironment which provides novel argument in human to favour its combination with immunotherapy. No significant financial relationships to disclose.
HLA-Haploidentical Related Hematopoietic Stem Cell Transplantation and Mesenchymal Stem Cell Transplantation in Patients with Hematologic Malignancies.
Authors: Xiaoyan Zhang, Jianyong Li, Kejiang Cao, Hanxin Wu, Hua Lu, Sixuan Qian, Wei Xu, Peng Liu, Lijuan Meng, Yu Zhu
Journal: Blood (2006)
Large Scale Alterations in Hepatic MRNA and MIRNA Expression in Human Extrahepatic Cholestasis
Authors: F.G. Schaap, Z. Soons, L. Fischer, M.J. Jetten, D. Jennen, J.C. Kleinjans, P.L. Jansen, S.W. Olde Damink
Journal: Journal of Hepatology (2016)
The Importance of CD33 Expression and Pro-Apoptotic Signalling for Gemtuzumab Ozogamicin-Induced Cytotoxic Effects on AML Cells
Authors: Marita Lagergren Lindberg, Petra Hååg, Kristina Viktorsson, Lena Kanter, Rolf Lewensohn, Leif Stenke
Journal: Blood (2008)
A Multicenter, Randomized, Open Label, Single- and Multiple-Dose, Dose Finding Study and Open-Label Extension to Assess the Effects of Obeticholic Acid in Pediatric Patients with Biliary Atresia
Authors: S. Karpen, L. Eliot, B. Scholz, M.M. Joshi, M.M. Merrigan, C. Sciacca, T. Marmon, R. Hooshmand-Rad, L. MacConell, D. Shapiro
Journal: Journal of Hepatology (2016)
Novel X-Linked Inhibitor of Apoptosis (XIAP) Inhibiting Compound as Sensitizer for TRAIL-Mediated Apoptosis In Chronic Lymphocytic Leukemia with Poor Prognosis
Authors: Lukas P. Frenzel, Michaela Patz, Christian P. Pallasch, Reinhild Brinker, Julia Claasen, Alexandra Schulz, Michael Hallek, Hamid Kashkar, Clemens-Martin Wendtner
Journal: Blood (2010)
Effect of a combination of atiprimod and the proteasome inhibitor bortezomib on apoptosis of mantle cell lymphoma in vitro and in vivo.
Authors: M. Wang, L. Zhang, L. Sun, J. Qian, J. Yang, Q. Yi
Journal: Journal of Clinical Oncology (2010)

e18529 Background: The proteasome inhibitor bortezomib (BTZ) induces apoptosis and sensitizes mantle cell lymphoma (MCL) cells to chemotherapy in relapsed or refractory MCL. Atiprimod (ATI), as a novel cationic amphophilic compound, displays significant anti-MCL effect in vitro and in xenograft mouse model. This study was to evaluate the effect of ATI and BTZ combination on MCL and to elucidate their therapeutic mechanisms. Methods: The established cells and freshly isolated MCL cells from refractory or relapsed MCL patients were incubated with ATI and/or BTZ and the effects on cell proliferation, cell cycle, and apoptosis were analyzed using 3H-thymidine incorporation assay, flow cytometry, immunoblotting, and MCL-bearing mouse model. Results: We found that ATI and BTZ synergistically induced the growth inhibition and apoptosis of both established MCL cells and freshly isolated tumor cells from relapsed or refractory MCL patients. Furthermore, ATI and BTZ induced apoptosis via two different signaling pathways. BTZ induced apoptosis via activation and cleavage of caspases-3, -8, -9, and PARP. The pan-caspase inhibitor Z-VAD-FMK completely blocked BTZ- but not ATI-induced apoptosis. ATI, but not BTZ, induced apoptosis by releasing apoptosis-inducing factor (AIF) from mitochondria to cytosol in MCL cells. Importantly, ATI plus BTZ synergistically delayed the tumor growth and prolonged the survival in MCL-bearing NOD-SCID mice. Conclusions: The results demonstrate that ATI and BTZ display synergistically therapeutic effects on MCL cells via activating two distinct apoptotic signaling pathways. The ATI and BTZ combination should be investigated in a clinical trial in patient with relapsed or refractory MCL. No significant financial relationships to disclose.
HBeAg Seroconversion Rates after Five Years of Follow-Up in Patients Treated with Peginterferon Alfa-2a (40kd) in Neptune: Final Results of the Son of Neptune Long-Term Follow-Up Study
Authors: W.-L. Chuang, J. Jia, H.L.-Y. Chan, K.-H. Han, T. Tanwandee, D. Tan, X. Chen, E. Gane, T. Piratvisuth, L. Chen, Q. Xie, J.J.-Y. Sung, D. Messinger, C. Wat, G. Bakalos, Y.-F. Liaw
Journal: Journal of Hepatology (2016)
Association of Medical School Pediatric Department Chairs Principles of Lifelong Learning in Pediatric Medicine
Authors: Valerie P. Opipari, Stephen R. Daniels, Robert W. Wilmott, Richard F. Jacobs
Journal: JAMA Pediatrics (2016)

Pediatric general and subspecialty care requires continuous effort to maintain knowledge and competencies in clinical practice. Equally important are efforts by investigators and educators to maintain knowledge and competencies in the conduct of research and training. The Association of Medical School Pediatric Department Chairs initiated a survey in July 2015 to define principles of lifelong learning in pediatric medicine and determine the approaches and strategies used by chairs to assess knowledge and competence across the care, research, and teaching missions. A total of 101 of 142 chairs (71%) completed the survey. Six of 7 proposed principles were endorsed by 84% to 96% of Association of Medical School Pediatric Department Chairs members. The focus areas included individual accountability, individually relevant activities, use of evidence-based guidelines/national standards, gaining cognitive expertise, learning as a continuous effort, affordability, and focus on individual understanding. The chairs endorsed a requirement for evidence of lifelong learning, competence, and compliance by all faculty members in clinical (n = 89 [88%]), research (n = 63 [62%]), and educational (n = 85 [84%]) practice. The survey identified the strategies to assess lifelong learning and faculty competence and compliance in clinical, research, and educational roles. Across missions, chairs endorsed an expectation for individual responsibility supplemented by formal evaluation practices and institutional and regulatory office oversight. While chairs endorsed an important role for the American Board of Pediatrics in assessing and verifying lifelong learning, knowledge, and competence in general and specialty certification, most (n = 91 [90%]) endorsed a need to revise current board requirements to better emphasize closing gaps in knowledge and using approaches that are evidence-based. This study provides the perspectives of pediatric department chairs on principles for lifelong learning and strategies and approaches used to assess faculty competence and commitment to lifelong learning across missions.
The NIH Chronic Gvhd Global Score and the CIBMTR Risk Score Correlate Well with Failure Free Survival Following Frontline Systemic Corticosteroid Therapy for Chronic Gvhd
Authors: Jieun Uhm, Nada Hamad, Elizabeth M Shin, Vikas Gupta, John Kuruvilla, Jeffrey H. Lipton, Hans A. Messner, Matthew Seftel, Dennis Dong Hwan Kim
Journal: Blood (2014)
PGE2 induces cyclin D1 in colon cancer via the Wnt pathway
Authors: Jinyi Shao, Hongmiao Sheng
Journal: Cancer Research (2005)

6124   Inhibition of cyclooxygenase-2 (COX-2), a key enzyme for conversion of arachidonic acid to prostaglandins including PGE 2 , is often associated with reduced proliferation of cancer cells; the underlying mechanism is not completely understood. A large body of studies demonstrates a strong link between COX-2/PGE 2  signaling and the APC/β-catenin/TCF pathway in intestinal neoplasia. The most convincing evidence was provided by clinical trials conducted in Familiar Adenomatous Polyposis (FAP) patients that result from germline mutations of the  APC  gene. Administration of sulindac or celecoxib, which inhibit COX enzyme activity, significantly reduces size and number of polyps in these patients. In the present study, we show that PGE 2  activated the Wnt signaling pathway and induced the expression of a Wnt target gene cyclin D1  in vitro  and  in vivo . Exposure to PGE 2  rapidly increased levels of cyclin D1 protein in colon cancer LS-174 cells. PGE 2  increased the activity of  cyclin D1  promoter driving reporter vector 4.5-fold. Furthermore, expression of stabilized β-catenin (Δ-89) increased the activity of the  cyclin D1  promoter; however, in combination, PGE 2  and mutated β-catenin (Δ-89) induced the activity of  cyclin D1  promoter in a synergistic manner.  Cyclin D1  promoter contains both TCF and CRE binding sites; mutation of the CRE did not attenuate PGE 2  induced  cyclin D1  transcription. In contrast, TCF elements were critical for PGE 2 -induced  cyclin D1  promoter activity. In animal experiments, administration of PGE 2  significantly increased the levels of cyclin D1 protein in  APC min/+   mouse polyps. To confirm that PGE 2  was able to activate the Wnt pathway directly, LS-174 cells were transfected with a TCF reporter vector, TOPflash, which contains a combination of TCF binding sites. Exposure to PGE 2  increased in the transcriptional activity of TCF ∼10-fold. PGE 2  induced TCF activity in a concentration-dependent fashion; as low as 1 nM PGE 2  clearly activated TCF elements. To investigate the effect of PGE 2  on endogenous activity of the Wnt pathway, HCA-7 colon cancer cells were treated with low concentration celecoxib to block the generation of endogenous PGE 2 . Celecoxib at 0.1 μM reduced TCF activity by ∼ 50%, suggesting that HCA-7 generated PGE 2  was partially responsible for the endogenous activity of the Wnt pathway. Activation of the cAMP/PKA pathway was required for PGE 2  stimulation of the Wnt pathway, as a specific PKA inhibitor, H-89, completely attenuated the PGE 2  induced Wnt activity. In summary, COX-2 generated PGE 2  may stimulate the Wnt pathway directly and activate Wnt target genes. Given the critical roles of Wnt target genes in regulation of cell proliferation, migration, transformation, and neo-angiogenesis, our results provide a novel mechanism by which COX-2/PGE 2  signaling exerts pro-oncogenic effects in colorectal carcinogenesis.
Study on Knowledge Awareness of HBV and HCV among Mongolian Population
Authors: O. Lhagva-Ochir, P. Bat-Ulzii, D. Boldbaatar, M. Enkhbat, G. Jargalsaikhan, B. Dashtseren, B. Bold, N. Dahdorj, N. Dahdorj
Journal: Journal of Hepatology (2016)
Swine flu vaccine is unlikely to raise risk of overall birth defects, study finds
Authors: Jacqui Wise
Journal: BMJ (2016)

Being given the H1N1 influenza vaccine during pregnancy does not seem to be associated with an increased risk of overall birth defects, a Swedish study published in Annals of Internal Medicine has found.1 However, the researchers did not completely rule out a raised risk for specific birth defects.

Previous research has shown conflicting risk estimates for congenital malformation in pregnant women from the Pandemrix vaccine in the first trimester, with odds ratios ranging from 0.67 to 2.18.

The World Health …
Biphasic Kinetics of HCV-RNA Decay is Accompanied by an even Faster Aminotransferases Normalization in All-Daa Treated Cirrhotic Patients: A Different Scenario from Interferon-Based Therapies
Authors: V. Cento, D. Di Carlo, T.H.T. Nguyen, E. Biliotti, C. Pasquazzi, L. Gianserra, D. Di Paolo, V. Calvaruso, E. Teti, M. Cerrone, D. Romagnoli, M. Melis, E. Danieli, B. Menzaghi, E. Polilli, M. Siciliano, L.A. Nicolini, A. Di Biagio, C.F. Magni, F.P. Antonucci, V.C. Di Maio, R. Alfieri, L. Sarmati, P. Casalino, S. Bernardini, V. Micheli, G. Rizzardini, E. Villa, G. Parruti, T. Quirino, M. Puoti, S. Babudieri, A. D’A. Monforte, M. Andreoni, A. Craxì, I. Lenci, M. Angelico, G. Taliani, J. Guedj, F. Ceccherini-Silberstein, C.F. Perno
Journal: Journal of Hepatology (2016)
Liver Transplantation in Severe Neurological Forms of Wilson Disease; The French Experience
Authors: R. Sobesky, A. Poujois, A.S. Brunet, E. Broussolle, O. Guillaud, E. Salame, F. Maillot, C. Vanlemmens, B. Hermeziu, W. Meissner, V. De Ledinghen, R. Adam, D. Cherqui, D. Castaing, D. Samuel, F. Woimant, J.C.D. Vallée
Journal: Journal of Hepatology (2016)
Emergence of Preexisting MET Y1230C Mutation as a Resistance Mechanism to Crizotinib in NSCLC with MET Exon 14 Skipping
Authors: Sai-Hong Ignatius Ou, Lauren Young, Alexa B. Schrock, Adrienne Johnson, Samuel J. Klempner, Viola W. Zhu, Vincent A. Miller, Siraj M. Ali
Journal: Journal of Thoracic Oncology (2016)
Targeting Isoprenylcysteine Carboxyl Methyltransferase to Overcome Resistance and Improve Responses in Chronic Myeloid Leukemia.
Authors: Wen Tian Sun, Bee Ling Ng, Li Yi Yang, Mei Wang, William Hwang, Junia V. Melo, Brian J. Druker, Patrick J Casey, Charles Chuah
Journal: Blood (2009)
Molecular profile of synchronous metastatic colon cancer and anaplastic thyroid cancer in a patient with Lynch Syndrome.
Authors: Jennifer Maria Johnson, Jason Chen, Inderpreet K Dardi, Madalina Tuluc, Siraj Mahamed Ali, David Cognetti, Barbara G. Campling, Ashwin Reddy Sama
Journal: Journal of Clinical Oncology (2015)

e22049 Background: Lynch Syndrome is an autosomal dominant disorder caused by either germline mutation in a DNA mismatch repair gene: MLH1, MSH2, MSH6, or PMS2, or epigenetic silencing of MSH2. The syndrome consists of early onset malignancies and multiplicity of cancers. Colonic malignancies predominate with the frequency and distribution of extracolonic cancers dictated by the mutated gene. Methods: A 54 year old man with a family history of Lynch Syndrome and a MSH6 mutation was found to have synchronous colonic adenocarcinomas on screening colonoscopy. Within weeks he presented with a rapidly enlarging anaplastic thyroid cancer (ATC). On PET/CT he was found to have liver metastases (biopsy confirmed as colonic) and pulmonary metastases (biopsy confirmed as ATC). Tumor tissue from his colon and thyroid was sent for FoundationOne analysis of 343 genes. Cell free circulating tumor DNA (CtDNA) was sequenced for 54 genes using Guardant360 technology with blood taken post-thyroidectomy. Results: FoundationOne sequencing is shown below. The only shared mutation was the germline MSH6. Of the 16 mutated genes, 4 were included in the Guardant360 panel. The APC and KRAS mutations were detected in the CtDNA, as was a separate FBXW7 mutation and EGFR and ERBB2 mutations not seen in the Foundation One data. Conclusions: This patient is 1 of 3 cases of ATC in Lynch Syndrome, and the first associated with MSH6 and synchronous colon cancer. Molecular profiling shows a hypermutated phenotype, consistent with a loss of mismatch repair. The unique signatures in the anaplastic and colonic primaries are more likely indicative of tissue-specificity while the discordance with CtDNA may represent tumor heterogeneity, evolution of the tumor during chemotherapy, or the limits of our current technology. FoundationOne Anaplastic Thyroid FoundationOne Colon Guardant360 ctDNA MSH6 G1105fs*3 G1105fs*3, R988fs*11 Not Tested (NT) AKT1 E17K APC G1412* G1412* ARID1A I106fs*4 NT ATM R3008H NT BLM N515fs*16 NT FBXW7 R179C, R465C R385C KRAS A146T A146T MLL3 K2797fs*26 NT NOTCH1 Y550fs*1 NT PI3KCa R38C E81K, H1047R NT PTEN R335* NT RB1 265-1G>T NT SOX9 Q412* NT TSC1 E945* NT TP53 R196* R267W ERBB2 Not Detected (ND) ND R340R EGFR ND ND T130T