tbuckley/cabot-search huggingface dataset:
EXTH-46. ALISERTIB POTENTIATES THE EFFECT OF CABOZANTINIB AND VANDETANIB AGAINST GLIOBLASTOMA CELLS
Authors: Brian Williams, Cory Zumbar, Caroline Mifsud, Kendall Smith, Muge Sak, Norman Lehman
Journal: Neuro-Oncology (2019)

Abstract Glioblastoma is the most common primary malignant brain tumor in adults and has a poor prognosis with current standard of care. Aurora-A (AURKA) is a serine-threonine kinase critical for mitotic progression through its role in centrosome maturation and mitotic spindle assembly. Vascular endothelial growth factor (VEGF) is a regulator of tumor angiogenesis and vasculogenesis. Both AURKA and VEGF are commonly over-expressed in glioblastoma. The AURKA inhibitor alisertib and inhibitors of VEGF have been shown to inhibit glioblastoma cell proliferation in vitro and in vivo, and both have been used in clinical trials for glioblastoma. Here we tested the ability of alisertib to potentiate the effects of the VEGF receptor (VEGFR) inhibitors cabozantinib and vandetanib using colony formation assays in U1242 and U87 glioblastoma cell lines. Chou-Talalay and Bliss independence models demonstrated synergistic growth inhibition in some cases. Annexin V binding assays were performed to assess the extent that apoptosis could account for the inhibitory effects in U87 cells, and a concentration of alisertib that did not cause apoptosis as a single agent was found to increase the induction of apoptosis caused by cabozantinib. These results support the rationale for further in vitro and in vivo studies of the combined use of alisertib and VEGFR inhibitors, including possible future clinical trials.
DDIS-02. DEVELOPMENT OF NOVEL SPRAY-TYPE FLUORESCENT PROBES FOR GLIOBLASTOMA DETECTION
Authors: Yosuke Kitagawa, Shota Tanaka, Yugo Kuriki, Kyoko Yamamoto, Takahide Nejo, Satoshi Takahashi, Masashi Nomura, Taijun Hana, Tsukasa Koike, Yoshihiro Kushihara, Erika Yamazawa, Shunsaku Takayanagi, Akitake Mukasa, Mako Kamiya, Yasuteru Urano, Nobuhito Saito
Journal: Neuro-Oncology (2019)

Abstract PURPOSE: ALA is commonly used as an intraoperative tool in malignant glioma surgery, which has been proven effective for radical tumor resection and extended progression-free survival. However, there are some limitations in its use, such as false positivity, false negativity, and inability of re-administration. We aim to develop a novel fluorescent labeling system which can be repeatedly administered by spray during surgery, using hydroxymethyl rhodamine green (HMRG) as fluorescent scaffold originally designed at our university for cancer detection. [Methods]Primary probe screening was performed using the homogenized glioblastoma (GBM) samples with the fluorescent probe library comprised of more than 320 kinds of HMRG fluorescent scaffold combined with various types of dipeptides. Second probe screening was performed using fresh GBM specimens and the selected probes in primary screening. To identify the responsible enzymes, diced electrophoresis gel (DEG) assay was performed. This method utilizes the combination of two dimensional electrophoresis (isoelectric point and molecular weight) and a multiwell-plate-based fluorometric assay to find protein spots with the specified activities. [Results] The prominent probes were selected based upon the above two-step screenings. We identified two enzymes by proteome analysis and experiments using inhibitors, which was further confirmed with real-time PCR and western blotting. [Discussion] This screening methodology is innovative in that it is based on selecting probes from the probe library that respond to clinical samples rather than creating probes from the responsible enzymes. Practical fluorescent probes can be established even for low-grade gliomas, which would be a breakthrough for rapid intraoperative diagnosis in glioma surgery. [Conclusion] HMRG-based aminopeptidase fluorescent probes may be effective for GBM detection.
Prognostic Impact of t(4;11)(q21;q23)/KMT2A-AFF1-Positivity in 926 BCR-ABL1-Negative B-Lineage Acute Lymphoblastic Leukemia Patients Treated in Gimema Clinical Trials Since 1996
Authors: Alfonso Piciocchi, Monica Messina, Loredana Elia, Antonella Vitale, Stefano Soddu, Anna Maria Testi, Sabina Chiaretti, Marco Mancini, Giorgina Specchia, Antonio Spadano, Mauro Krampera, Roberto Cairoli, Francesco Di Raimondo, Felicetto Ferrara, Giuseppe Cimino, Renato Bassan, Paola Fazi, Marco Vignetti
Journal: Blood (2019)
DC Vaccination Induces Antigen Specific Immune Responses in AML Patients: A 1-Year Interim Assessment
Authors: Judith Eckl, Silke Raffegerst, Frauke Schnorfeil, Petra Prinz-Schulz, Christiane Fingerhut, Yngvar Floisand, Dag Josefsen, Iris Bigalke, Kai Pinkernell, Gunnar Kvalheim, Dolores Schendel, Anna Tafuri
Journal: Blood (2019)
Acute Leukemia and High-Risk Myelodysplastic Syndromes in HIV-Positive Patients: 25-Years' Experience of the Rete Ematologica Lombarda (REL)
Authors: Chiara Cattaneo, Massimo Bernardi, Valentina Mancini, Chiara Pagani, Monica Fumagalli, Patrizia Zappasodi, Erika Borlenghi, Alessandro Re, Fabio Ciceri, Margherita Sciumé, Roberto Cairoli, Giuseppe Rossi
Journal: Blood (2019)
TMOD-28. AUTHENTIC HUMAN GLIOMA MODELING USING GENETICALLY ENGINEERED INDUCED PLURIPOTENT STEM CELLS
Authors: Tomoyuki Koga, Isaac Chaim, Sebastian Markmiller, Jorge Benitez, Alison Parisian, Shunichiro Miki, Florian Hessenauer, Kristen Turner, Sriram Venneti, Denise Malicki, Robert Wechsler-Reya, Paul Mischel, Clark Chen, Gene Yeo, Frank Furnari
Journal: Neuro-Oncology (2019)

Abstract Many mouse and human glioma models have been utilized to study the genetic alterations involved in the genesis of these tumors, but they have not been fully evaluated for how closely they recapitulate pathobiology, including tumor heterogeneity, which is an inherent feature making patient treatment difficult. Here we present new glioma models using genetically engineered human pluripotent stem cells, in which authentic pathobiology is recapitulated through precision gene editing. Specifically, we show that neural progenitor cells (NPCs) derived from human induced pluripotent stem cells (iPSCs), with different combinations of genetic drivers introduced by CRISPR/Cas9-mediated editing give rise to distinct intracranial tumors recapitulating authentic pathobiology of the disease when engrafted in immunocompromised mice. NPCs deficient in PTEN and NF1, a genotype associated with the mesenchymal molecular subtype, and NPCs deficient in TP53 and expressing a PDGFRA activating mutation (PDGFRAΔ8–9), a genotype associated with the proneural glioblastoma molecular subtype, give rise to distinct tumors resembling glioblastoma. Both models presented inter and intra-tumor heterogeneity based on single-cell RNA sequencing, with the former model showing proneural signature and the latter a mesenchymal signature, and both having different degrees of cycling, and stem cell-enriched populations. The TP53/PDGFRA model had more clonal variability related with striking karyotype abnormalities including extrachromosomal DNA. Additionally, we expanded this approach to pediatric gliomas. Brainstem tumors derived from NPCs introduced with TP53 R248Q and H3F3A K27M mutations presented features of glial tumors with global expression of histone H3 K27M accompanied by suppression of histone H3K27 trimethylation, compatible with H3 K27M-mutant pediatric diffuse midline glioma. Using these isogenic human brain tumor models, we aim to advance our understanding of the pathobiology associated with different driver mutations and further, to provide a platform for development of targeted therapy.
Clinical validation of an NGS-based assay for detecting multiple genomic alterations in Chinese patients with non-small cell lung cancer
Authors: H. Ge, X. Chen, L. Ruan, Q. Gao, X. Yang, W. Shi, X. Li, G. Zhu
Journal: Annals of Oncology (2019)

Background: Patients with non-small cell lung cancer (NSCLC) often harbors driver mutations in multiple oncogenes, including EGFR, KRAS, ALK, ROS1, BRAF, HER2, RET, etc. Driver genetic alterations are used as predictive biomarkers for molecular targeted therapies. Therefore, identifying mutations in oncogenes and tailoring therapy accordingly become a standard in clinical cancer management. A genetic testing assay based on next-generation sequencing (NGS) technology, named AmoyDx Essential NGS Panel, has been developed for multiplexed and targeted deep sequencing of variants in 10 driver genes. Clinical validation was conducted in the present study. Methods: A total of 372 formalin-fixed and paraffin-embedded (FFPE) tissue samples collected from Chinese patients with NSCLC were detected by AmoyDx Essential NGS Panel, which enables the simultaneous detection of single-nucleotide variants (SNVs), insertions/deletions and fusions in 10 driver genes (EGFR, KRAS, NRAS, BRAF, PIK3CA, ALK, ROS1, HER2, RET, and MET) in DNA samples. DNA sequencing was performed on the Illumina platform. Golden standard Sanger sequencing as reference method was used as a reference method to test the same cohort. The concordance of variants determined with the AmoyDx Essential NGS Panel was assessed compared to the reference method. Results: In total of 372 samples, 98.39% (366/372) of patients were successfully detected by both AmoyDx Essential NGS Panel and Sanger sequencing. 73.50% (269/366) were identified to shown variants by NGS as listed in the table . The overall concordance rate of mutations determined with AmoyDx Essential NGS Panel compared with reference was 98.80%.Table9P Variants detected by NGSVariant typeNumber of patientsPositive rateEGFR mutation21057.38%KRAS mutation226.01%NRAS mutation00.00%BRAF mutation71.91%PIK3CA mutation51.37%ALK fusion133.55%ROS1 fusion10.27%HER2 mutation82.19%RET fusion61.64%MET mutation10.27%Total26973.50% Open table in a new tab Conclusions: The NGS analysis with AmoyDx Essential NGS Panel represents an accurate and efficient approach to detect genomic alterations in 10 driver genes with high concordance rate of 98.80% compared with Sanger sequencing. Legal entity responsible for the study: Amoy Diagnostics Co., Ltd. Funding: Has not received any funding. Disclosure: H. Ge, L. Ruan, Q. Gao, X. Yang, W. Shi, X. Li, G. Zhu: Employee: Amoy Diagnostics Co., Ltd. All other authors have declared no conflicts of interest.
Real World Treatment Patterns and Toxicity Among Elderly Patients with Multiple Myeloma
Authors: Jesus D Gonzalez-Lugo, Ana Acuna-Villaorduna, Joshua Heisler, Niyati Goradia, Daniel Cole, Mateo Mejia Saldarriaga, Aditi Shastri, Gurbakhash Kaur, Ira Braunschweig, Noah Kornblum, Amit Verma, Murali Janakiram, Ioannis Mantzaris
Journal: Blood (2019)
Reduced Intensity Conditioning and Dual T-Cell Modulation Improves Gvhd Free, Relapse Free Survival in AML Patients Compared with Myeloablative Conditioning
Authors: Maria Queralt Salas, Shiyi Chen, Wilson Lam, David Loach, Fotios V. Michelis, Zeyad Al-Shaibani, Dennis Dong Hwan Kim, Jeffrey H. Lipton, Auro Viswabandya, Rajat Kumar, Jonas Mattsson, Arjun Law
Journal: Blood (2019)
Peri-Transplant Administration of Ruxolitinib Is Safe and Feasible in Patients with Myelofibrosis: Primary Results of a Pilot Open-Label Study of Ruxolitinib Administration in Combination with Reduced Intensity Conditioning
Authors: Haris Ali, David Snyder, Tracy Stiller, Timothy Synold, Saloomeh Mokhtari, Joycelynne Palmer, Amandeep Salhotra, Vinod A. Pullarkat, Ji-lian Cai, Stephen J Forman, Matthew Mei, Ryotaro Nakamura
Journal: Blood (2019)
Clinical, Laboratory and Molecular Characterization of Factor VII, Factor X and Their Combined Deficiencies in a Tertiary Care Center
Authors: Bereczky Zsuzsanna, Speker Marianna, Al-Muhanna Marie, Balogh Gábor, Boda Zoltán, Pfliegler György, Schlammadinger Ágota, Kerényi Adrienn, Csongor Kiss
Journal: Blood (2019)
Changing the Natural History of Fanconi Anemia Complementation Group-A with Gene Therapy: Early Results of U.S. Phase I Study of Lentiviral-Mediated Ex-VivoFANCA Gene Insertion in Human Stem and Progenitor Cells
Authors: Agnieszka Czechowicz, Maria Grazia Roncarolo, Brian C Beard, Ken Law, Eileen Nicoletti, Paula Río, Juan A. Bueren, Jonathan D Schwartz, Sandeep Soni
Journal: Blood (2019)
Abstract #LB-76: Identification of neuroblastoma tumour-initiating cells by micro-array time-course analysis of neurospheres
Authors: Nicole Gross, Aurélie Coulon, Annick Mühlethaler-Mottet, Marjorie Flahaut, Lukas Sommer
Journal: Cancer Research (2009)

Solid tumours are believed to arise from a minor population of tumour-initiating cells (TICs) with typical stem cell markers and properties. TICs would possess the exclusive ability to initiate and maintain the tumour. Rare populations of undifferentiated cells with stem cell characteristics have been identified in several malignancies. The identification of TICs therefore establishes a new putative cellular target for more effective therapies in aggressive cancers. Neuroblastoma (NB), the most common extracranial childhood solid tumour originates from neural crest-derived malignant sympathoadrenal cells. We have identified cells within primary NB tissue and cell lines that express neural crest stem cells markers. Moreover, NB primary tumours were shown to include differentiated cell types normally generated from neural crest cells, leading us to postulate the existence of TICs in NB tumour that recapitulate the properties of sympathetic precursor cells. As reliable and specific cell surface markers to isolate TICs are not available for solid tumours, functional assays such as ability of stem cells to grow as spheres in non-adherent conditions have been developed to reliably detect and quantify TICs. By serial passages of neurospheres generated from a dissociated NB tumour, a subset of cells was gradually selected and its specific gene expression profile identified by micro-array time-course analysis. GeneOntology analysis revealed in the set of differentially expressed genes from neurospheres, an enrichment in genes implicated in development, including the known CD133, WNT and NOTCH TICs markers. We compared these results with genes enriched in neural crest and other stem cells types by overlap. Interestingly, these markers were found to be highly expressed by NB primary tumour cells propagated in a serum-free medium preventing cell differentiation. We also showed the presence of a cell population expressing these markers within the tumour. This preliminary study uncovers putatively relevant markers for the isolation and further investigation of the in vitro and in vivo tumourigenic potential of TICs in tumours.  Citation Information: In: Proc Am Assoc Cancer Res; 2009 Apr 18-22; Denver, CO. Philadelphia (PA): AACR; 2009. Abstract nr LB-76.
Treatment Discontinuation Patterns for Patients with CLL in the Real-World Settings: Results from a Multi-Center Study
Authors: Mazyar Shadman, Kavita Sail, Beenish S Manzoor, Maryam Sarraf Yazdy, Brian T. Hill, Hande H. Tuncer, John N. Allan, Chaitra S. Ujjani, Nnadozie Emechebe, Rajesh Kamalakar, Simon Sharmokh, Daniel Dingfeng Jiang, German Pena, Thomas Marshall, Jacqueline Nielsen, Paul M. Barr, Jennifer R. Brown, Anna Schuh, Toby A. Eyre, Nicole Lamanna, William G. Wierda, Alan Skarbnik, Lindsey E. Roeker, Rajat Bannerji, James M. Pauff, Stephen J. Schuster, George A Follows, Bruce D. Cheson, Barbara F. Eichhorst, Danielle M. Brander, Irina Pivneva, Annie Guerin, Anthony R. Mato
Journal: Blood (2019)
SEL120 - a First-in-Class CDK8/19 Inhibitor As a Novel Option for the Treatment of Acute Myeloid Leukemia and High-Risk Myelodysplastic Syndrome - Data from Preclinical Studies and Introduction to a Phase Ib Clinical Trial
Authors: Gautam M. Borthakur, William B. Donnellan, Scott R. Solomon, Camille Abboud, Aziz Nazha, Milena Mazan, Michal Mikula, Eliza Majewska, Katarzyna Wiklik, Aniela Golas, Marcus Järås, Marion Chapellier, Anna Polak, Arkadiusz Bialas, Renata Windak, Jerzy Ostrowski, Przemyslaw Juszczynski, Pawel Chrom, Tomasz Rzymski, Krzysztof Brzózka
Journal: Blood (2019)
Autologous Platelet Rich Plasma (PRP) Provoke Immunomodulatory Response By an Increase of Regulatory T Cells (CD4+ CD25+ FOXP3+) with a Decrease of Activated NK Cells (CD16+ CD56+ CD69+) in a Longitudinal Study of Patients with BehçEt's Disease
Authors: Stephany Cares Huber, Silmara Aparecida De Lima Montalvão, Zoraida Sachetto, Erich Vinicius De Paula, Joyce Maria Annichino-Bizzacchi
Journal: Blood (2016)
Decitabine Containing Conditioning Regimen for Allogeneic Hematopoietic Stem Cell Transplantation in Patients with Intermediate- and High-Risk Myelodysplastic Syndrome/Acute Myeloid Leukemia: Potential Decrease in the Incidence of Acute Graft Versus Host Disease
Authors: Yuan Li, Qing Ya Wang, Ze Yin Liang, Yue Yin, Wei Liu, Qian Wang, Yujun Dong, YuHua Sun, Wei Lin Xu, Hanyun Ren
Journal: Blood (2019)
Homeobox Transcription Factor Hhex Promotes Myeloid Leukemia in Cooperation with Mutant ASXL1
Authors: Reina Takeda, Shuhei Asada, Sung-Joon Park, Akihiko Yokoyama, Akinori Kanai, Valeria Visconte, Courtney Hershberger, Yasutaka Hayashi, Taishi Yonezawa, Moe Tamura, Tomofusa Fukuyama, Akiko Matsumoto, Satoshi Yamasaki, Kenta Nakai, Toshiya Inaba, Tatsuhiro Shibata, Daichi Inoue, Hiroaki Honda, Susumu Goyama, Jaroslaw P. Maciejewski, Toshio Kitamura
Journal: Blood (2019)
Shared Decision Making in Cancer Treatment: Findings from a Large Survey of Lymphoma (LYM) Patients and Survivors
Authors: Kendall H Sullivan, Michael Toscani, Tayla Poretta, Ciera Patzke, Thushara Korattyil, Denalee O'Malley, Victor Gonzalez, Joseph Barone, Andrew M. Evens
Journal: Blood (2019)
Anti-Leukemic Activity of Single Agent Venetoclax in Newly Diagnosed Acute Myeloid Leukemia: A Sub-Set Analysis of the Caveat Study
Authors: Chong Chyn Chua, John Reynolds, Jessica M Salmon, Chun Fong, Stephen B Ting, Ing Soo Tiong, Shaun Fleming, Sarah MacRaild, Donia M Moujalled, Giovanna Pomilio, Nik Cummings, Julie McManus, Adam Ivey, Purvi M Kakadia, Stefan K. Bohlander, Andrew W. Roberts, Andrew H. Wei
Journal: Blood (2019)
Metagenome-wide association study of gut microbiome revealed novel aetiology of rheumatoid arthritis in the Japanese population
Authors: Toshihiro Kishikawa, Yuichi Maeda, Takuro Nii, Daisuke Motooka, Yuki Matsumoto, Masato Matsushita, Hidetoshi Matsuoka, Maiko Yoshimura, Shoji Kawada, Satoru Teshigawara, Eri Oguro, Yasutaka Okita, Keisuke Kawamoto, Shinji Higa, Toru Hirano, Masashi Narazaki, Atsushi Ogata, Yukihiko Saeki, Shota Nakamura, Hidenori Inohara, Atsushi Kumanogoh, Kiyoshi Takeda, Yukinori Okada
Journal: Annals of the Rheumatic Diseases (2019)

The causality and pathogenic mechanism of microbiome composition remain elusive in many diseases, including autoimmune diseases such as rheumatoid arthritis (RA). This study aimed to elucidate gut microbiome's role in RA pathology by a comprehensive metagenome-wide association study (MWAS).We conducted MWAS of the RA gut microbiome in the Japanese population (ncase=82, ncontrol=42) by using whole-genome shotgun sequencing of high depth (average 13 Gb per sample). Our MWAS consisted of three major bioinformatic analytic pipelines (phylogenetic analysis, functional gene analysis and pathway analysis).Phylogenetic case-control association tests showed high abundance of multiple species belonging to the genus Prevotella (e.g., Prevotella denticola) in the RA case metagenome. The non-linear machine learning method efficiently deconvoluted the case-control phylogenetic discrepancy. Gene functional assessments showed that the abundance of one redox reaction-related gene (R6FCZ7) was significantly decreased in the RA metagenome compared with controls. A variety of biological pathways including those related to metabolism (e.g., fatty acid biosynthesis and glycosaminoglycan degradation) were enriched in the case-control comparison. A population-specific link between the metagenome and host genome was identified by comparing biological pathway enrichment between the RA metagenome and the RA genome-wide association study results. No apparent discrepancy in alpha or beta diversities of metagenome was found between RA cases and controls.Our shotgun sequencing-based MWAS highlights a novel link among the gut microbiome, host genome and pathology of RA, which contributes to our understanding of the microbiome's role in RA aetiology.
Clinical and Biological Characteristics and Outcomes of Richter Transformation : A French Multicenter Study from the Filo Group
Authors: Charline Moulin, Romain Morizot, Thomas Remen, Hélène Augé, Florian Bouclet, Marion Divoux, Sandra Lomazzi, Caroline Dartigeas, Anne Quinquenel, Hélène Busby, Cecile Tomowiak, Veronique Leblond, Catherine Thieblemont, Florence Cymbalista, Marie C Bene, Romain Guièze, Julien Broseus, Pierre Feugier
Journal: Blood (2019)
Interaction of Mantle Cell Lymphoma with the Microenvironment Induces Phospho Akt-Mediated Resistance Against BTK Inhibition and Can be Overcome By Co-Treatment with a Specific Akt Inhibitor (MK-2206)
Authors: Elisabeth Silkenstedt, Claudia Schwandner, Johanna Deuss, Natalie Mack, Yvonne Zimmermann, Martin Dreyling
Journal: Blood (2019)
Peripheral Blood Cell Sorting Strategies for Transcriptomic Analysis in Chronic Myelomonocytic Leukemia
Authors: Moritz Binder, Ryan Carr, Nathalie Droin, Abhishek A Mangaonkar, Giacomo Coltro, Luciana L Almada, David Marks, Kurt Berger, Terra Lasho, Naseema Gangat, Christopher Pin, Martin Fernandez-Zapico, Eric Solary, Mrinal M Patnaik
Journal: Blood (2019)
Review: Diabetes, Obesity, and Cancer—Pathophysiology and Clinical Implications
Authors: Iliana C Lega, Lorraine L Lipscombe
Journal: Endocrine Reviews (2019)

Abstract Obesity and diabetes have both been associated with an increased risk of cancer. In the face of increasing obesity and diabetes rates worldwide, this is a worrying trend for cancer rates. Factors such as hyperinsulinemia, chronic inflammation, antihyperglycemic medications, and shared risk factors have all been identified as potential mechanisms underlying the relationship. The most common obesity- and diabetes-related cancers are endometrial, colorectal, and postmenopausal breast cancers. In this review, we summarize the existing evidence that describes the complex relationship between obesity, diabetes, and cancer, focusing on epidemiological and pathophysiological evidence, and also reviewing the role of antihyperglycemic agents, novel research approaches such as Mendelian Randomization, and the methodological limitations of existing research. In addition, we also describe the bidirectional relationship between diabetes and cancer with a review of the evidence summarizing the risk of diabetes following cancer treatment. We conclude this review by providing clinical implications that are relevant for caring for patients with obesity, diabetes, and cancer and provide recommendations for improving both clinical care and research for patients with these conditions.
Impact of α-Gene Deletions and β-Globin Cluster Haplotypes on Biological Parameters at Baseline and on Hydroxyurea in Children with Sickle Cell Anemia
Authors: Francoise Bernaudin, Cécile Arnaud, Annie Kamdem, Serge Pissard, Isabelle Hau, Ralph Epaud, Corinne Pondarré
Journal: Blood (2016)
Nutrient Deficiencies in Breast-Fed Infants
Journal: New England Journal of Medicine (1978)

An editorial in a previous issue of the New England Journal of Medicine August 17, 1978, recommends iron supplementation as a countermeasure to the iron deficiency of breast-fed infants. However, the dosage suggested may saturate the binding capacity of lactoferrin, an iron-binding protein found in human milk. Since lactoferrin, in combination with specific antibody, is essential for the beneficial bacteriostatic effects of milk against Escherichia coli, an added regimen of iron may impair this effect and prove detrimental to the infant. The question, then, of iron deficiency becomes essential. Evidence shows that the hemoglobin values of infants fed by normal mothers for approximately 7 months and infants fed by iron-deficient mothers are normal. The need for additional iron seems unlikely, especially if the infant diet is supplemented with food containing iron.