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Article ; Online: A comparative medical genomics approach may facilitate the interpretation of rare missense variation.

Haque, Bushra / Guirguis, George / Curtis, Meredith / Mohsin, Hera / Walker, Susan / Morrow, Michelle M / Costain, Gregory

Journal of medical genetics

2024

Abstract: Purpose: To determine the degree to which likely causal missense variants of single-locus traits in domesticated species have features suggestive of pathogenicity in a human genomic context.: Methods: We extracted missense variants from the Online ... ...

Abstract	Purpose: To determine the degree to which likely causal missense variants of single-locus traits in domesticated species have features suggestive of pathogenicity in a human genomic context. Methods: We extracted missense variants from the Online Mendelian Inheritance in Animals database for nine animals (cat, cattle, chicken, dog, goat, horse, pig, rabbit and sheep), mapped coordinates to the human reference genome and annotated variants using genome analysis tools. We also searched a private commercial laboratory database of genetic testing results from >400 000 individuals with suspected rare disorders. Results: Of 339 variants that were mappable to the same residue and gene in the human genome, 56 had been previously classified with respect to pathogenicity: 31 (55.4%) pathogenic/likely pathogenic, 1 (1.8%) benign/likely benign and 24 (42.9%) uncertain/other. The odds ratio for a pathogenic/likely pathogenic classification in ClinVar was 7.0 (95% CI 4.1 to 12.0, p<0.0001), compared with all other germline missense variants in these same 220 genes. The remaining 283 variants disproportionately had allele frequencies and REVEL scores that supported pathogenicity. Conclusion: Cross-species comparisons could facilitate the interpretation of rare missense variation. These results provide further support for comparative medical genomics approaches that connect big data initiatives in human and veterinary genetics.
Language	English
Publishing date	2024-03-20
Publishing country	England
Document type	Journal Article
ZDB-ID	220881-7
ISSN	1468-6244 ; 0022-2593
ISSN (online)	1468-6244
ISSN	0022-2593
DOI	10.1136/jmg-2023-109760
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Article ; Online: Weekly Proactive Telephone Breastfeeding Standard Care by Lactation Consultants in the First Month Postpartum Prolongs Breastfeeding for Up to 6 Months.

Fan, Wei Qi / Chan, Christopher / Paterson, Susan / Foster, Kathryn / Morrow, Michelle / Bourne, Debra / Ashworth, Jodie

Nutrients

2023 Volume 15, Issue 9

Abstract: Many mothers, especially those with co-morbidities, do not achieve exclusive breastfeeding (EBF) for the first 6 months, with the loss of multiple health benefits including enhanced infant nutrition. We wished to evaluate whether proactive lactation ... ...

Abstract	Many mothers, especially those with co-morbidities, do not achieve exclusive breastfeeding (EBF) for the first 6 months, with the loss of multiple health benefits including enhanced infant nutrition. We wished to evaluate whether proactive lactation consultant telephone advice in the first month postpartum improved breastfeeding rates for up to 6 months. A prospective cohort observational study was performed. Mother groupings included the following: Control (CG,
MeSH term(s)	Infant ; Female ; Humans ; Breast Feeding ; Consultants ; Prospective Studies ; Postpartum Period ; Lactation ; Telephone
Language	English
Publishing date	2023-04-25
Publishing country	Switzerland
Document type	Observational Study ; Journal Article
ZDB-ID	2518386-2
ISSN	2072-6643 ; 2072-6643
ISSN (online)	2072-6643
ISSN	2072-6643
DOI	10.3390/nu15092075
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Article ; Online: Durable response of anaplastic thyroid carcinoma to FS118, a bispecific LAG-3/PD-L1 antibody, after checkpoint inhibitor progression: a case report.

Kroloff, Maxwell J / Holz, Josefin-Beate / Stern, Omer / Shepherd, Christopher J / Morrow, Michelle / Kayitalire, Louis / Wong, Deborah J

Journal for immunotherapy of cancer

2022 Volume 10, Issue 10

Abstract: Anaplastic thyroid cancer represents a rare, highly aggressive form of thyroid cancer with a poor prognosis and an overall survival ranging from 5 to 12 months. Unfortunately, treatment options remain limited, even for patients with a targetable driver ... ...

Abstract	Anaplastic thyroid cancer represents a rare, highly aggressive form of thyroid cancer with a poor prognosis and an overall survival ranging from 5 to 12 months. Unfortunately, treatment options remain limited, even for patients with a targetable driver mutation. Here, we present a case of a patient with a BRAF V600E-mutated, PD-L1 positive (tumor proportion score of 95%) anaplastic thyroid cancer refractory to standard therapies, including debulking surgery, followed by chemoradiation, who had further progressed on PD-1 monotherapy, and was unable to tolerate BRAF/MEK inhibition. Ongoing treatment with FS118, a bispecific LAG-3/PD-L1 antagonist, has afforded 3 years of disease control, including a late confirmed partial response, with excellent tolerability. Given this response, further investigation is required to delineate the mechanism by which dual PD-L1/LAG-3 blockade by FS118 overcomes initial PD-1 pathway resistance, and therefore, identify which patients are most likely to benefit. Simultaneously, expanded use should be considered for those with refractory disease, especially if PD-L1 positive. Insights Dual PD-L1/LAG-3 blockade may be an effective treatment strategy for refractory metastatic tumors, including anaplastic thyroid cancer.
MeSH term(s)	Antibodies, Bispecific/therapeutic use ; Antineoplastic Agents/therapeutic use ; B7-H1 Antigen ; Humans ; Mitogen-Activated Protein Kinase Kinases/therapeutic use ; Programmed Cell Death 1 Receptor ; Proto-Oncogene Proteins B-raf ; Thyroid Carcinoma, Anaplastic/drug therapy ; Thyroid Carcinoma, Anaplastic/pathology ; Thyroid Neoplasms/pathology
Chemical Substances	Antibodies, Bispecific ; Antineoplastic Agents ; B7-H1 Antigen ; Programmed Cell Death 1 Receptor ; Proto-Oncogene Proteins B-raf (EC 2.7.11.1) ; Mitogen-Activated Protein Kinase Kinases (EC 2.7.12.2)
Language	English
Publishing date	2022-10-06
Publishing country	England
Document type	Case Reports ; Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2719863-7
ISSN	2051-1426 ; 2051-1426
ISSN (online)	2051-1426
ISSN	2051-1426
DOI	10.1136/jitc-2022-005225
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Article ; Online: Mutation update: Variants of the ENPP1 gene in pathologic calcification, hypophosphatemic rickets, and cutaneous hypopigmentation with punctate keratoderma.

Ralph, Douglas / Levine, Michael A / Richard, Gabriele / Morrow, Michelle M / Flynn, Elizabeth K / Uitto, Jouni / Li, Qiaoli

Human mutation

2022 Volume 43, Issue 9, Page(s) 1183–1200

Abstract: ENPP1 encodes ENPP1, an ectonucleotidase catalyzing hydrolysis of ATP to AMP and inorganic pyrophosphate (PPi), and an endogenous plasma protein physiologically preventing ectopic calcification of connective tissues. Mutations in ENPP1 have been reported ...

Abstract	ENPP1 encodes ENPP1, an ectonucleotidase catalyzing hydrolysis of ATP to AMP and inorganic pyrophosphate (PPi), and an endogenous plasma protein physiologically preventing ectopic calcification of connective tissues. Mutations in ENPP1 have been reported in association with a range of human genetic diseases. In this mutation update, we provide a comprehensive review of all the pathogenic variants, likely pathogenic variants, and variants of unknown significance in ENPP1 associated with three autosomal recessive disorders-generalized arterial calcification of infancy (GACI), autosomal recessive hypophosphatemic rickets type 2 (ARHR2), and pseudoxanthoma elasticum (PXE), as well as with a predominantly autosomal dominant disorder-Cole disease. The classification of all variants is determined using the latest ACMG guidelines. A total of 140 ENPP1 variants were curated consisting of 133 previously reported variants and seven novel variants, with missense variants being the most prevalent (70.0%, 98/140). While the pathogenic variants are widely distributed in the ENPP1 gene of patientsgen without apparent genotype-phenotype correlation, eight out of nine variants associated with Cole disease are confined to the somatomedin-B-like (SMB) domains critical for homo-dimerization of the ENPP1 protein.
MeSH term(s)	Humans ; Hypopigmentation/genetics ; Mutation ; Phosphoric Diester Hydrolases/genetics ; Pyrophosphatases/genetics ; Rickets, Hypophosphatemic/complications ; Rickets, Hypophosphatemic/genetics ; Vascular Calcification/genetics
Chemical Substances	Phosphoric Diester Hydrolases (EC 3.1.4.-) ; ectonucleotide pyrophosphatase phosphodiesterase 1 (EC 3.1.4.1) ; Pyrophosphatases (EC 3.6.1.-)
Language	English
Publishing date	2022-05-18
Publishing country	United States
Document type	Journal Article ; Review ; Research Support, Non-U.S. Gov't ; Research Support, N.I.H., Extramural
ZDB-ID	1126646-6
ISSN	1098-1004 ; 1059-7794
ISSN (online)	1098-1004
ISSN	1059-7794
DOI	10.1002/humu.24391
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Article ; Online: Age-induced changes in anti-tumor immunity alter the tumor immune infiltrate and impact response to immuno-oncology treatments.

Sitnikova, Suzanne I / Walker, Jennifer A / Prickett, Laura B / Morrow, Michelle / Valge-Archer, Viia E / Robinson, Matthew J / Wilkinson, Robert W / Dovedi, Simon J

Frontiers in immunology

2023 Volume 14, Page(s) 1258291

Abstract: Introduction: Immuno-oncology (IO) research relies heavily on murine syngeneic tumor models. However, whilst the average age for a cancer diagnosis is 60 years or older, for practical purposes the majority of preclinical studies are conducted in young ... ...

Abstract	Introduction: Immuno-oncology (IO) research relies heavily on murine syngeneic tumor models. However, whilst the average age for a cancer diagnosis is 60 years or older, for practical purposes the majority of preclinical studies are conducted in young mice, despite the fact that ageing has been shown to have a significant impact on the immune response. Methods: Using aged (60-72 weeks old) mice bearing CT26 tumors, we investigated the impact of ageing on tumor growth as well as the immune composition of the tumor and peripheral lymphoid organs. Results: We found many differences in the immune cell composition of both the tumor and tumor-draining lymph node between aged and young mice, such as a reduction in the naïve T cell population and a decreased intratumoral CD8/Treg ratio in aged animals. We hypothesized that these differences may contribute to impaired anti-cancer immune responses in aged mice and therefore assessed the anti-tumor efficacy of different IO therapies in aged mice, including both co-stimulation (using an anti-OX40 antibody) and immune checkpoint blockade (using anti-PD-L1 and anti-CTLA-4 antibodies). Whilst aged mice retained the capacity to generate anti-tumor immune responses, these were significantly attenuated when compared to the responses observed in young mice. Discussion: These differences highlight the importance of age-related immunological changes in assessing and refining the translational insights gained from preclinical mouse models.
MeSH term(s)	Mice ; Animals ; Neoplasms ; Immunotherapy
Language	English
Publishing date	2023-10-18
Publishing country	Switzerland
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2606827-8
ISSN	1664-3224 ; 1664-3224
ISSN (online)	1664-3224
ISSN	1664-3224
DOI	10.3389/fimmu.2023.1258291
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Article ; Online: TELO2-related syndrome (You-Hoover-Fong syndrome): Description of 14 new affected individuals and review of the literature.

Albokhari, Daniah / Pritchard, Amanda Barone / Beil, Adelyn / Muss, Candace / Bupp, Caleb / Grange, Dorothy K / Delplancq, Geoffroy / Heeley, Jennifer / Zuteck, Melissa / Morrow, Michelle M / Kuentz, Paul / Palculict, Timothy Blake / Hoover-Fong, Julie E

American journal of medical genetics. Part A

2023 Volume 191, Issue 5, Page(s) 1261–1272

Abstract: You-Hoover-Fong syndrome (YHFS) is an autosomal recessive condition caused by pathogenic variants in the TELO2 gene. Affected individuals were reported to have global developmental delay, intellectual disability, microcephaly, dysmorphic facial features, ...

Abstract	You-Hoover-Fong syndrome (YHFS) is an autosomal recessive condition caused by pathogenic variants in the TELO2 gene. Affected individuals were reported to have global developmental delay, intellectual disability, microcephaly, dysmorphic facial features, ocular involvement including cortical visual impairment, strabismus, cataract and rotatory nystagmus, movement disorder, hypertonia and spasticity, balance disturbance and ataxia, and abnormal sleep pattern. Other features reported include poor growth, cleft palate, cardiac malformations, epilepsy, scoliosis, and hearing loss. To date, 12 individuals with YHFS have been reported in the literature. Here we describe 14 new individuals with YHFS from 10 families. Their clinical presentation provides additional support of the phenotype recognized previously and delineates the clinical spectrum associated with YHFS syndrome. In addition, we present a review of the literature including follow-up data on four previously reported individuals with YHFS.
MeSH term(s)	Humans ; Brain Diseases/complications ; Epilepsy/complications ; Intellectual Disability/pathology ; Microcephaly/pathology ; Syndrome
Chemical Substances	TELO2 protein, human
Language	English
Publishing date	2023-02-16
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	2108614-X
ISSN	1552-4833 ; 0148-7299 ; 1552-4825
ISSN (online)	1552-4833
ISSN	0148-7299 ; 1552-4825
DOI	10.1002/ajmg.a.63142
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Zs.A 1376/A: Show issues

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Article ; Online: De novo variants implicate chromatin modification, transcriptional regulation, and retinoic acid signaling in syndromic craniosynostosis.

Timberlake, Andrew T / McGee, Stephen / Allington, Garrett / Kiziltug, Emre / Wolfe, Erin M / Stiegler, Amy L / Boggon, Titus J / Sanyoura, May / Morrow, Michelle / Wenger, Tara L / Fernandes, Erica M / Caluseriu, Oana / Persing, John A / Jin, Sheng Chih / Lifton, Richard P / Kahle, Kristopher T / Kruszka, Paul

American journal of human genetics

2023 Volume 110, Issue 5, Page(s) 846–862

Abstract: Craniosynostosis (CS) is the most common congenital cranial anomaly. Several Mendelian forms of syndromic CS are well described, but a genetic etiology remains elusive in a substantial fraction of probands. Analysis of exome sequence data from 526 ... ...

Abstract	Craniosynostosis (CS) is the most common congenital cranial anomaly. Several Mendelian forms of syndromic CS are well described, but a genetic etiology remains elusive in a substantial fraction of probands. Analysis of exome sequence data from 526 proband-parent trios with syndromic CS identified a marked excess (observed 98, expected 33, p = 4.83 × 10
MeSH term(s)	Humans ; Mutation ; Tretinoin ; Craniosynostoses/genetics ; Gene Expression Regulation ; Chromatin ; Genetic Predisposition to Disease
Chemical Substances	Tretinoin (5688UTC01R) ; Chromatin
Language	English
Publishing date	2023-04-21
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	219384-x
ISSN	1537-6605 ; 0002-9297
ISSN (online)	1537-6605
ISSN	0002-9297
DOI	10.1016/j.ajhg.2023.03.017
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Article ; Online: CD137/OX40 Bispecific Antibody Induces Potent Antitumor Activity that Is Dependent on Target Coengagement.

Gaspar, Miguel / Pravin, John / Rodrigues, Leonor / Uhlenbroich, Sandra / Everett, Katy L / Wollerton, Francisca / Morrow, Michelle / Tuna, Mihriban / Brewis, Neil

Cancer immunology research

2020 Volume 8, Issue 6, Page(s) 781–793

Abstract: Following the success of immune checkpoint blockade therapy against cancer, agonistic antibodies targeting T-cell costimulatory pathways are in clinical trials. The TNF superfamily of receptors (TNFRSF) members CD137 and OX40 are costimulatory receptors ... ...

Abstract	Following the success of immune checkpoint blockade therapy against cancer, agonistic antibodies targeting T-cell costimulatory pathways are in clinical trials. The TNF superfamily of receptors (TNFRSF) members CD137 and OX40 are costimulatory receptors that stimulate T-cell proliferation and activation upon interaction with their cognate ligands. Activating CD137 and OX40 with agonistic mAbs stimulates the immune system due to their broad expression on CD4
MeSH term(s)	Animals ; Antibodies, Bispecific/pharmacology ; Apoptosis ; Cell Proliferation ; Colonic Neoplasms/immunology ; Colonic Neoplasms/metabolism ; Colonic Neoplasms/pathology ; Colonic Neoplasms/therapy ; Female ; Humans ; Immunotherapy ; Killer Cells, Natural/immunology ; Lymphocyte Activation/immunology ; Mice ; Mice, Inbred BALB C ; Receptors, OX40/immunology ; T-Lymphocytes, Regulatory/immunology ; Tumor Cells, Cultured ; Tumor Necrosis Factor Receptor Superfamily, Member 9/immunology ; Xenograft Model Antitumor Assays
Chemical Substances	Antibodies, Bispecific ; Receptors, OX40 ; TNFRSF9 protein, human ; Tumor Necrosis Factor Receptor Superfamily, Member 9
Language	English
Publishing date	2020-04-09
Publishing country	United States
Document type	Journal Article
ZDB-ID	2732489-8
ISSN	2326-6074 ; 2326-6066
ISSN (online)	2326-6074
ISSN	2326-6066
DOI	10.1158/2326-6066.CIR-19-0798
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Article ; Online: A recurrent missense variant in the E3 ubiquitin ligase substrate recognition subunit FEM1B causes a rare syndromic neurodevelopmental disorder.

Lecoquierre, François / Punt, A Mattijs / Ebstein, Frédéric / Wallaard, Ilse / Verhagen, Rob / Studencka-Turski, Maja / Duffourd, Yannis / Moutton, Sébastien / Tran Mau-Them, Frédédic / Philippe, Christophe / Dean, John / Tennant, Stephen / Brooks, Alice S / van Slegtenhorst, Marjon A / Jurgens, Julie A / Barry, Brenda J / Chan, Wai-Man / England, Eleina M / Martinez Ojeda, Mayra /

Engle, Elizabeth C / Robson, Caroline D / Morrow, Michelle / Innes, A Micheil / Lamont, Ryan / Sanderson, Matthea / Krüger, Elke / Thauvin, Christel / Distel, Ben / Faivre, Laurence / Elgersma, Ype / Vitobello, Antonio

Genetics in medicine : official journal of the American College of Medical Genetics

2024 Volume 26, Issue 6, Page(s) 101119

Abstract: Purpose: Fem1 homolog B (FEM1B) acts as a substrate recognition subunit for ubiquitin ligase complexes belonging to the CULLIN 2-based E3 family. Several biological functions have been proposed for FEM1B, including a structurally resolved function as a ... ...

Abstract	Purpose: Fem1 homolog B (FEM1B) acts as a substrate recognition subunit for ubiquitin ligase complexes belonging to the CULLIN 2-based E3 family. Several biological functions have been proposed for FEM1B, including a structurally resolved function as a sensor for redox cell status by controlling mitochondrial activity, but its implication in human disease remains elusive. Methods: To understand the involvement of FEM1B in human disease, we made use of Matchmaker exchange platforms to identify individuals with de novo variants in FEM1B and performed their clinical evaluation. We performed functional validation using primary neuronal cultures and in utero electroporation assays, as well as experiments on patient's cells. Results: Five individuals with a recurrent de novo missense variant in FEM1B were identified: NM_015322.5:c.377G>A NP_056137.1:p.(Arg126Gln) (FEM1B Conclusion: Overall, our data indicate that p.(Arg126Gln) induces aberrant FEM1B activation, resulting in a gain-of-function mechanism associated with a severe syndromic developmental disorder in humans.
Language	English
Publishing date	2024-03-07
Publishing country	United States
Document type	Journal Article
ZDB-ID	1455352-1
ISSN	1530-0366 ; 1098-3600
ISSN (online)	1530-0366
ISSN	1098-3600
DOI	10.1016/j.gim.2024.101119
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Article ; Online: FS118, a Bispecific Antibody Targeting LAG-3 and PD-L1, Enhances T-Cell Activation Resulting in Potent Antitumor Activity.

Kraman, Matthew / Faroudi, Mustapha / Allen, Natalie L / Kmiecik, Katarzyna / Gliddon, Daniel / Seal, Claire / Koers, Alexander / Wydro, Mateusz M / Batey, Sarah / Winnewisser, Julia / Young, Lesley / Tuna, Mihriban / Doody, Jacqueline / Morrow, Michelle / Brewis, Neil

Clinical cancer research : an official journal of the American Association for Cancer Research

2020 Volume 26, Issue 13, Page(s) 3333–3344

Abstract: Purpose: Although programmed death-ligand 1 (PD-L1) antibody-based therapy has improved the outcome of patients with cancer, acquired resistance to these treatments limits their clinical efficacy. FS118 is a novel bispecific, tetravalent antibody (mAb!## ...

Abstract	Purpose: Although programmed death-ligand 1 (PD-L1) antibody-based therapy has improved the outcome of patients with cancer, acquired resistance to these treatments limits their clinical efficacy. FS118 is a novel bispecific, tetravalent antibody (mAb Experimental design: This study characterizes the binding activity and immune function of FS118 in cell lines and human peripheral blood mononuclear cells and further investigates its antitumor activity and mechanism of action using a surrogate murine bispecific antibody (mLAG-3/PD-L1 mAb Results: FS118 demonstrated simultaneous binding to LAG-3 and PD-L1 with high affinity and comparable or better activity than the combination of the single component parts of the mAb Conclusions: This study demonstrates a novel benefit of the bispecific approach over a combination of mAbs and supports the further development of FS118 for the treatment of patients with cancer.
MeSH term(s)	Animals ; Antibodies, Bispecific/pharmacology ; Antibody Affinity ; Antigens, CD/metabolism ; Antineoplastic Agents, Immunological/pharmacology ; B7-H1 Antigen/antagonists & inhibitors ; Biomarkers, Tumor ; Cell Line, Tumor ; Disease Models, Animal ; Humans ; Immunophenotyping ; Lymphocyte Activation/drug effects ; Lymphocyte Activation/immunology ; Mice ; Protein Binding ; T-Lymphocytes/drug effects ; T-Lymphocytes/immunology ; T-Lymphocytes/metabolism ; Xenograft Model Antitumor Assays
Chemical Substances	Antibodies, Bispecific ; Antigens, CD ; Antineoplastic Agents, Immunological ; B7-H1 Antigen ; Biomarkers, Tumor ; CD223 antigen ; CD274 protein, human
Language	English
Publishing date	2020-04-16
Publishing country	United States
Document type	Journal Article
ZDB-ID	1225457-5
ISSN	1557-3265 ; 1078-0432
ISSN (online)	1557-3265
ISSN	1078-0432
DOI	10.1158/1078-0432.CCR-19-3548
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