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Article ; Online: The pro-tumorigenic host response to cancer therapies.

Shaked, Yuval

2019 Volume 19, Issue 12, Page(s) 667–685

Abstract: Resistance to cancer therapy remains a major challenge in clinical oncology. Although the initial treatment phase is often successful, eventual resistance, characterized by tumour relapse or spread, is discouraging. The majority of studies devoted to ... ...

Abstract	Resistance to cancer therapy remains a major challenge in clinical oncology. Although the initial treatment phase is often successful, eventual resistance, characterized by tumour relapse or spread, is discouraging. The majority of studies devoted to investigating the basis of resistance have focused on tumour-related changes that contribute to therapy resistance and tumour aggressiveness. However, over the last decade, the diverse roles of various host cells in promoting therapy resistance have become more appreciated. A growing body of evidence demonstrates that cancer therapy can induce host-mediated local and systemic responses, many of which shift the delicate balance within the tumour microenvironment, ultimately facilitating or supporting tumour progression. In this Review, recent advances in understanding how the host response to different cancer therapies may promote therapy resistance are discussed, with a focus on therapy-induced immunological, angiogenic and metastatic effects. Also summarized is the potential of evaluating the host response to cancer therapy in an era of precision medicine in oncology.
MeSH term(s)	Animals ; Antineoplastic Agents/pharmacology ; Carcinogenesis ; Cell Lineage ; Disease Progression ; Disease-Free Survival ; Drug Resistance, Neoplasm ; Epigenesis, Genetic ; Humans ; Immune System ; Immunotherapy ; Mice ; Neoplasm Metastasis ; Neoplasm Recurrence, Local ; Neoplasms/therapy ; Neovascularization, Pathologic ; Precision Medicine ; Tumor Microenvironment
Chemical Substances	Antineoplastic Agents
Language	English
Publishing date	2019-10-23
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	2062767-1
ISSN	1474-1768 ; 1474-175X
ISSN (online)	1474-1768
ISSN	1474-175X
DOI	10.1038/s41568-019-0209-6
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Zs.A 5563: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (2.OG) ab Jg. 2022: Lesesaal (EG)
Zs.MG 24: Show issues

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Article ; Online: The role of host response to chemotherapy: resistance, metastasis and clinical implications.

Deo, Abhilash / Sleeman, Jonathan P / Shaked, Yuval

Clinical & experimental metastasis

2023

Abstract: Chemotherapy remains the primary treatment for most metastatic cancers. However, the response to chemotherapy and targeted agents is often transient, and concurrent development of resistance is the primary impediment to effective cancer therapy. ... ...

Abstract	Chemotherapy remains the primary treatment for most metastatic cancers. However, the response to chemotherapy and targeted agents is often transient, and concurrent development of resistance is the primary impediment to effective cancer therapy. Strategies to overcome resistance to treatment have focused on cancer cell intrinsic factors and the tumor microenvironment (TME). Recent evidence indicates that systemic chemotherapy has a significant impact on the host that either facilitates tumor growth, allowing metastatic spread, or renders treatment ineffective. These host responses include the release of bone marrow-derived cells, activation of stromal cells in the TME, and induction of different molecular effectors. Here, we provide an overview of chemotherapy-induced systemic host responses that support tumor aggressiveness and metastasis, and which contribute to therapy resistance. Studying host responses to chemotherapy provides a solid basis for the development of adjuvant strategies to improve treatment outcomes and delay resistance to chemotherapy. This review discusses the emerging field of host response to cancer therapy, and its preclinical and potential clinical implications, explaining how under certain circumstances, these host effects contribute to metastasis and resistance to chemotherapy.
Language	English
Publishing date	2023-11-24
Publishing country	Netherlands
Document type	Journal Article ; Review
ZDB-ID	604952-7
ISSN	1573-7276 ; 0262-0898
ISSN (online)	1573-7276
ISSN	0262-0898
DOI	10.1007/s10585-023-10243-5
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Zs.A 1855: Show issues

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Article ; Online: Balancing efficacy of and host immune responses to cancer therapy: the yin and yang effects.

Shaked, Yuval

Nature reviews. Clinical oncology

2016 Volume 13, Issue 10, Page(s) 611–626

Abstract: Local and systemic treatments for cancer include surgery, radiation, chemotherapy, hormonal therapy, molecularly targeted therapies, antiangiogenic therapy, and immunotherapy. Many of these therapies can be curative in patients with early stage disease, ... ...

Abstract	Local and systemic treatments for cancer include surgery, radiation, chemotherapy, hormonal therapy, molecularly targeted therapies, antiangiogenic therapy, and immunotherapy. Many of these therapies can be curative in patients with early stage disease, but much less frequently is this the case when they are used to treat advanced-stage metastatic disease. In the latter setting, innate and/or acquired resistance are among the reasons for reduced responsiveness or nonresponsiveness to therapy, or for tumour relapse after an initial response. Most studies of resistance or reduced responsiveness focus on 'driver' genetic (or epigenetic) changes in the tumour-cell population. Several studies have highlighted the contribution of therapy-induced physiological changes in host tissues and cells that can reduce or even nullify the desired antitumour effects of therapy. These unwanted host effects can promote tumour-cell proliferation (repopulation) and even malignant aggressiveness. These effects occur as a result of systemic release of numerous cytokines, and mobilization of various host accessory cells, which can invade the treated tumour microenvironment. In short, the desired tumour-targeting effects of therapy (the 'yin') can be offset by a reactive host response (the 'yang'); proactively preventing or actively suppressing the latter represents a possible new approach to improving the efficacy of both local and systemic cancer therapies.
MeSH term(s)	Angiogenesis Inhibitors/therapeutic use ; Antineoplastic Combined Chemotherapy Protocols/immunology ; Antineoplastic Combined Chemotherapy Protocols/therapeutic use ; Humans ; Immunity, Cellular/immunology ; Molecular Targeted Therapy/methods ; Neoplasms/immunology ; Neoplasms/therapy ; Yin-Yang
Chemical Substances	Angiogenesis Inhibitors
Language	English
Publishing date	2016-10
Publishing country	England
Document type	Journal Article ; Review
ZDB-ID	2491410-1
ISSN	1759-4782 ; 1759-4774
ISSN (online)	1759-4782
ISSN	1759-4774
DOI	10.1038/nrclinonc.2016.57
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Zs.A 6029: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 2021: Bestellungen von Artikeln über das Online-Bestellformular ab Jg. 2022: Lesesaal (EG)
Zs.MG 103: Show issues

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Article ; Online: Oncogenic ASPM Is a Regulatory Hub of Developmental and Stemness Signaling in Cancers.

Tsai, Kelvin K / Bae, Byoung-Il / Hsu, Chung-Chi / Cheng, Li-Hsin / Shaked, Yuval

Cancer research

2023 Volume 83, Issue 18, Page(s) 2993–3000

Abstract: Despite recent advances in molecularly targeted therapies and immunotherapies, the effective treatment of advanced-stage cancers remains a largely unmet clinical need. Identifying driver mechanisms of cancer aggressiveness can lay the groundwork for the ... ...

Abstract	Despite recent advances in molecularly targeted therapies and immunotherapies, the effective treatment of advanced-stage cancers remains a largely unmet clinical need. Identifying driver mechanisms of cancer aggressiveness can lay the groundwork for the development of breakthrough therapeutic strategies. Assembly factor for spindle microtubules (ASPM) was initially identified as a centrosomal protein that regulates neurogenesis and brain size. Mounting evidence has demonstrated the pleiotropic roles of ASPM in mitosis, cell-cycle progression, and DNA double-strand breaks (DSB) repair. Recently, the exon 18-preserved isoform 1 of ASPM has emerged as a critical regulator of cancer stemness and aggressiveness in various malignant tumor types. Here, we describe the domain compositions of ASPM and its transcript variants and overview their expression patterns and prognostic significance in cancers. A summary is provided of recent progress in the molecular elucidation of ASPM as a regulatory hub of development- and stemness-associated signaling pathways, such as the Wnt, Hedgehog, and Notch pathways, and of DNA DSB repair in cancer cells. The review emphasizes the potential utility of ASPM as a cancer-agnostic and pathway-informed prognostic biomarker and therapeutic target.
MeSH term(s)	Humans ; Nerve Tissue Proteins/metabolism ; Neoplasms/genetics ; Signal Transduction ; Mitosis ; DNA
Chemical Substances	Nerve Tissue Proteins ; DNA (9007-49-2) ; ASPM protein, human
Language	English
Publishing date	2023-06-27
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	1432-1
ISSN	1538-7445 ; 0008-5472
ISSN (online)	1538-7445
ISSN	0008-5472
DOI	10.1158/0008-5472.CAN-23-0158
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Article ; Online: Pathogenic Variants of Scavenger Receptor

Canavati, Christina / Siam, Ahmad / Labes, Sapir / Trabelsi, Nirit / Regev, Eshcar / Parnasa, Elchanan / Barhoum, Barhoum / Magadle, Nur / Perzon, Ofer / Braun, Maya / Mor-Shaked, Hagar / Schueler-Furman, Ora / Tabach, Yuval / Mevorach, Dror

Circulation

2024 Volume 149, Issue 3, Page(s) 270–273

MeSH term(s)	Humans ; BNT162 Vaccine/adverse effects ; COVID-19/prevention & control ; Efferocytosis ; Myocarditis/chemically induced ; Vaccination/adverse effects
Chemical Substances	BNT162 Vaccine
Language	English
Publishing date	2024-01-16
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	80099-5
ISSN	1524-4539 ; 0009-7322 ; 0069-4193 ; 0065-8499
ISSN (online)	1524-4539
ISSN	0009-7322 ; 0069-4193 ; 0065-8499
DOI	10.1161/CIRCULATIONAHA.123.064884
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Ui IV Zs.60: Show issues

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Article ; Online: Elucidating the roles of ASPM isoforms reveals a novel prognostic marker for pancreatic cancer.

Timaner, Michael / Shaked, Yuval

The Journal of pathology

2019 Volume 250, Issue 2, Page(s) 123–125

Abstract: Pancreatic ductal adenocarcinoma (PDAC) is one of the deadliest cancers worldwide. Late diagnosis, desmoplastic tissue and intrinsic resistance to therapy are among the main reasons for its aggressive phenotype. In addition, it is now appreciated that ... ...

Abstract	Pancreatic ductal adenocarcinoma (PDAC) is one of the deadliest cancers worldwide. Late diagnosis, desmoplastic tissue and intrinsic resistance to therapy are among the main reasons for its aggressive phenotype. In addition, it is now appreciated that cancer stem cells - a rare subpopulation of tumor cells highly resistant to therapy - are crucial players in PDAC initiation, progression and resistance to therapy. In a recent article in The Journal of Pathology, Hsu et al elucidated the specific roles of abnormal spindle-like, microcephaly-associated protein (ASPM) isoforms in PDAC. The authors reported that ASPM isoform I (ASPM-iI) is mainly expressed in the cytoplasm of PDAC cells. Its expression is associated with the Wnt signaling pathway, which promotes stemness and maintains the cancer stem cell niche. Clinically, expression of ASPM-iI correlates with poor survival in PDAC patients. Thus, this study revealed a novel prognostic marker as well as a potential therapeutic target for PDAC. © 2019 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd.
MeSH term(s)	Carcinoma, Pancreatic Ductal ; Humans ; Nerve Tissue Proteins ; Pancreatic Neoplasms ; Prognosis ; Protein Isoforms ; United Kingdom
Chemical Substances	ASPM protein, human ; Nerve Tissue Proteins ; Protein Isoforms
Language	English
Publishing date	2019-12-02
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Comment
ZDB-ID	3119-7
ISSN	1096-9896 ; 0022-3417
ISSN (online)	1096-9896
ISSN	0022-3417
DOI	10.1002/path.5355
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Book ; Online: Incorporating Context into Subword Vocabularies

Yehezkel, Shaked / Pinter, Yuval

2022

Abstract: Most current popular subword tokenizers are trained based on word frequency statistics over a corpus, without considering information about co-occurrence or context. Nevertheless, the resulting vocabularies are used in language models' highly ... ...

Abstract	Most current popular subword tokenizers are trained based on word frequency statistics over a corpus, without considering information about co-occurrence or context. Nevertheless, the resulting vocabularies are used in language models' highly contextualized settings. We present SaGe, a tokenizer that tailors subwords for their downstream use by baking in the contextualized signal at the vocabulary creation phase. We show that SaGe does a better job than current widespread tokenizers in keeping token contexts cohesive, while not incurring a large price in terms of encoding efficiency or domain robustness. SaGe improves performance on English GLUE classification tasks as well as on NER, and on Inference and NER in Turkish, demonstrating its robustness to language properties such as morphological exponence and agglutination. Comment: EACL 2023
Keywords	Computer Science - Computation and Language
Publishing date	2022-10-13
Publishing country	us
Document type	Book ; Online
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Article ; Online: A new screening method for ATP-independent kinase inhibitors identifies repurposed anti-cancer drugs.

Timaner, Michael / Shaked, Yuval

EBioMedicine

2018 Volume 37, Page(s) 21–22

MeSH term(s)	Antineoplastic Agents/pharmacology ; Drug Repositioning ; Drug Screening Assays, Antitumor/methods ; Enzyme Inhibitors/pharmacology ; Humans ; Phosphotransferases/antagonists & inhibitors ; Protein Kinase Inhibitors/pharmacology
Chemical Substances	Antineoplastic Agents ; Enzyme Inhibitors ; Protein Kinase Inhibitors ; Phosphotransferases (EC 2.7.-)
Language	English
Publishing date	2018-10-24
Publishing country	Netherlands
Document type	Letter
ZDB-ID	2851331-9
ISSN	2352-3964
ISSN (online)	2352-3964
DOI	10.1016/j.ebiom.2018.10.020
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Zs.A 7090: Show issues

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Article ; Online: Sperm Inspection for In Vitro Fertilization via Self-Assembled Microdroplet Formation and Quantitative Phase Microscopy.

Atzitz, Yuval / Dudaie, Matan / Barnea, Itay / Shaked, Natan T

Cells

2021 Volume 10, Issue 12

Abstract: We present a new method for the selection of individual sperm cells using a microfluidic device that automatically traps each cell in a separate microdroplet that then individually self-assembles with other microdroplets, permitting the controlled ... ...

Abstract	We present a new method for the selection of individual sperm cells using a microfluidic device that automatically traps each cell in a separate microdroplet that then individually self-assembles with other microdroplets, permitting the controlled measurement of the cells using quantitative phase microscopy. Following cell trapping and droplet formation, we utilize quantitative phase microscopy integrated with bright-field imaging for individual sperm morphology and motility inspection. We then perform individual sperm selection using a single-cell micromanipulator, which is enhanced by the microdroplet-trapping procedure described above. This method can improve sperm selection for intracytoplasmic sperm injection, a common type of in vitro fertilization procedure.
MeSH term(s)	Cell Movement ; Fertilization in Vitro ; Humans ; Male ; Microfluidics ; Microscopy ; Spermatozoa/cytology
Language	English
Publishing date	2021-11-26
Publishing country	Switzerland
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2661518-6
ISSN	2073-4409 ; 2073-4409
ISSN (online)	2073-4409
ISSN	2073-4409
DOI	10.3390/cells10123317
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Article: The Dichotomous Role of Bone Marrow Derived Cells in the Chemotherapy-Treated Tumor Microenvironment.

Vorontsova, Avital / Kan, Tal / Raviv, Ziv / Shaked, Yuval

Journal of clinical medicine

2020 Volume 9, Issue 12

Abstract: Bone marrow derived cells (BMDCs) play a wide variety of pro- and anti-tumorigenic roles in the tumor microenvironment (TME) and in the metastatic process. In response to chemotherapy, the anti-tumorigenic function of BMDCs can be enhanced due to ... ...

Abstract	Bone marrow derived cells (BMDCs) play a wide variety of pro- and anti-tumorigenic roles in the tumor microenvironment (TME) and in the metastatic process. In response to chemotherapy, the anti-tumorigenic function of BMDCs can be enhanced due to chemotherapy-induced immunogenic cell death. However, in recent years, a growing body of evidence suggests that chemotherapy or other anti-cancer drugs can also facilitate a pro-tumorigenic function in BMDCs. This includes elevated angiogenesis, tumor cell proliferation and pro-tumorigenic immune modulation, ultimately contributing to therapy resistance. Such effects do not only contribute to the re-growth of primary tumors but can also support metastasis. Thus, the delicate balance of BMDC activities in the TME is violated following tumor perturbation, further requiring a better understanding of the complex crosstalk between tumor cells and BMDCs. In this review, we discuss the different types of BMDCs that reside in the TME and their activities in tumors following chemotherapy, with a major focus on their pro-tumorigenic role. We also cover aspects of rationally designed combination treatments that target or manipulate specific BMDC types to improve therapy outcomes.
Language	English
Publishing date	2020-12-02
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2662592-1
ISSN	2077-0383
ISSN	2077-0383
DOI	10.3390/jcm9123912
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