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Article ; Online: p53 and its mutants on the slippery road from stemness to carcinogenesis.

Molchadsky, Alina / Rotter, Varda

2017 Volume 38, Issue 4, Page(s) 347–358

Abstract: Normal development, tissue homeostasis and regeneration following injury rely on the proper functions of wide repertoire of stem cells (SCs) persisting during embryonic period and throughout the adult life. Therefore, SCs employ robust mechanisms to ... ...

Abstract	Normal development, tissue homeostasis and regeneration following injury rely on the proper functions of wide repertoire of stem cells (SCs) persisting during embryonic period and throughout the adult life. Therefore, SCs employ robust mechanisms to preserve their genomic integrity and avoid heritage of mutations to their daughter cells. Importantly, propagation of SCs with faulty DNA as well as dedifferentiation of genomically altered somatic cells may result in derivation of cancer SCs, which are considered to be the driving force of the tumorigenic process. Multiple experimental evidence suggest that p53, the central tumor suppressor gene, plays a critical regulatory role in determination of SCs destiny, thereby eliminating damaged SCs from the general SC population. Notably, mutant p53 proteins do not only lose the tumor suppressive function, but rather gain new oncogenic function that markedly promotes various aspects of carcinogenesis. In this review, we elaborate on the role of wild type and mutant p53 proteins in the various SCs types that appear under homeostatic conditions as well as in cancer. It is plausible that the growing understanding of the mechanisms underlying cancer SC phenotype and p53 malfunction will allow future optimization of cancer therapeutics in the context of precision medicine.
MeSH term(s)	Animals ; Carcinogenesis/genetics ; Humans ; Mutation/genetics ; Neoplasms/genetics ; Neoplastic Stem Cells/metabolism ; Oncogenes/genetics ; Phenotype ; Tumor Suppressor Protein p53/genetics
Chemical Substances	Tumor Suppressor Protein p53
Language	English
Publishing date	2017-04-01
Publishing country	England
Document type	Journal Article ; Review
ZDB-ID	603134-1
ISSN	1460-2180 ; 0143-3334
ISSN (online)	1460-2180
ISSN	0143-3334
DOI	10.1093/carcin/bgw092
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Article ; Online: Dysfunctional diversity of p53 proteins in adult acute myeloid leukemia: projections on diagnostic workup and therapy.

Prokocimer, Miron / Molchadsky, Alina / Rotter, Varda

Blood

2017 Volume 130, Issue 6, Page(s) 699–712

Abstract: The heterogeneous nature of acute myeloid leukemia (AML) and its poor prognosis necessitate therapeutic improvement. Current advances in AML research yield important insights regarding AML genetic, epigenetic, evolutional, and clinical diversity, all in ... ...

Abstract	The heterogeneous nature of acute myeloid leukemia (AML) and its poor prognosis necessitate therapeutic improvement. Current advances in AML research yield important insights regarding AML genetic, epigenetic, evolutional, and clinical diversity, all in which dysfunctional p53 plays a key role. As p53 is central to hematopoietic stem cell functions, its aberrations affect AML evolution, biology, and therapy response and usually predict poor prognosis. While in human solid tumors
MeSH term(s)	Adult ; Animals ; Antineoplastic Agents/pharmacology ; Antineoplastic Agents/therapeutic use ; DNA Damage/drug effects ; Gene Expression Regulation, Leukemic/drug effects ; Genomic Instability/drug effects ; Hematopoiesis/drug effects ; Humans ; Karyopherins/genetics ; Karyopherins/metabolism ; Leukemia, Myeloid, Acute/diagnosis ; Leukemia, Myeloid, Acute/drug therapy ; Leukemia, Myeloid, Acute/genetics ; Leukemia, Myeloid, Acute/metabolism ; MicroRNAs/genetics ; MicroRNAs/metabolism ; Molecular Targeted Therapy/methods ; Mutation/drug effects ; Nuclear Proteins/genetics ; Nuclear Proteins/metabolism ; Nucleophosmin ; Protein Interaction Maps/drug effects ; Receptors, Cytoplasmic and Nuclear/genetics ; Receptors, Cytoplasmic and Nuclear/metabolism ; Signal Transduction/drug effects ; Translocation, Genetic ; Tumor Suppressor Protein p53/analysis ; Tumor Suppressor Protein p53/genetics ; Tumor Suppressor Protein p53/metabolism ; fms-Like Tyrosine Kinase 3/genetics ; fms-Like Tyrosine Kinase 3/metabolism ; Exportin 1 Protein
Chemical Substances	Antineoplastic Agents ; Karyopherins ; MicroRNAs ; Nuclear Proteins ; Receptors, Cytoplasmic and Nuclear ; Tumor Suppressor Protein p53 ; Nucleophosmin (117896-08-9) ; FLT3 protein, human (EC 2.7.10.1) ; fms-Like Tyrosine Kinase 3 (EC 2.7.10.1)
Language	English
Publishing date	2017-06-12
Publishing country	United States
Document type	Journal Article ; Review
ZDB-ID	80069-7
ISSN	1528-0020 ; 0006-4971
ISSN (online)	1528-0020
ISSN	0006-4971
DOI	10.1182/blood-2017-02-763086
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Article ; Online: Oncogenic Mutant p53 Gain of Function Nourishes the Vicious Cycle of Tumor Development and Cancer Stem-Cell Formation.

Shetzer, Yoav / Molchadsky, Alina / Rotter, Varda

Cold Spring Harbor perspectives in medicine

2016 Volume 6, Issue 10

Abstract: More than half of human tumors harbor an inactivated p53 tumor-suppressor gene. It is well accepted that mutant p53 shows an oncogenic gain-of-function (GOF) activity that facilitates the transformed phenotype of cancer cells. In addition, a growing body ...

Abstract	More than half of human tumors harbor an inactivated p53 tumor-suppressor gene. It is well accepted that mutant p53 shows an oncogenic gain-of-function (GOF) activity that facilitates the transformed phenotype of cancer cells. In addition, a growing body of evidence supports the notion that cancer stem cells comprise a seminal constituent in the initiation and progression of cancer development. Here, we elaborate on the mutant p53 oncogenic GOF leading toward the acquisition of a transformed phenotype, as well as placing mutant p53 as a major component in the establishment of cancer stem cell entity. Therefore, therapy targeted toward cancer stem cells harboring mutant p53 is expected to pave the way to eradicate tumor growth and recurrence.
MeSH term(s)	Animals ; Antineoplastic Agents/pharmacology ; Gain of Function Mutation ; Humans ; Mice ; Molecular Targeted Therapy ; Neoplasms/genetics ; Neoplasms/metabolism ; Neoplasms/pathology ; Neoplastic Stem Cells/metabolism ; Neoplastic Stem Cells/pathology ; Phenotype ; Tumor Suppressor Protein p53/genetics
Chemical Substances	Antineoplastic Agents ; Tumor Suppressor Protein p53
Language	English
Publishing date	2016-10-03
Publishing country	United States
Document type	Journal Article ; Review
ISSN	2157-1422
ISSN (online)	2157-1422
DOI	10.1101/cshperspect.a026203
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Article ; Online: p53 on the crossroad between regeneration and cancer.

Charni, Meital / Aloni-Grinstein, Ronit / Molchadsky, Alina / Rotter, Varda

Cell death and differentiation

2017 Volume 24, Issue 1, Page(s) 8–14

Abstract: Regeneration and tumorigenesis share common molecular pathways, nevertheless the outcome of regeneration is life, whereas tumorigenesis leads to death. Although the process of regeneration is strictly controlled, malignant transformation is unrestrained. ...

Abstract	Regeneration and tumorigenesis share common molecular pathways, nevertheless the outcome of regeneration is life, whereas tumorigenesis leads to death. Although the process of regeneration is strictly controlled, malignant transformation is unrestrained. In this review, we discuss the involvement of TP53, the major tumor-suppressor gene, in the regeneration process. We point to the role of p53 as coordinator assuring that regeneration will not shift to carcinogenesis. The fluctuation in p53 activity during the regeneration process permits a tight control. On one hand, its inhibition at the initial stages allows massive proliferation, on the other its induction at advanced steps of regeneration is essential for preservation of robustness and fidelity of the regeneration process. A better understanding of the role of p53 in regulation of regeneration may open new opportunities for implementation of TP53-based therapies, currently available for cancer patients, in regenerative medicine.
Language	English
Publishing date	2017-01
Publishing country	England
Document type	Review ; Journal Article
ZDB-ID	1225672-9
ISSN	1476-5403 ; 1350-9047
ISSN (online)	1476-5403
ISSN	1350-9047
DOI	10.1038/cdd.2016.117
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Zs.A 4230: 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)
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Article ; Online: Various stress stimuli rewire the profile of liver secretome in a p53-dependent manner.

Charni-Natan, Meital / Solomon, Hilla / Molchadsky, Alina / Jacob-Berger, Adi / Goldfinger, Naomi / Rotter, Varda

Cell death & disease

2018 Volume 9, Issue 6, Page(s) 647

Abstract: Liver is an important secretory organ that consistently manages various insults in order to retain whole-body homeostasis. Importantly, it was suggested that the tumor-suppressor p53 plays a role in a variety of liver physiological processes and thus it ... ...

Abstract	Liver is an important secretory organ that consistently manages various insults in order to retain whole-body homeostasis. Importantly, it was suggested that the tumor-suppressor p53 plays a role in a variety of liver physiological processes and thus it is being regarded as a systemic homeostasis regulator. Using high-throughput mass spectrometric analysis, we identified various p53-dependent liver secretome profiles. This allowed a global view on the role of p53 in maintaining the harmony of liver and whole-body homeostasis. We found that p53 altered the liver secretome differently under various conditions. Under physiological conditions, p53 controls factors that are related mainly to lipid metabolism and injury response. Upon exposure to various types of cancer therapy agents, the hepatic p53 is activated and induces the secretion of proteins related to additional pathways, such as hemostasis, immune response, and cell adhesion. Interestingly, we identified a possible relationship between p53-dependent liver functions and lung tumors. The latter modify differently liver secretome profile toward the secretion of proteins mainly related to cell migration and immune response. The notion that p53 may rewire the liver secretome profile suggests a new non-cell autonomous role of p53 that affect different liver functions and whole organism homeostasis.
MeSH term(s)	Animals ; Antineoplastic Agents/pharmacology ; Cell Line, Tumor ; Gene Expression Regulation, Neoplastic ; Humans ; Liver/metabolism ; Liver/physiology ; Lung Neoplasms/genetics ; Lung Neoplasms/pathology ; Mice, Inbred C57BL ; Mice, Knockout ; Stress, Physiological ; Tumor Suppressor Protein p53/metabolism
Chemical Substances	Antineoplastic Agents ; Tumor Suppressor Protein p53
Language	English
Publishing date	2018-05-29
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2541626-1
ISSN	2041-4889 ; 2041-4889
ISSN (online)	2041-4889
ISSN	2041-4889
DOI	10.1038/s41419-018-0697-4
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Article ; Online: Immune deficiency augments the prevalence of p53 loss of heterozygosity in spontaneous tumors but not bi-directional loss of heterozygosity in bone marrow progenitors.

Shetzer, Yoav / Napchan, Yael / Kaufman, Tom / Molchadsky, Alina / Tal, Perry / Goldfinger, Naomi / Rotter, Varda

International journal of cancer

2017 Volume 140, Issue 6, Page(s) 1364–1369

Abstract: p53 loss of heterozygosity (LOH) is a frequent event in tumors of somatic and Li-Fraumeni syndrome patients harboring p53 mutation. Here, we focused on resolving a possible crosstalk between the immune-system and p53 LOH. Previously, we reported that p53 ...

Abstract	p53 loss of heterozygosity (LOH) is a frequent event in tumors of somatic and Li-Fraumeni syndrome patients harboring p53 mutation. Here, we focused on resolving a possible crosstalk between the immune-system and p53 LOH. Previously, we reported that p53 heterozygous bone-marrow mesenchymal progenitor cells undergo p53 LOH in-vivo. Surprisingly, the loss of either the wild-type p53 allele or mutant p53 allele was detected with a three-to-one ratio in favor of losing the mutant allele. In this study, we examined whether the immune-system can affect the LOH directionality in bone marrow progenitors. We found that mesenchymal progenitor cells derived from immune-deficient mice exhibited the same preference of losing the mutant p53 allele as immune-competent matched cells, nevertheless, these animals showed a significantly shorter tumor-free survival, indicating the possible involvement of immune surveillance in this model. Surprisingly, spontaneous tumors of p53 heterozygous immune-deficient mice exhibited a significantly higher incidence of p53 LOH compared to that observed in tumors derived of p53 heterozygous immune-competent mice. These findings indicate that the immune-system may affect the p53 LOH prevalence in spontaneous tumors. Thus suggesting that the immune-system may recognize and clear cells that underwent p53 LOH, whereas in immune-compromised mice, those cells will form tumors with shorter latency. In individuals with a competent immune-system, p53 LOH independent pathways may induce malignant transformation which requires a longer tumor latency. Moreover, this data may imply that the current immunotherapy treatment aimed at abrogating the inhibition of cellular immune checkpoints may be beneficial for LFS patients.
MeSH term(s)	Alleles ; Animals ; Bone Marrow/pathology ; Genes, p53 ; Genotype ; Homeodomain Proteins/genetics ; Immunocompromised Host ; Immunologic Surveillance/genetics ; Immunologic Surveillance/immunology ; Interleukin-2/deficiency ; Interleukin-2/genetics ; Loss of Heterozygosity/genetics ; Loss of Heterozygosity/immunology ; Lymphoma/genetics ; Lymphoma/immunology ; Lymphoma/pathology ; Mesenchymal Stromal Cells/metabolism ; Mesenchymal Stromal Cells/pathology ; Mice ; Mice, Inbred C57BL ; Mice, Inbred NOD ; Mice, Knockout ; Polymorphism, Single Nucleotide ; Sarcoma, Experimental/genetics ; Sarcoma, Experimental/immunology ; Sarcoma, Experimental/pathology ; Tumor Escape ; Tumor Suppressor Protein p53/deficiency ; Tumor Suppressor Protein p53/genetics
Chemical Substances	Homeodomain Proteins ; Interleukin-2 ; Tumor Suppressor Protein p53 ; RAG-1 protein (128559-51-3)
Language	English
Publishing date	2017-03-15
Publishing country	United States
Document type	Journal Article
ZDB-ID	218257-9
ISSN	1097-0215 ; 0020-7136
ISSN (online)	1097-0215
ISSN	0020-7136
DOI	10.1002/ijc.30554
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Zs.A 478: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (1.OG) ab Jg. 2022: Lesesaal (EG)
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Article ; Online: A Mutant p53-Dependent Embryonic Stem Cell Gene Signature Is Associated with Augmented Tumorigenesis of Stem Cells.

Koifman, Gabriela / Shetzer, Yoav / Eizenberger, Shay / Solomon, Hilla / Rotkopf, Ron / Molchadsky, Alina / Lonetto, Giuseppe / Goldfinger, Naomi / Rotter, Varda

Cancer research

2018 Volume 78, Issue 20, Page(s) 5833–5847

Abstract: Mutations in the tumor suppressor p53 are the most frequent alterations in human cancer. These mutations include p53-inactivating mutations as well as oncogenic gain-of-function (GOF) mutations that endow p53 with capabilities to promote tumor ... ...

Abstract	Mutations in the tumor suppressor p53 are the most frequent alterations in human cancer. These mutations include p53-inactivating mutations as well as oncogenic gain-of-function (GOF) mutations that endow p53 with capabilities to promote tumor progression. A primary challenge in cancer therapy is targeting stemness features and cancer stem cells (CSC) that account for tumor initiation, metastasis, and cancer relapse. Here we show that
MeSH term(s)	Animals ; Biomarkers, Tumor ; CRISPR-Cas Systems ; Carcinogenesis/genetics ; Cell Line, Tumor ; Cell Proliferation ; Embryonic Stem Cells/cytology ; Gene Expression Regulation, Neoplastic ; Humans ; Mesenchymal Stem Cells/cytology ; Mice ; Mice, Inbred C57BL ; Mutation ; Neoplasm Recurrence, Local/pathology ; Neoplastic Stem Cells/pathology ; Prognosis ; Tumor Suppressor Protein p53/genetics
Chemical Substances	Biomarkers, Tumor ; TP53 protein, human ; Trp53 protein, mouse ; Tumor Suppressor Protein p53
Language	English
Publishing date	2018-08-28
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-18-0805
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Article ; Online: p53 in liver pathologies-taking the good with the bad.

Charni, Meital / Rivlin, Noa / Molchadsky, Alina / Aloni-Grinstein, Ronit / Rotter, Varda

Journal of molecular medicine (Berlin, Germany)

2014 Volume 92, Issue 12, Page(s) 1229–1234

Abstract: The distinct physiology of the liver makes it a unique ground with respect to its cross talk with p53, the "guardian of the genome." The stressful environment in the liver frequently leads to the activation of p53, which is associated with alterations in ...

Abstract	The distinct physiology of the liver makes it a unique ground with respect to its cross talk with p53, the "guardian of the genome." The stressful environment in the liver frequently leads to the activation of p53, which is associated with alterations in metabolic pathways and induction of apoptosis. The latter serves as a mechanism that controls the deposal of DNA-damaged cells. However, accentuated apoptosis may eventually lead to liver pathologies, mainly steatosis, which can develop into a more severe disease such as steatohepatitis, fibrosis, and cirrhosis. These pathologies, together with other apoptosis outcome such as chronic inflammation, may pave the way toward cancer development. In addition to this unique scenario that connects the ongoing response of wild-type (WT) p53 to stress and cancer development, hepatocarcinoma may develop in other well-described mechanisms involving p53. One such example is hepatitis virus-induced liver cancer whereby p53 is inactivated upon the binding of a specific viral protein, leading to the loss of its tumor suppressive activity. Furthermore, the accumulations of carcinogens such as aflatoxin were shown to yield an oncogenic mutated p53 protein. In this review, we will demonstrate the diverse activities of p53 in the liver. Interestingly, some of these activities may protect the liver from cancer in the short term, yet in the long term, p53 may lead to malignant transformation. A better understanding of the complex clinical outcome of p53 function in the liver may shed light on future therapies.
MeSH term(s)	Animals ; Carcinoma, Hepatocellular/genetics ; Carcinoma, Hepatocellular/metabolism ; Carcinoma, Hepatocellular/pathology ; Fatty Liver/genetics ; Fatty Liver/metabolism ; Fatty Liver/pathology ; Humans ; Liver/metabolism ; Liver/pathology ; Liver Neoplasms/genetics ; Liver Neoplasms/metabolism ; Liver Neoplasms/pathology ; Tumor Suppressor Protein p53/analysis ; Tumor Suppressor Protein p53/genetics ; Tumor Suppressor Protein p53/metabolism
Chemical Substances	Tumor Suppressor Protein p53
Language	English
Publishing date	2014-12
Publishing country	Germany
Document type	Journal Article ; Review
ZDB-ID	1223802-8
ISSN	1432-1440 ; 0946-2716
ISSN (online)	1432-1440
ISSN	0946-2716
DOI	10.1007/s00109-014-1223-5
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Article ; Online: The paradigm of mutant p53-expressing cancer stem cells and drug resistance.

Shetzer, Yoav / Solomon, Hilla / Koifman, Gabriela / Molchadsky, Alina / Horesh, Stav / Rotter, Varda

Carcinogenesis

2014 Volume 35, Issue 6, Page(s) 1196–1208

Abstract: It is well accepted that expression of mutant p53 involves the gain of oncogenic-specific activities accentuating the malignant phenotype. Depending on the specific cancer type, mutant p53 can contribute to either the early or the late events of the ... ...

Abstract	It is well accepted that expression of mutant p53 involves the gain of oncogenic-specific activities accentuating the malignant phenotype. Depending on the specific cancer type, mutant p53 can contribute to either the early or the late events of the multiphase process underlying the transformation of a normal cell into a cancerous one. This multifactorial system is evident in ~50% of human cancers. Mutant p53 was shown to interfere with a variety of cellular functions that lead to augmented cell survival, cellular plasticity, aberration of DNA repair machinery and other effects. All these effects culminate in the acquisition of drug resistance often seen in cancer cells. Interestingly, drug resistance has also been suggested to be associated with cancer stem cells (CSCs), which reside within growing tumors. The notion that p53 plays a regulatory role in the life of stem cells, coupled with the observations that p53 mutations may contribute to the evolvement of CSCs makes it challenging to speculate that drug resistance and cancer recurrence are mediated by CSCs expressing mutant p53.
MeSH term(s)	Animals ; Drug Resistance, Neoplasm/genetics ; Gene Expression Regulation, Neoplastic ; Genomic Instability ; Humans ; Mutation ; Neoplastic Stem Cells/drug effects ; Neoplastic Stem Cells/metabolism ; Signal Transduction ; Tumor Suppressor Protein p53/genetics ; Tumor Suppressor Protein p53/metabolism
Chemical Substances	Tumor Suppressor Protein p53
Language	English
Publishing date	2014-06
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	603134-1
ISSN	1460-2180 ; 0143-3334
ISSN (online)	1460-2180
ISSN	0143-3334
DOI	10.1093/carcin/bgu073
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Article ; Online: Differential regulated microRNA by wild type and mutant p53 in induced pluripotent stem cells.

Grespi, Francesca / Landré, Vivien / Molchadsky, Alina / Di Daniele, Nicola / Marsella, Luigi Tonino / Melino, Gerry / Rotter, Varda

Cell death & disease

2016 Volume 7, Issue 12, Page(s) e2567

Abstract: The tumour suppressor p53 plays an important role in somatic cell reprogramming. While wild-type p53 reduces reprogramming efficiency, mutant p53 exerts a gain of function activity that leads to increased reprogramming efficiency. Furthermore, induced ... ...

Abstract	The tumour suppressor p53 plays an important role in somatic cell reprogramming. While wild-type p53 reduces reprogramming efficiency, mutant p53 exerts a gain of function activity that leads to increased reprogramming efficiency. Furthermore, induced pluripotent stem cells expressing mutant p53 lose their pluripotency in vivo and form malignant tumours when injected in mice. It is therefore of great interest to identify targets of p53 (wild type and mutant) that are responsible for this phenotype during reprogramming, as these could be exploited for therapeutic use, that is, formation of induced pluripotent stem cells with high reprogramming efficiency, but no oncogenic potential. Here we studied the transcriptional changes of microRNA in a series of mouse embryonic fibroblasts that have undergone transition to induced pluripotent stem cells with wild type, knock out or mutant p53 status in order to identify microRNAs whose expression during reprogramming is dependent on p53. We identified a number of microRNAs, with known functions in differentiation and carcinogenesis, the expression of which was dependent on the p53 status of the cells. Furthermore, we detected several uncharacterised microRNAs that were regulated differentially in the different p53 backgrounds, suggesting a novel role of these microRNAs in reprogramming and pluripotency.
MeSH term(s)	Animals ; Cell Differentiation/genetics ; Cellular Reprogramming/genetics ; Down-Regulation/genetics ; Embryo, Mammalian/cytology ; Fibroblasts/metabolism ; Gene Expression Regulation ; Induced Pluripotent Stem Cells/cytology ; Induced Pluripotent Stem Cells/metabolism ; Mice ; MicroRNAs/genetics ; MicroRNAs/metabolism ; Mutation/genetics ; Response Elements/genetics ; Tumor Suppressor Protein p53/metabolism ; Up-Regulation/genetics
Chemical Substances	MicroRNAs ; Tumor Suppressor Protein p53
Language	English
Publishing date	2016-12-29
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2541626-1
ISSN	2041-4889 ; 2041-4889
ISSN (online)	2041-4889
ISSN	2041-4889
DOI	10.1038/cddis.2016.419
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