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Article: Strategies of the War on Cancer: To Kill or to Neutralize?

Lichtenstein, Anatoly V

2019 Volume 8, Page(s) 667

Language	English
Publishing date	2019-01-10
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2649216-7
ISSN	2234-943X
ISSN	2234-943X
DOI	10.3389/fonc.2018.00667
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: Genetic Mosaicism and Cancer: Cause and Effect.

Lichtenstein, Anatoly V

Cancer research

2018 Volume 78, Issue 6, Page(s) 1375–1378

Abstract: Increasing theoretical and experimental evidence suggests that the genomes of both normal and cancer cells are subject to continuous changes as a result of copying errors during replication, defects in chromosome segregation during mitosis, and direct ... ...

Abstract	Increasing theoretical and experimental evidence suggests that the genomes of both normal and cancer cells are subject to continuous changes as a result of copying errors during replication, defects in chromosome segregation during mitosis, and direct chemical attacks by reactive oxygen species. The process of cellular genetic diversification begins during embryonic development and continues throughout life, leading to the phenomenon of somatic mosaicism. New information about the genetic diversity of cells composing the body makes us reconsider the existing concepts of cancer etiology and pathogenesis. Here, I suggest that a progressively deteriorating microenvironment ("soil") generates the cancerous "seed" and favors its development.
MeSH term(s)	Aging/genetics ; Animals ; Cell Transformation, Neoplastic/genetics ; Humans ; Mosaicism ; Mutation Rate ; Neoplasms/genetics ; Neoplasms/pathology
Language	English
Publishing date	2018-02-22
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	1432-1
ISSN	1538-7445 ; 0008-5472
ISSN (online)	1538-7445
ISSN	0008-5472
DOI	10.1158/0008-5472.CAN-17-2769
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Article ; Online: Aberrant methylation scanning by quantitative DNA melting analysis with hybridization probes as exemplified by liquid biopsy of SEPT9 and HIST1H4F in colorectal cancer.

Botezatu, Irina V / Kondratova, Valentina N / Stroganova, Anna M / Dranko, Svetlana L / Lichtenstein, Anatoly V

Clinica chimica acta; international journal of clinical chemistry

2023 Volume 551, Page(s) 117591

Abstract: Objective: The generally accepted method of quantifying hypermethylated DNA by qPCR using methylation-specific primers has the risk of underestimating DNA methylation and requires data normalization. This makes the analysis complicated and less reliable. ...

Abstract	Objective: The generally accepted method of quantifying hypermethylated DNA by qPCR using methylation-specific primers has the risk of underestimating DNA methylation and requires data normalization. This makes the analysis complicated and less reliable. Methods: The end-point PCR method, called qDMA-HP (for quantitative DNA Melting Analysis with hybridization probes), which excludes the normalization procedure, is multiplexed and quantitative, has been proposed. qDMA-HP is characterized by the following features: (i) asymmetric PCR with methylation-independent primers; (ii) fluorescent dual-labeled, self-quenched probes (commonly known as TaqMan probes) covering several interrogated CpGs; (iii) post-PCR melting analysis of amplicon/probe hybrids; (iv) quantitation of unmethylated and methylated DNA alleles by measuring the areas under the corresponding melt peaks. Results: qDMA-HP was tested in liquid biopsy of colorectal cancer by evaluating SEPT9 and HIST1H4F methylations simultaneously in the single-tube reaction. Differences in the methylation levels in healthy donors versus cancer patients were statistically significant (p < 0.0001), AUCROC values were 0.795-0.921 for various marker combinations. Conclusions: This proof-of-concept study shows that qDMA-HP is a simple, normalization-independent, quantitative, multiplex and "closed tube" method easily adapted to clinical settings. It is demonstrated, for the first time, that HIST1H4F is a perspective marker for liquid biopsy of colorectal cancer.
MeSH term(s)	Humans ; Nucleic Acid Denaturation ; DNA Methylation ; DNA ; Cytoskeletal Proteins/genetics ; DNA Primers ; Colorectal Neoplasms/diagnosis ; Colorectal Neoplasms/genetics ; Colorectal Neoplasms/pathology ; Liquid Biopsy
Chemical Substances	DNA (9007-49-2) ; Cytoskeletal Proteins ; DNA Primers
Language	English
Publishing date	2023-10-11
Publishing country	Netherlands
Document type	Journal Article
ZDB-ID	80228-1
ISSN	1873-3492 ; 0009-8981
ISSN (online)	1873-3492
ISSN	0009-8981
DOI	10.1016/j.cca.2023.117591
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Article ; Online: Cancer: evolutionary, genetic and epigenetic aspects.

Lichtenstein, Anatoly V

Clinical epigenetics

2010 Volume 1, Issue 3-4, Page(s) 85–100

Abstract: There exist two paradigms about the nature of cancer. According to the generally accepted one, cancer is a by-product of design limitations of a multi-cellular organism (Greaves, Nat Rev Cancer 7:213-221, 2007). The essence of the second resides in the ... ...

Abstract	There exist two paradigms about the nature of cancer. According to the generally accepted one, cancer is a by-product of design limitations of a multi-cellular organism (Greaves, Nat Rev Cancer 7:213-221, 2007). The essence of the second resides in the question "Does cancer kill the individual and save the species?" (Sommer, Hum Mutat 3:166-169, 1994). Recent data on genetic and epigenetic mechanisms of cell transformation summarized in this review support the latter point of view, namely that carcinogenesis is an evolutionary conserved phenomenon-a programmed death of an organism. It is assumed that cancer possesses an important function of altruistic nature: as a mediator of negative selection, it serves to preserve integrity of species gene pool and to mediate its evolutionary adjustment. Cancer fulfills its task due apparently to specific killer function, understanding mechanism of which may suggest new therapeutic strategy.
Language	English
Publishing date	2010-09-14
Publishing country	Germany
Document type	Journal Article
ZDB-ID	2553921-8
ISSN	1868-7083 ; 1868-7075
ISSN (online)	1868-7083
ISSN	1868-7075
DOI	10.1007/s13148-010-0010-6
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Article: Cancer: shift of the paradigm.

Lichtenstein, Anatoly V

Medical hypotheses

2008 Volume 71, Issue 6, Page(s) 839–850

Abstract: ... from a specific activity (killer function) of cancer cell and (v) evolutionary conservation indicates that cancer ...

Abstract	Cancer is usually considered to be a by-product of design limitations of a multicellular organism and its intrinsic fallibility. However, recent data prompt a revision of some established notions about carcinogenesis and form a new paradigm of carcinogenesis as a highly conserved biological phenomenon - a programmed death of an organism. This altruistic program, which is unleashed when mutagenesis surpasses a certain critical threshold, gives a population the important benefit acting as a guardian of the gene pool against the spread of certain mutant genes. A growing body of evidence supports this point of view: (i) epigenetic changes leading to cancer arise early, simultaneously in many cells and look like deterministic regulation; (ii) concept of cancer stem cell suggests a view of carcinogenesis not as vague transformation but as well known differentiation; (iii) tumor/host relations usually perceived as antagonistic are, in reality, synergistic; (iv) death of an individual from cancer is predetermined and results apparently from a specific activity (killer function) of cancer cell and (v) evolutionary conservation indicates that cancer comes with a general advantage that explains its evolutionary success. A holistic approach to carcinogenesis suggests new avenues of research and new therapeutic strategy.
MeSH term(s)	Cell Communication ; Cell Physiological Phenomena ; Cell Transformation, Neoplastic ; Humans ; Models, Biological ; Mutation ; Neoplasms/genetics ; Neoplasms/mortality ; Neoplasms/physiopathology
Language	English
Publishing date	2008-12
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	193145-3
ISSN	1532-2777 ; 0306-9877
ISSN (online)	1532-2777
ISSN	0306-9877
DOI	10.1016/j.mehy.2008.07.041
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Article: Clonal heterogeneity of tumor may be due to continuous influx of newly transformed cells.

Lichtenstein, Anatoly V

Cancer biology & therapy

2006 Volume 5, Issue 10, Page(s) 1263–1264

MeSH term(s)	Cell Division ; Cell Transformation, Neoplastic ; Genetic Heterogeneity ; Humans ; Neoplasms/genetics ; Neoplasms/pathology
Language	English
Publishing date	2006-10-05
Publishing country	United States
Document type	Journal Article
ZDB-ID	2146305-0
ISSN	1538-4047
ISSN	1538-4047
DOI	10.4161/cbt.5.10.3347
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Article ; Online: Asymmetric mutant-enriched polymerase chain reaction and quantitative DNA melting analysis of KRAS mutation in colorectal cancer.

Botezatu, Irina V / Kondratova, Valentina N / Shelepov, Valery P / Mazurenko, Natalia N / Tsyganova, Irina V / Susova, Olga Y / Lichtenstein, Anatoly V

Analytical biochemistry

2019 Volume 590, Page(s) 113517

Abstract: Identification of mutant genes in tumor tissues and blood plasma (solid and liquid biopsy samples, respectively) is a necessity for individualized treatment of cancer patients. Here we report the use of a novel mutant-enriched PCR - quantitative DNA ... ...

Abstract	Identification of mutant genes in tumor tissues and blood plasma (solid and liquid biopsy samples, respectively) is a necessity for individualized treatment of cancer patients. Here we report the use of a novel mutant-enriched PCR - quantitative DNA melting curve analysis (mePCR-qDMA) with TaqMan probes. The TaqMan probes served as blocking agents during PCR and as hybridization probes during DNA melting curve analyses. The end-point measurement of melt peaks areas by PeakFit software, a nonlinear iterative curve-fitting program, permitted quantification of the mutant/wild-type allele ratios. Approximately 6% and 0.1% of mutant KRAS allele in an excess of wild-type allele is detected with the standard and mePCR-qDMA processes, respectively. The application of the approach was tested for detecting the KRAS codon 12/13 mutation in paired tumor and blood plasma samples from 20 colorectal cancer patients. KRAS mutants were detected in 7 and 18 FFPE tumor samples, and in 3 and 7 plasma samples by the standard and mePCR-qDMA process, respectively. The results were confirmed by Sanger sequencing. This simple, rapid, cost-effective, and quantitative method carried out in a closed-tube format could be applied for the clinical analyses of other cancer genes.
MeSH term(s)	Adult ; Aged ; Aged, 80 and over ; Colorectal Neoplasms/genetics ; DNA Mutational Analysis/methods ; DNA, Neoplasm/blood ; Female ; Humans ; Male ; Middle Aged ; Mutation ; Polymerase Chain Reaction/methods ; Proto-Oncogene Proteins p21(ras)/genetics
Chemical Substances	DNA, Neoplasm ; KRAS protein, human ; Proto-Oncogene Proteins p21(ras) (EC 3.6.5.2)
Language	English
Publishing date	2019-11-26
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	1110-1
ISSN	1096-0309 ; 0003-2697
ISSN (online)	1096-0309
ISSN	0003-2697
DOI	10.1016/j.ab.2019.113517
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Article: On evolutionary origin of cancer.

Lichtenstein, Anatoly V

Cancer cell international

2005 Volume 5, Issue 1, Page(s) 5

Abstract: BACKGROUND: The necessary and sufficient capabilities of cancer cell have been identified. Strikingly, this list does not include one that would seem to be a key property, namely the ability of cancer cells to kill their "host". This is believed to be a ... ...

Abstract	BACKGROUND: The necessary and sufficient capabilities of cancer cell have been identified. Strikingly, this list does not include one that would seem to be a key property, namely the ability of cancer cells to kill their "host". This is believed to be a self-evident consequence of the other capabilities (e.g., metastasis), although the available evidence suggests a distinct killer function. Taking into account this unlisted property can significantly affect the current paradigm of carcinogenesis. PRESENTATION OF THE HYPOTHESIS: On the assumption that killer function is a key capability of the cancer cell, it is suggested that cancer has evolved as a mechanism of negative selection of mutant alleles of vitally important genes present in population. Similarly to apoptosis, which is an altruistic suicidal act of a damaged cell, cancer is an altruistic suicidal act of an individual who carries dangerous alleles and presents a hazard for genetic stability of the population. From this point of view, apoptosis is not a protection means against cancer as generally believed, but rather they are the first and second lines of defense against genome instability, respectively. TESTING THE HYPOTHESIS: The modern DNA array technology is capable of revealing gene expression profiles responsible for killer function of cancer cell as well as those specific targets in the body that are most strongly affected by the tumor growth. IMPLICATIONS OF THE HYPOTHESIS: This hypothesis suggests new avenues of cancer research as well as principally new therapeutic strategies.
Language	English
Publishing date	2005-03-02
Publishing country	England
Document type	Journal Article
ISSN	1475-2867
ISSN	1475-2867
DOI	10.1186/1475-2867-5-5
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Article: Asymmetric mutant-enriched polymerase chain reaction and quantitative DNA melting analysis of KRAS mutation in colorectal cancer

Botezatu, Irina V / Kondratova, Valentina N / Shelepov, Valery P / Mazurenko, Natalia N / Tsyganova, Irina V / Susova, Olga Y / Lichtenstein, Anatoly V

Analytical biochemistry. 2020 Feb. 01, v. 590

2020

Abstract	Identification of mutant genes in tumor tissues and blood plasma (solid and liquid biopsy samples, respectively) is a necessity for individualized treatment of cancer patients. Here we report the use of a novel mutant-enriched PCR - quantitative DNA melting curve analysis (mePCR-qDMA) with TaqMan probes. The TaqMan probes served as blocking agents during PCR and as hybridization probes during DNA melting curve analyses. The end-point measurement of melt peaks areas by PeakFit software, a nonlinear iterative curve-fitting program, permitted quantification of the mutant/wild-type allele ratios. Approximately 6% and 0.1% of mutant KRAS allele in an excess of wild-type allele is detected with the standard and mePCR-qDMA processes, respectively. The application of the approach was tested for detecting the KRAS codon 12/13 mutation in paired tumor and blood plasma samples from 20 colorectal cancer patients. KRAS mutants were detected in 7 and 18 FFPE tumor samples, and in 3 and 7 plasma samples by the standard and mePCR-qDMA process, respectively. The results were confirmed by Sanger sequencing. This simple, rapid, cost-effective, and quantitative method carried out in a closed-tube format could be applied for the clinical analyses of other cancer genes.
Keywords	DNA ; alleles ; biopsy ; blood plasma ; colorectal neoplasms ; computer software ; cost effectiveness ; hybridization probes ; melting ; melting curve analysis ; mutants ; mutation ; patients ; polymerase chain reaction ; quantitative analysis ; tissues
Language	English
Dates of publication	2020-0201
Publishing place	Elsevier Inc.
Document type	Article
ZDB-ID	1110-1
ISSN	1096-0309 ; 0003-2697
ISSN (online)	1096-0309
ISSN	0003-2697
DOI	10.1016/j.ab.2019.113517
Database	NAL-Catalogue (AGRICOLA)

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Article ; Online: On evolutionary origin of cancer

Lichtenstein Anatoly V

Cancer Cell International, Vol 5, Iss 1, p

2005 Volume 5

Abstract: Abstract Background The necessary and sufficient capabilities of cancer cell have been identified. Strikingly, this list does not include one that would seem to be a key property, namely the ability of cancer cells to kill their "host". This is believed ... ...

Abstract	Abstract Background The necessary and sufficient capabilities of cancer cell have been identified. Strikingly, this list does not include one that would seem to be a key property, namely the ability of cancer cells to kill their "host". This is believed to be a self-evident consequence of the other capabilities (e.g., metastasis), although the available evidence suggests a distinct killer function. Taking into account this unlisted property can significantly affect the current paradigm of carcinogenesis. Presentation of the hypothesis On the assumption that killer function is a key capability of the cancer cell, it is suggested that cancer has evolved as a mechanism of negative selection of mutant alleles of vitally important genes present in population. Similarly to apoptosis, which is an altruistic suicidal act of a damaged cell, cancer is an altruistic suicidal act of an individual who carries dangerous alleles and presents a hazard for genetic stability of the population. From this point of view, apoptosis is not a protection means against cancer as generally believed, but rather they are the first and second lines of defense against genome instability, respectively. Testing the hypothesis The modern DNA array technology is capable of revealing gene expression profiles responsible for killer function of cancer cell as well as those specific targets in the body that are most strongly affected by the tumor growth. Implications of the hypothesis This hypothesis suggests new avenues of cancer research as well as principally new therapeutic strategies.
Keywords	Neoplasms. Tumors. Oncology. Including cancer and carcinogens ; RC254-282 ; Internal medicine ; RC31-1245 ; Medicine ; R ; DOAJ:Oncology ; DOAJ:Medicine (General) ; DOAJ:Health Sciences
Subject code	610
Language	English
Publishing date	2005-03-01T00:00:00Z
Publisher	BioMed Central
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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