Lung cancer stem cells—origin, characteristics and therapy

Prabavathy, D.; Swarnalatha, Y; Ramadoss, Niveditha

doi:10.21037/sci.2018.02.01

Cited by 85 publications

(73 citation statements)

References 76 publications

(67 reference statements)

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“…These stem cells express markers such as high aldehyde dehydrogenase (ALDH) activity, CD44, CD133 and can be identified by flow cytometry as a side population (Hoechst exclusion) and be potentially responsible for tumor relapse like dormant/quiescent/persister cells [22][23][24][25][26]. Furthermore, the link between stemness properties and dormancy has been already established in various cancer types including for instance glioblastoma [27], sarcoma [25], colon [28], breast [29,30], prostate [31], lung [32,33], and ovarian cancers [34].…”

Section: Dormant Quiescent Tolerant and Persister Cells In Cancermentioning

confidence: 99%

Dormant, quiescent, tolerant and persister cells: Four synonyms for the same target in cancer

Vallette

Olivier

Lezot

et al. 2019

Biochemical Pharmacology

142

126

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Although many drugs/treatments are now available for most diseases, too often, resistance to these treatments impedes complete therapeutic success. Acquired resistance is a major problem in many pathologies but it is an acute one in cancers and infections. This is probably because these diseases often require long durations of treatment, which ascribe to the selection of resistant cells. However, the actual mechanisms implicated in the selection process are still under debate. It is becoming increasingly clear that resistance is associated with the heterogeneity of cancer cells or microorganisms and that multiple mechanisms underlie the emergence of drug-resistant subpopulations. Recently, it has been suggested that a subpopulation of drug tolerant cells present in cancer populations and called "persisters" play a major role in this resistance. Recent studies have shown that microorganisms share similar properties. Still, how persister/tolerant cells intervene in the development of resistance is not completely elucidated but seems to be related to epigenetic changes in treated cells and the capacity of persisters to modulate and/or highjack their microenvironment. Due to the complexity of this process, the input from mathematicians, as well as new methods of bioinformatics and statistics, is necessary to fully comprehend the acquisition of resistance/tolerance deriving from and leading to the heterogeneous cell populations. The present review will give a brief overview of the most recent data available on drug tolerant cells in cancers and their similarities with microorganisms.

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Section: Dormant Quiescent Tolerant and Persister Cells In Cancermentioning

confidence: 99%

Dormant, quiescent, tolerant and persister cells: Four synonyms for the same target in cancer

Vallette

Olivier

Lezot

et al. 2019

Biochemical Pharmacology

142

126

View full text Add to dashboard Cite

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“…However, none of the commonly used markers (including CD133, ALDH, CD44, EpCAM, or CD90) can standalone as an ubiquitous marker for hepatic CSCs due to heterogeneity of the tumoral process [108]. Additionally, ALDH was used as a biomarker for distinguishing normal from CSCs, making it a powerful predictor of poor clinical outcome [105,[109][110][111]. However, a recent study demonstrated that deletion of the Aldh1a gene did not affect LPC proliferation or HCC progression [21].…”

Section: Aldh and Cancer Stem Cellsmentioning

confidence: 99%

“…However, the biological functions of ALDHs extend beyond detoxification, as the enzymes are involved in other biochemical processes, such as retinoic acid (RA) biosynthesis, catalysis of folate and amino acid and lipid peroxidation [2]. Additionally, altered ALDH activity is associated with certain behavioral deficits [3,4], endocrine disorders, cardiovascular and lung diseases [5], oral and gastrointestinal cancers, Fanconi anemia, and dermatitis [6].…”

Section: Introductionmentioning

confidence: 99%

Aldehyde Dehydrogenase, Liver Disease and Cancer

Wang

et al. 2020

Int. J. Biol. Sci.

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Acetaldehyde dehydrogenase 2 (ALDH2) is the key enzyme responsible for metabolism of the alcohol metabolite acetaldehyde in the liver. In addition to conversion of the acetaldehyde molecule, ALDH is also involved in other cellular functions. Recently, many studies have investigated the involvement of ALDH expression in viral hepatitis, alcoholic liver disease (ALD), non-alcoholic fatty liver disease (NAFLD), liver fibrosis, and liver cancer. Notably, ALDH2 expression has been linked with liver cancer risk, as well as pathogenesis and prognosis, and has emerged as a promising therapeutic target. Of note, approximately 8% of the world's population, and approximately 30-40% of the population in East Asia carry an inactive ALDH2 gene. This review summarizes new progress in understanding tissue-specific acetaldehyde metabolism by ALDH2 as well as the association of ALDH2 gene polymorphisms with liver disease and cancer. New research directions emerging in the field are also briefly discussed.

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“…Despite the availability of diagnostic and genetic technologies, the five-years survival rate is poor, and the reason why the mortality rates still remain higher than other cancers [29]. This is also due to the presence of cancer stem cells (CSCs) or tumor-initiating cells (T-ICs) in the tumor mass, that are a highly undifferentiated cellular population, resistant to chemotherapy and responsible to the high recurrence [30].…”

Section: Top Five Lethal Solid Cancersmentioning

confidence: 99%

Retinoic Acids in the Treatment of Most Lethal Solid Cancers

Costantini

Molinari

Farinon

et al. 2020

JCM

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Although the use of oral administration of pharmacological all-trans retinoic acid (ATRA) concentration in acute promyelocytic leukaemia (APL) patients was approved for over 20 years and used as standard therapy still to date, the same use in solid cancers is still controversial. In the present review the literature about the top five lethal solid cancers (lung, stomach, liver, breast, and colon cancer), as defined by The Global Cancer Observatory of World Health Organization, and retinoic acids (ATRA, 9-cis retinoic acid, and 13-cis retinoic acid, RA) was compared. The action of retinoic acids in inhibiting the cell proliferation was found in several cell pathways and compartments: from membrane and cytoplasmic signaling, to metabolic enzymes, to gene expression. However, in parallel in the most aggressive phenotypes several escape routes have evolved conferring retinoic acids-resistance. The comparison between different solid cancer types pointed out that for some cancer types several information are still lacking. Moreover, even though some pathways and escape routes are the same between the cancer types, sometimes they can differently respond to retinoic acid therapy, so that generalization cannot be made. Further studies on molecular pathways are needed to perform combinatorial trials that allow overcoming retinoic acids resistance.

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Lung cancer stem cells—origin, characteristics and therapy

Abstract: This review will focus on stem cell origins, role of signaling pathways, stem cell markers and therapeutic approaches specific to lung cancer.

Cited by 85 publications

References 76 publications

Dormant, quiescent, tolerant and persister cells: Four synonyms for the same target in cancer

Dormant, quiescent, tolerant and persister cells: Four synonyms for the same target in cancer

Aldehyde Dehydrogenase, Liver Disease and Cancer

Retinoic Acids in the Treatment of Most Lethal Solid Cancers

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