Analysis of octamer-binding transcription factor-4 expression in oral leukoplakia

Tegginamani, Anand S; Shivakumar, V; Kallarakkal, Thomas George; Ismail, Siti Mazlipah; Abraham, Mannil Thomas; Zamzuri, Ahmad

doi:10.4103/jomfp.jomfp_272_19

Cited by 5 publications

(2 citation statements)

References 32 publications

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“…[ 31 ] In cervical cancers, OSCC, and cutaneous SCC, the expression was dramatically reduced, indicating that CD138 can be used for the identification. [ 32 , 33 ] Reduced expression is considered a precursor to MT or a sign that malignancy is more likely to develop. Few studies have examined the immunoreactivity of CD138 and CD43 in OL.…”

Section: Discussionmentioning

confidence: 99%

Comparison of the IHC Markers CD138 and CD43 in Oral Leukoplakia: An Original Research

Akkaloori,

Saikia,

Kuppusamy

et al. 2023

Journal of Pharmacy and Bioallied Sciences

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Background: In the clinical practice, one of the most common suspicious lesions that may be potentially malignant is oral leukoplakia. Globally, the rate at which it turns malignant varies. This study examines the levels of markers CD138 and 43 in oral leukoplakia. Materials and Methods: Twenty archival blocks of confirmed epithelial dysplasia were taken from the Department of Oral Pathology. These were processed for the identification of markers CD138 and 43 through Immuno Histo Chemistry (IHC). The blocks were divided equally for both the markers. Results: There was a noticeable difference in staining intensity between dysplastic tissue and nondysplastic epithelium. However, CD138 expression was low or weak in dysplastic epithelium. CD43 expression was negative in all nonhematopoietic tissues. Conclusion: Genes that are cancer associated have been found to have incredibly different impacts in numerous tissues during the multistep process of oral carcinogenesis. In tissues undergoing dysplastic changes, CD138 expression was shown to be decreased, which could point out the malignant changes initiated in the epithelium of the oral tissues.

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Section: Discussionmentioning

confidence: 99%

Comparison of the IHC Markers CD138 and CD43 in Oral Leukoplakia: An Original Research

Akkaloori,

Saikia,

Kuppusamy

et al. 2023

Journal of Pharmacy and Bioallied Sciences

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“…However, do they share some common markers that make them a cancer stem cell? As pointed out previously, if the cancer stem cell is derived from a normal organ-specific adult stem cell, and if one marker, namely, the Oct4A gene, is shared by all cancer stem cells, as seems to be indicated by many published papers [60][61][62][63][64][65][66][67][68][69][70][71][72][73][74][75][76][77], then it would seem that some strategy should be developed to find ways to either shut down this gene in order to force the cells to differentiate or apoptose. In addition, if the connexin genes and functional gap junctions are not found in either the normal stem cells or cancer stem cells, agents that might induce the connexin genes to be expressed could induce either differentiation or apoptosis.…”

Section: Are All "Cancer Stem Cells" Identical?mentioning

confidence: 99%

The Concept of “Cancer Stem Cells” in the Context of Classic Carcinogenesis Hypotheses and Experimental Findings

Trosko

2021

Life

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In this Commentary, the operational definition of cancer stem cells or cancer initiating cells includes the ability of certain cells, found in a heterogeneous mixture of cells within a tumor, which are able to sustain growth of that tumor. However, that concept of cancer stem cells does not resolve the age-old controversy of two opposing hypotheses of the origin of the cancer, namely the stem cell hypothesis versus the de-differentiation or re-programming hypothesis. Moreover, this cancer stem concept has to take into account classic experimental observations, techniques, and concepts, such as the multi-stage, multi-mechanism process of carcinogenesis; roles of mutagenic, cytotoxic and epigenetic mechanisms; the important differences between errors of DNA repair and errors of DNA replication in forming mutations; biomarkers of known characteristics of normal adult organ-specific stem cells and of cancer stem cells; and the characteristics of epigenetic mechanisms involved in the carcinogenic process. In addition, vague and misleading terms, such as carcinogens, immortal and normal cells have to be clarified in the context of current scientific facts. The ultimate integration of all of these historic factors to provide a current understanding of the origin and characteristics of a cancer stem cell, which is required for a rational strategy for prevention and therapy for cancer, does not follow a linear path. Lastly, it will be speculated that there exists evidence of two distinct types of cancer stem cells, one that has its origin in an organ-specific adult stem cell that is ‘initiated’ in the stem cell stage, expressing the Oct4A gene and not expressing any connexin gene or having functional gap junctional intercellular communication (GJIC). The other cancer stem cell is derived from a stem cell that is initiated early after the Oct4A gene is suppressed and the connexin gene is expressed, which starts early differentiation, but it is blocked from terminal differentiation.

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On the potential origin and characteristics of cancer stem cells

Trosko

2021

Carcinogenesis

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The “cancer stem cell” hypothesis has pointed to a specific target for new cancer therapies. The hypothesis is based on the observation that only the “cancer stem cell” among the other heterogeneous cancer cells can sustain the growth of the cancer. The goal is to identify biomarkers of “cancer stem cells” to distinguish them from the “cancer non-stem cells” and normal adult tissue-specific stem cells. This analyst posits a hypothesis that, while all cancers originated from a single cell, there exist two types of “cancer stem cells” either by the “Stem Cell hypothesis” or from the “De-differentiation hypothesis”. It is proposed that there exist two different “cancer stem cells”. Some “cancer stem cells” (a) lack the expression of connexins or gap junction genes and lack any form of gap junctional intercellular communication (GJIC) or (b) they have the expressed connexin -coded proteins for functional GJIC but are dysfunctional by some expressed oncogene. This is consistent with the Loewenstein hypothesis that a universal characteristic of cancer cells is they do not have growth control, nor terminally differentiate. This review speculates the normal organ-specific adult stem cell, that is “initiated”, is the origin of the “cancer stem cells” with expressed Oct4A gene and no expressed connexin genes; while the other cancer stem cell has no expressed Oct4A genes but expressed connexin gene, whose coded protein is dysfunctional. Hence. both types of “cancer stem cells” lack GJIC, for two different reasons, the selective therapies have to be different for these different cell types.

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Analysis of octamer-binding transcription factor-4 expression in oral leukoplakia

Cited by 5 publications

References 32 publications

Comparison of the IHC Markers CD138 and CD43 in Oral Leukoplakia: An Original Research

Comparison of the IHC Markers CD138 and CD43 in Oral Leukoplakia: An Original Research

The Concept of “Cancer Stem Cells” in the Context of Classic Carcinogenesis Hypotheses and Experimental Findings

On the potential origin and characteristics of cancer stem cells

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