REVIEW OF SCIENTIFIC ARTICLES
|Year : 2003 | Volume
| Issue : 2 | Page : 58-59
Review of scientific articles
T Bertin A Einstein, N Gururaj, A Anuradha
Department of Oral and Maxillo Facial Pathology, Meenakshi Ammal Dental College and Hospital, Chennai, India
T Bertin A Einstein
Department of Oral and Maxillo Facial Pathology, Meenakshi Ammal Dental College and Hospital, Chennai
Source of Support: None, Conflict of Interest: None
|How to cite this article:|
Einstein T B, Gururaj N, Anuradha A. Review of scientific articles. J Oral Maxillofac Pathol 2003;7:58-9
| An Introduction to Stem Cells|| |
Alison MR, Poulsom R, Forbes S and Wright NA
J PATHOL 2002, 197: 419-423
The field of stem cell research has gained worldwide attention in the recent years, because of a genuine belief that stem cells may be the answer to mankind's prayer to be able to replace tissues worn out by age and ravaged by disease. In spite of the remarkable progress made with embryonic stem (ES) cells, growing opposition to the use of early human embryos or aborted fetuses for procuring the stem cells have led to search for other sources of stem cells with similar levels of clonogenecity. Certain adult stem cells such as the haematopoietic compartment have been identified as having the capacity to differentiate into cells of another organ system. This article summarizes the important attributes of such tissue specific stem cells.
Tissue specific stem cells are a self-maintaining population with a high level of clonogenecity and a slow cycling potential. They appear to be located in most organs of the body with perhaps the possible exception of the heart and can be identified by various markers, such as β-1 integrin for epidermal stem cells. The authors suggest that these tissue based stem cells could be implicated in cancers of continuously renewing cells, as only these stem cells persist for a sufficient length of time to acquire the necessary number of genetic changes for neoplastic transformation. Also, the tissue stem cells are possibly governed by the local microenvironment through a combination of cells and extracellular matrix.
Advent of tissue specific stem cells assumes significance given the ethical issues concerning the use of ES cells. Also, these newly discovered pathways of tissue regeneration may lead to a revolution in terms of how we treat cardiovascular disease, neurodegenerative disease, cancer, diabetes, and the like. Further, the suggested role of tissue specific stem cells in cancers of continuously renewing cells, should provide a better insight into the pathogenesis of oral cancer.
| Clinical, Cellular, and Molecular Aspects of Cancer Invasion|| |
Mareel M, Leroy A
PHYSIOL REV 83: 337-376, 2003
Invasion causes malignancy. The authors extensively review recent data about cellular and molecular mechanisms of invasion, focusing on cross talk between the invaders and the host. The discussion centers on the invasion promoter and suppressor genes such as Ecadherin gene CDH1, N-cadherin gene CDH2, E-catenin gene CTNNA1, N-catenin gene CTNNB1, kinase and phosphatase genes, and the non-cancer invasion promoter and suppressor genes. Various cellular activities associated with the invasive phenotype such as cell-cell adhesion, cell-matrix interactions, migration and proteolysis are discussed in detail.
The highlight of the article is however the molecular cross talk between the host cells (myofibroblasts, blood and lymph vessels, tumour infiltrated leukocytes, osteoclasts) and the cancer cells, leading to cancer invasion. It is interesting to note that similar invasion of cells is also noticed during embryonic development (migration of neural crest cells), in healthy organisms (leukocytes moving from the tissue of origin in bone marrow into circulation to reach specific sites), and in many non cancerous diseases (entry of microorganisms into the host through the skin, to reach the circulation and produce secondary lesions). The interaction between the host cells and the cancer cells asserts the fact that cancer invasion is a subject of tissue restriction and these restrictions seem to be disturbed during tumour progression. The ultimate goal of future research would thus be restoration of these tissue restrictions by manipulation of the positive and negative invasion pathways in cancer cells or in host cells.
| A Genetic Explanation of Slaughter's Concept of Field Cancerization: Evidence and Clinical Implications|| |
Braakhuis BJM, Tabor MP, Kummer JA, Leemans CR, Brakenhoff RH
CANCER RESEARCH 63, 1737-1730, 2003
'Field cancerization' refers to the existence of pre neoplastic processes at multiple sites, often with the unproven assumption that these have developed independently. It is already an established fact that an accumulation of genetic alterations forms the basis for the progression from a normal cell to a cancer cell, referred to as the process of mutistep carcinogenesis. Thus, the process of 'field cancerization' could be best understood in molecular terms. Molecular analyses of tumour adjacent 'normal tissue' and tumour margins, using markers such as LOH, microsatellite alterations, chromosomal instability, and mutations in the TP53 gene detected by DNA amplification techniques, immunohistochemistry and in situ hybridisation, have revealed the presence of one or more areas consisting of epithelial cells with genetic alterations. This has led the authors to define such areas as comprising a 'preneoplastic field', which might show dysplasia histologically; in fact all moderately and severly dysplastic lesions show genetic alterations.
Based on these findings, a model of multistep carcinogenesis as related to 'field cancerization' has been proposed. Initially, a stem cell which acquires genetic alterations forms a 'patch', a clonal unit of altered daughter cells. Additional genetic alterations lead to the conversion of this 'patch' into an expanding proliferating field which gradually displaces the normal mucosa. Ultimately, clonal divergence leads to the development of one or more tumours within a contiguous field of preneoplastic cells. The persistence of the fields after surgery of the primary tumour, leads to new cancers, designated by clinicians as 'a second primary tumour' or 'local recurrence'. For the clinician, this concept of the expanding field has important consequences. In future, the diagnosis and treatment of epithelial cancers should not only be focused on the tumour but also on the field from which it developed
| Prostaglandins as Modulators of Immunity|| |
Harris SG, Padilla J, Koumas L, Ray D and Phipps RP
TRENDS IN IMMUNOLOGY, VOL.23, No.3, MAR 2002
Prostaglandins (PG) are unsaturated hydroxy acids with 5-numbered ring in a 20-carbon skeleton. They regulate numerous processes in the body including kidney function, platelet aggregation, neurotransmitter release and modulation of immune function. As oral pathologists, we are familiar with the actions of PG in inflammation. This review provides the highlights of recent research data concerning the role of a well-studied prostaglandin E 2 (PGE ) in cells of the immune system and disease states. As regarding the immune cells, PGE 2 has a diverse effect on the T cells; plays an important role in the development and activity of B cells; modulates the activity of 'professional' antigen presenting cells and regulates the cytokine production by activated macrophages. The authors introduce a newly discovered, prominent prostaglandin 15-deoxy-? 12,14 -PGJ 2 or 15-d-PGJ2, produced by a variety of cells including mast cells, T cells, platelets and alveolar macrophages. 15-d-PGJ 2 plays an active role in regulating diverse processes such as adipogenesis, inflammation, and tumorigenesis.
Of significant interest to the readers is the central role PGE 2 plays in the disease progression in periodontal disease and certain cancers. PGE 2 , a marker for periodontitis, causes increased vasopermeability and vasodilation and further induces the synthesis of matrix metalloproteinases (MMPs) by monocytes and fibroblasts. MMPs cause connective tissue degradation and osteoclastic bone destruction, both of which are hallmarks of periodontal disease. In carcinogenesis, PGE 2 promotes tumour cell survival by inhibiting tumour cell apoptosis, increasing tumour cell proliferation, altering cell morphology, and increasing cell motility and migration. Indirectly, PGE 2 helps in tumorigenesis by stimulating angiogenesis and by acting as an immune modulator.
| Keratin Expression in Human Tissues and Neoplasms|| |
Chu PG, Weiss LM
HISTOPATHOLOGY 2002, 40, 403-439
All mammalian cells contain a complex intracytoplasmic skeleton composed of microfilaments, microtubules and intermediate filaments. Keratin filaments (Type I and II) are the intermediate filaments of the epithelial cells. So far 20 different subunits of keratin have been extracted with their molecular weight ranging between 40-70 kDa. Keratin can be thus divided into low/high molecular weight keratins or acidic/basic keratins.
This article provides an in depth analysis of the expression of keratin in different human tissues and neoplasms, with a brief description of the underlying biologic processes. Given the widespread usage of keratin in the field of immunohistochemistry as an epithelial marker in the recent years, this review clarifies the rationale behind using various types of keratins for typing diverse epithelial tissues.
The fact that keratin expression is developmentally regulated and not universally expressed during embryonic development, accounts for the expression of different sets of keratins at different stages of epithelial cell development during odontogenesis. Further, when an epithelium undergoes malignant transformation, its keratin profile usually remains constant. Thus keratins have been widely used in the finger printing of various carcinomas, the keratin expression varying so greatly among different epithelia. Other interesting aspects of the article include the discussion about the various diseases and mutations associated with keratin subtypes, like white sponge nevus and the various types of antibodies available against the 20 keratins.
| Extent of Extracapsular Spread: A Critical Prognosticator in Oral Tongue Cancer|| |
Greenberg JS, Fowler R, Gomez J, Mo V, Roberts D, El Naggar AK, Myers JN
CANCER 2003; 97: 1464-70
Extracapsular spread (ECS) of metastatic squamous cell carcinoma of the head and neck to regional lymph nodes is the most reliable predictor of poor treatment outcomes. ECS is significantly associated with higher rates of locoregional recurrence, distant metastasis, and decreased survival in patients with squamous cell carcinoma of the oral tongue. This study has been carried out to assess if the degree of ECS influences distant metastasis rates and survival. Results have indicated no significant difference in the survival of patients with ECS of 2 mm or >2 mm. However, patients with both ECS and multiple positive lymph nodes, compared to those with a single positive lymph node with ECS, had decreased overall survival, disease specific survival and a shorter disease free survival. Those with multiple ECS positive lymph nodes had the worst prognosis.