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Telomeres are repetitive nucleotide sequences located at the ends of the chromosomes. Their role is to preserve genome integrity. During cell divisions, telomeres shorten and reach a critical size leading to a mechanism of apoptosis. To postpone replicative senescence and acquire immortality, tumor cells must maintain functional telomeres. Two telomere length maintenance mechanisms are involved: reactivation of telomerase, an enzyme specialized in the replication of telomeric sequences, and an alternative mechanism called ''Alternative lenghtening of telomeres pathway'', using chromosomal recombination. Colorectal cancer does not deviate from this rule. Over the past 25 years, telomeric features in colorectal cancer, including telomere length and telomerase activity, have been studied on several occasions. However, many points remain unsolved. Following a reminder on telomeres, this mini-review attempts to summarize, concisely, these main characteristics and their potential uses in clinical practice. [ABSTRACT FROM AUTHOR]

Eukaryotic cells contain linear DNA molecules whose ends can potentially be recognized as DNA breaks and induce an apoptosis process. Specific terminal DNA sequences, known as telomeres, act as a protection system against this phenomenon. It has been evidenced that in somatic cells, telomeres tend to decrease in length over time, which has been suggested to be the biological substrate of aging. In order to counter this process, certain cells express an enzyme called telomerase that has the ability to elongate telomeric ends. During gametogenesis, and especially during spermatogenesis, telomeres participate in homologous chromosomes pairing and to their accurate segregation through the formation of a structure called the telomere bouquet. Their length increases over time in men, which could act as a sort of "guarantee" of the transmission of an acceptable telomeric length to the offspring. The precise mechanisms of this transmission, as well as the implication of telomeres on certain idiopathic male-factor infertilities, remain to be elucidated. [ABSTRACT FROM AUTHOR]

Abstract: Telomeres are specialized structures that cap and protect the end of chromosomes. Telomeres progressively shorten after each cellular division unless an enzyme, the telomerase, counteracts. Telomeres are implicated in cellular senescence, acting like a biological clock. Telomere length and telomerase activity are important in the physiopathology of cancer. In the past years, research has focused on them in order to find new therapeutic targets. Yet, oxidative stress, inflammation and increased leucocytes renewal are major environmental factors associated with telomeres shortening acceleration and thus in concordance with biological age. Thus, telomeric erosion induces cell apoptosis; indeed, apoptotic cell clearance is impaired in systemic lupus. Considering these elements and data resulting from oncology, telomere/telomerase couple was studied during the last decade in systemic lupus erythematosus. The objective was to know if this couple could have an implication in the physiopathology of this disease. A systematic review of literature is proposed about telomere and/or telomerase in systemic lupus erythematosus in order to discuss their physiopathological implication. Among 273 tested patients, telomere seems to be eroded and telomerase activity insufficiently increased but correlated to the activity of the disease. The analysis of telomere length and telomerase activity could be useful as prognosis factor or disease activity index. Telomere erosion could reflect an accelerated replicative senescence of the immune system. The role of the regulator T lymphocytes has not yet been precised. Standardized studies on larger population could be realized in systemic lupus and open new avenues of research and/or therapy based upon the telomere/telomerase biology. [Copyright &y& Elsevier]

The development of oral and head and neck squamous cell carcinomas occurs in relation with multiple events including mainly: loss of cycle cell control, evasion from apoptosis, telomerase reactivation. Complex interactions between a set of molecules, cell cycle proteins, tumour suppressor genes, oncogenes and the telomerase, occur in the multiple step process of carcinogenesis. The 2 main ways of control of the cell cycle rely on 2 tumour suppressor genes: the P53 gene and the retinoblastoma gene or RB gene. One of the regulation pathways or the 2 regulation pathways are disabled during the development of oral and head and neck squamous cell carcinomas. Most of the time, the inactivation of the P53 pathway results from a loss of function of the p53 protein, secondary to mutation and/or deletion of the P53 gene; It may also result of the amplification of the MDM2 gene and of the inactivation of the arf protein. The RB pathway leads to cell proliferation by loss of the p16 protein, by amplification of the cyclin D1 gene and less frequently by mutation of the RB gene or loss of the retinoblastoma protein. In India and South-East Asia, the activation of RAS and MYC oncogenes appears to be related with the presence of specific carcinogens in snuff and tobacco. By blocking apoptosis, the Bcl2 protein seems to increase the resistance of tumours to radiotherapy and chemotherapy. [Copyright &y& Elsevier]