Telomerase expression in B-cell chronic lymphocytic leukemia predicts survival and delineates subgroups of patients with the same igVH mutation status and different outcome

Terrin, Liliana; Trentin, Livio; Degan, Massimo; Corradini, Irene; Bertorelle, Roberta; Carli, Piero De; Maschio, Nilla; Bo, Michele Dal; Noventa, Franco; Gattei, Valter; Semenzato, Gianpietro; Rossi, Anita De

doi:10.1038/sj.leu.2404607

Cited by 57 publications

(60 citation statements)

References 39 publications

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“…un-mutated IGHV with long telomere and mutated IGHV with short telomeres (Ricca et al, 2007). It seems possible therefore that TL analysis could be used to risk stratify CLL patients, resulting in patients who are low risk being spared unnecessary treatment (Terrin et al, 2007). This study also highlighted another consideration for TL as a useful marker in clinical practice for patient prognosis.…”

Section: Chronic Lymphocytic Leukaemiamentioning

confidence: 77%

Telomere dysfunction and its role in haematological cancer

Jones¹,

Pepper²,

Baird

2012

Br J Haematol

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SummaryObservations in human tumours, as well as mouse models, have indicated that telomere dysfunction may be a key event driving genomic instability and disease progression in many solid tumour types. In this scenario, telomere shortening ultimately results in telomere dysfunction, fusion and genomic instability, creating the large-scale rearrangements that are characteristic of these tumours. It is now becoming apparent that this paradigm may also apply to haematological malignancies; indeed these conditions have provided some of the most convincing evidence of telomere dysfunction in any malignancy. Telomere length has been shown in several malignancies to provide clinically useful prognostic information, implicating telomere dysfunction in disease progression. In these malignancies extreme telomere shortening, telomere dysfunction and fusion have all been documented and correlate with the emergence of increased genomic complexity. Telomeres may therefore represent both a clinically useful prognostic tool and a potential target for therapeutic intervention.

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Section: Chronic Lymphocytic Leukaemiamentioning

confidence: 77%

Telomere dysfunction and its role in haematological cancer

Jones¹,

Pepper²,

Baird

2012

Br J Haematol

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“…The quantification of all hTERT transcripts (hTERT-AT) in CRC samples was carried out by real-time PCR, exactly as previously described (Terrin et al, 2007(Terrin et al, , 2008, and normalised for 10 3 copies of the housekeeping hypoxanthine guanine phosphoribosyl transferase 1 (HPRT1) gene (Terrin et al, 2008).…”

Section: Quantification Of Htert Transcriptsmentioning

confidence: 99%

Relationship between telomere shortening, genetic instability, and site of tumour origin in colorectal cancers

et al. 2010

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BACKGROUND: Telomeres, located at chromosome ends, are progressively shortened during each cell cycle by replication-dependent loss of DNA termini. Although maintenance of telomere length is critical for cell-replicative potential and tumourigenesis, the erosion of telomeres can lead to genetic instability, a pivotal mechanism in the neoplastic process. PATIENTS AND METHODS: A total of 118 colorectal cancer (CRC) samples (53 right-colon, 30 left-colon, and 35 rectal tumours) and corresponding adjacent non-cancerous tissues were evaluated for telomere length, p53 mutation, and microsatellite instability (MSI). Telomere length was estimated by real-time PCR. RESULTS: Telomeres were significantly shorter in CRCs than in adjacent tissues, regardless of tumour stage and grade, site, or genetic alterations (Po0.0001). Moreover, in normal tissues, but not in tumours, telomere length inversely correlated with age (r ¼ À0.24, P ¼ 0.017). Telomere length in CRCs did not differ with tumour progression or p53 status; however, in CRCs carrying the wild-type p53, telomeres were significantly shorter in tumours with MSI than in those with stable microsatellites (P ¼ 0.027). Furthermore, telomere length differed according to tumour location, being longer in rectal cancers (P ¼ 0.03). CONCLUSIONS: These findings suggest that telomere shortening is a key initial event in colorectal carcinogenesis. The extent of telomere erosion is related to tumour origin site and may be influenced by the mismatch repair pathway.

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“…A number of reports have shown that short telomeres and expression of h-tert, the catalytic subunit of telomerase, are poor prognostic factors in this neoplasm. [24][25][26][27] Although early studies postulated that telomere length (TL) was mostly acting as a surrogate marker for IGHV-MS, a number of subsequent reports indicated that in discordant cases TL performed better than IGHV-MS, suggesting that TL deserved further consideration as a prognostic biomarker in CLL. 28,29 Despite these encouraging results, additional experience needs to be accumulated on TL as a prognostic marker in CLL.…”

Section: Introductionmentioning

confidence: 99%