PT  - JOURNAL ARTICLE
AU  - Paola Anna Erba
AU  - Enrica Tusi
AU  - Chiara Manfredi
AU  - Maria Teresa Locci
AU  - Martina Sollini
AU  - Elena Lazzeri
AU  - Katrin Massri
AU  - Luisa Locantore
AU  - Giuliano Mariani
TI  - 99mTc-Annexin-V and 99mTc-Sestamibi uptake as indicators of chemotherapy induced apoptosis.
DP  - 2009 May 01
TA  - Journal of Nuclear Medicine
PG  - 1575--1575
VI  - 50
IP  - supplement 2
4099  - http://jnm.snmjournals.org/content/50/supplement_2/1575.short
4100  - http://jnm.snmjournals.org/content/50/supplement_2/1575.full
SO  - J Nucl Med2009 May 01; 50
AB  - 1575 Objectives 99mTc-Annexin-V can be employed to monitor apoptosis in vivo.99mTc-Sestamibi has been shown to be inversely correlated with levels of Bcl-2: reduction of 99mTc-Sestamibi uptake in response to an antiblastic agent would reflect resistance to apoptosis.We evaluated 99mTc-Annexin V and 99mTc-Sestamibi uptake in a virus-induced model of mouse breast cancer . Methods Biodistribution was evaluated in tumor-bearing mice in baseline conditions and 1, 3, 6 and 24 hr after 0.02 mg/g bw Paclitaxel given iv.Biodistribution was assessed 1 hr after injection of 99mTc-Annexin V and 20 min after 99mTc-Sestamibi.Tumour samples were also processed by WB and IF to identify apoptotic cells (TUNEL) and expression of Caspase-3, Caspase-8 and Bcl-2. Results A highly significant correlation between 99mTc-Annexin V and 99mTc-Sestamibi with a peak 3-hr uptake was found,suggesting that they both may be used as indicators of apoptosis.TUNEL was significantly correlated with uptake of both 99mTc-Annexin V (p&amp;lt;0.0001) and 99mTc-Sestamibi (p=0.0122).Caspase-3 and -8 expression was prevalent in baseline condition and 6-24 hr after treatment, while Bcl-2 was high in baseline condition, reached a nadir at 3 hr and subsequent recovered. Conclusions These observations confirm the anti-apoptotic role of Bcl-2 and suggest the co-existence of two apoptotic cell populations: an early apoptotic response probably mediated by Caspase-10 and a later, minor apoptotic event mediated by Caspase-3.