17p(p53) (MM, CLL)
17p(p53) (MM, CLL)
د.إ 750.00 د.إ 600.00 Book Now

17p(p53) (MM, CLL)

د.إ 750.00 د.إ 600.00


Clinical and laboratory data were collected from CLL patients (pts) enrolled in the ICLL001 – BOMP phase II trial of the French CLL intergroup (NCT01612988) evaluating a paraphrase of ofatumumab (300 mg) followed by 6 monthly courses of BOMP including bendamustine (70 mg/m2 d1-2), ofatumumab 1000 mg TD (d1 and d15 on 1st and 2nd courses) and high dose methylprednisolone (1 g/m2 d1-3) in fit patients with relapsing CLL and IWCLL treatment criteria

17p(p53) (MM, CLL) outcome time: 12 working days

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Sometimes a baby will be born early no matter what the mother and her health care providers do. But there is one thing some women can do to help increase their chances of having a full-term baby — 17P.

17P is a progesterone medicine that can help prevent preterm birth in some pregnant women who have already had a preterm birth. Progesterone is a hormone that a woman’s body makes naturally during pregnancy. Extra progesterone for some women can help to prevent another preterm birth.

17p (p53)(CLL):

CLL patients with 17P/TP53 frequently progress earlier to symptomatic disease and have shorter response durations with traditional chemoimmunotherapy. In 2013, two new targeted therapies, ibrutinib and idelalisib, were introduced into the CLL market. Both are indicated for patients tested positive for either 17P/TP53 or patients who have received at least one previous treatment.


Despite the improvement in treatment strategies, virtually all chronic lymphocytic leukaemia (CLL) patients will relapse and experience tumour resistance. The 17p deletion resulting in loss of the TP53 gene, found in up to 20-40% of relapsing patients, is strongly associated with impaired response to genotoxic agents, reduced progression-free survival and poor overall survival.

The 17p deletion usually coincides with TP53 mutation, leading to the impairment of the p53-associated pathway. Also, individual TP53 mutations (without 17p deletion) appear also associated with poor outcome in prospective trials. However, TP53 mutation screening is time-consuming, can be not exhaustive, and the respective impact of different patterns of TP53 gene impairment on p53 function and prognostic remains unclear

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