SCIENTIFIC PROGRAMME
SESSION I
THE GENOMIC AND
EPIGENOMIC LANDSCAPE
OF CLL AND CLINICAL
CONSEQUENCES
SESSION II
THE ROLE OF BCR
ACTIVATION AND
SIGNALLING FOR CLL
SESSION III
THERAPEUTIC OPTIONS
FOR CLL
SESSION IV
LONG TERM FOLLOW
UP OF CLINICAL TRIALS
VERSUS REAL WORLD
DATA (OUTSIDE CLINICAL
TRIALS DATA-OCT)
SESSION V
THE INCREASING ROLE
OF THE LEUKAEMIC
MICROENVIRONMENT
SESSION VI
THERAPEUTIC OPTIONS 2 :
THE USE OF CELLULAR
AND NON-CELLULAR
IMMUNOTHERAPIES IN
CLL
SESSION VII
EFFICACY THROUGH
SAFETY
SESSION VIII
CLONAL HETEROGENEITY,
CLONAL EVOLUTION AND
MECHANISMS OF DRUG
RESISTANCE
SESSION IX
CONTRASTING
THERAPEUTIC CONCEPTS
SELECTED ABSTRACTS
FOR AN ORAL
PRESENTATION
SELECTED ABSTRACTS
FOR A POSTER
PRESENTATION
FACULTY DISCLOSURES
PI3K p110d inhibitor idelalisib, dAEs were noted in 23-58% of patients (17,18); these rashes
were classified as “maculopapular”. In addition to colitis, pneumonitis and hepatitis, flares of
and new onset psoriasis and rarely pityriasis rubra pilaris have since been reported (19,20).
Patients with psoriasis are managed with skin directed and systemic therapies known to be
effective in this disorder. PRP-like eruptions appear to require PI3K inhibitor interruption and
are managed with topical steroids, retinoids and systemic immune suppression when needed.
Identification of these dAEs and the approach to management will be reviewed.
In nearly all cases, collaborative multidisciplinary care with classification of rash types and
institution of appropriate, specific therapies aimed at dAE mechanisms will best allow for
patients to maintain their anticancer regimen – an ideally their quality of life as well.
References
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