Cardiff University Oncology Society have been busy raising money for Pancreatic Cancer UK via The Th

Pancreatic cancer’s notoriety can be partly attributed to its combination of often late stage at

diagnosis and subsequent refractory response to treatment. It therefore bears an extremely poor

prognosis. Pancreatic Cancer UK has contributed £4 million in an effort to tackle this devastating

disease. The driver mutation, KRAS , dominates the tumorigenesis and unhappily tumours

characterised by KRAS mutations have a notorious ability to evade traditional cancer treatment

strategies. Developing targeted therapeutics and better understanding this disease therefore

remains the compelling focus of research efforts. Some of the latest developments include:

● A novel means of genetic engineering that involves using inhibitory exosomes to target the

KRAS mutants using siRNA’s that attenuate PDAC tumour growth specifically has shown

promise in vivo. Preliminary results suggest this technique looks to be more effective than

use of liposomes as a means of delivering targeted therapeutics.

● Use of adjuvant gemcitabine plus capecitabine in patients with surgically resected PDAC has

demonstrated improvements versus gemcitabine monotherapy in 5-year overall survival in a

large randomized phase II trial, changing the standard of care for this patient group.

● Advances in genetic sequencing technology has allowed insight into other driver mutations

implicated in the tumorigenesis of PDAC, namely those involved in homologous DNA repair

and epigenetic regulation. Success in treating such mutations in breast and ovarian cancers

has been achieved by using PARP inhibitors and platinum agents leading to the exploration

of a repurposing of these agents in PDAC.

While these developments into pancreatic cancer research looks promising many remain in their

preliminary stages, highlighting the importance of supporting efforts to overcome the many and

complex challenges such a merciless cancer poses. Newer treatments that target the driver mutation

KRAS and its


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