A glimmer of progress, and more on U Penn-Novartis partnership

So today I came in for a scheduled RBC transufusion, as my Hgb was 7.7 last Friday when got my second ofatumumab dose. I expected to also need platelets again especially since have had an ongoing bloody nose...got both and was delighted to hear my total WBC was down to 18.7, presumably due to the partial dose of Arzerra I recieved last week.

There was an expanded story on the U Penn partnership with Novartis in the Daily Pennsylvanian, the college newspaper.

Some excerpts thereof:

The first steps in the Penn-Novartis collaboration involve a focus on developing cell production facilities, bringing to Penn the first Center for Advanced Cellular Therapies. This new building will allow researchers to develop and manufacture chimeric antigen receptor technology for the treatment of cancer, according to Novartis’ press release. Research collaborations will also begin during the first year

The construction of new cancer research facilities at Penn will allow for the expansion of the number of patients who can be treated. “Because the clinical results were so striking, Penn had more than 5,000 patients or families contacting us wanting to enroll on clinical trials,” said Bruce Levine, a professor of pathology and laboratory medicine at the medical school

Not hard to believe since CLL is most common  adult leukemia, and justifies my prior skepticism about getting into that trial, even though the patient profiled in New England Journal article sounds a lot like me (except for the 17p deletion part, so far not applicable to me)

The patient received a diagnosis of stage I CLL in 1996. He first required treatment after 6 years of observation for progressive leukocytosis and adenopathy. In 2002, he was treated with two cycles of rituximab plus fludarabine; this treatment resulted in normalization of blood counts and partial resolution of adenopathy. In 2006, he received four cycles of rituximab and fludarabine for disease progression, again with normalization of blood counts and partial regression of adenopathy. This response was followed by a 20-month progression-free interval and a 2-year treatment-free interval. In February 2009, he had rapidly progressive leukocytosis and recurrent adenopathy. His bone marrow was extensively infiltrated with CLL. Cytogenetic analysis showed that 3 of 15 cells contained a deletion of chromosome 17p, and fluorescence in situ hybridization (FISH) testing showed that 170 of 200 cells had a deletion involving TP53 on chromosome 17p. He received rituximab with bendamustine for one cycle and three additional cycles of bendamustine without rituximab (because of a severe allergic reaction). This treatment resulted in only transient improvement in lymphocytosis. Progressive adenopathy was documented by means of computed tomography (CT) after therapy.

 Now however with this new push, many more patients could be studied, hopefully to include moi!