Appeal No. 2006-2466 Page 10
Application No. 09/835,759
Id. In fact, as stated by the examiner, Tachibana teaches that, with cyclophosphamide,
“generation of potent cytotoxic T cells was comparable to that of immunized hosts and
was followed by curative antitumor effect.” Page 461.
Both Apostolopoulos and Tachibana teach that antitumor activity is associated
with producing cellular rather than humoral immunity. Apostolopoulos, page 930, col. 2;
Tachibana, page 461. In order to achieve this goal, Tachibana teaches administering
the immunogenic hybrid cells with cyclophosphamide “as an immunosuppressant to
depress humoral response . . . and/or regulatory cells.” Id., page 456. In addition,
Tachibana suggests that “humoral immune response existing beforehand in
tumor-bearing mice was accelerated by inoculations of immunogenic hybrid cells and
the resulting immune complexes interfere with cell-mediated immunity to cause
enhancement of tumor growth.” Id., page 458. Based on these teachings, we conclude
that the examiner has set forth a prima facie case that it would have been obvious to
administer a tumor-associated antigen with components other than cyclophosphamide
that would depress the humoral response.
Parkhouse teaches that ricin-anti-CD22 conjugate depletes both normal and
neoplastic B cells. Abstract. Specifically, Parkhouse describes anti-CD22 mAb coupled
to ricin A chain. Page 333. As noted by the examiner, “B cells produce antibodies;
antibodies mediate humoral immunity.” Examiner’s Answer, page 20. We agree with
Appellant that “[d]isclosing that humoral immune responses inhibit cell mediated
antitumor activity is not the same as disclosing or suggesting depletion of B cells or
depletion of B cells with anti-CD22 antibody to eliminate a humoral immune response.”
However, because B cells produce the antibodies that mediate humoral immunity, we
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