Appeal No. 1999-1732
Application No. 08/308,879
The examiner relies on the following references:
Kopchick et al. (Kopchick) 5,350,836 Sep. 27, 1994
Phares, “Regression of Rat Mammary Tumors Associated with Suppressed Growth
Hormone,” Anticancer Research, Vol. 6, pp. 845-848 (1986).
Watahiki et al. (Watahiki), “Conserved and Unique Amino Acid Residues in the Domains
of the Growth Hormones,” J. Biol. Chem., Vol. 264, pp. 312-316 (1989).
Chen et al. (Chen), “Expression of a mutated bovine growth hormone gene suppresses
growth of transgenic mice,” Proc. Natl. Acad. Sci., Vol. 87, pp. 5061-5065 (1990).
Claims 1 and 3-7, which stand or fall together, stand rejected under 35 U.S.C.
§ 103(a) as being obvious over Kopchick. In addition, claims 1 and 3-7 stand rejected
under 35 U.S.C. § 103(a) over the combination of Chen, Phares and Watahiki. After
careful review of the record before us, we reverse both rejections.
BACKGROUND
Growth hormone is a member of a homologous hormone family that also includes
prolactins, placental lactogens, and other genetic and species variants of growth hormone.
Human growth hormone not only binds to its own receptor, but can also bind to either
cloned somatogenic or prolactin receptors. See Specification, page 3. The human growth
hormone sequence is known, and the hormone has been cloned. See id. at pages 3-4.
Prolactin and growth hormone are known to play a role in the development and
progression of breast cancer. The majority of breast cancer cells overexpress the prolactin
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