Table 5.

The proposed interpretation of possible mechanisms behind distribution of Ki-67 values among subgroups of different immunohistochemical cancer phenotypes

HER2 & ER/PgR Breast cancer phenotypes		Model proposed subdivision of breast cancers, based on mitotic activity
		LMA (low mitotic activity) Ki67 < 25%	IMA (intermediate mitotic activity)Ki-67 25–65%	HMA (high mitotic activity)Ki-67 > 65%
HER2 0+ to 3+	ER + PgR+	~67% of all patients probably HER2 dependent mitotic rates, thus intermediate mitotic rates seem dependent on the increased HER2 expression		~ 1% of all patients high mitotic rate due to unknown promiotic mechanism
	ER + PgR-	~26% of all patients mitotic rates do not seem closely regulated by normal HER2 expression (0+ to 2+), HER2 3+ increases number of IMA tumors
	ER-PgR-			~6% of all patients high mitotic rate due to unknown promiotic mechanism, HER2 3+ reduces number of HMA tumors
Open questions		168 out of 769 LMA cancers were HER2 3+ Can HER2 molecules in HER2 3+ & LMA cancers be dysfunctional?	99 out of 323 IMA cancers were HER2 absent Is there another promitotic mechanism in HER2 absent & IMA tumors, particularly in 55 ER + PgR+ cancers?	43 out of 106 triple-negative & HER2 absent cancers were HMA What promotes the highest mitotic rates in HER2 absent ER-PgR- tumors?