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+ | ERÂ +Â 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 | |
ERÂ +Â 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 ERÂ +Â 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? | |