African Health Sciences
Makerere University Medical School
Vol. 21, No. 1, 2021, pp. 41-46
Bioline Code: hs21015
Full paper language: English
Document type: Research Article
Document available free of charge
African Health Sciences, Vol. 21, No. 1, 2021, pp. 41-46
© Copyright 2021 - Latifa M et al.
Intra-tumoral distribution of Ki-67 and Cyclin D1 in ER+ mammary carcinoma: quantitative evaluation|
Latifa, Mohammedi; Fatima, Djillali Doula; Farida, Mesli & Rachid, Senhadji
Background: In spite of the strong evidence demonstrating the role of overexpression of Ki-67 and Cyclin D1 markers
in breast carcinomas, clinical and pathological data remain to be discussed. This can be explained partly by intratumor heterogeneity.
Objectives: To define the prevalence and clinical significance of Ki-67 and Cyclin D1 overexpression in primary breast
tumors ER positive, while highlighting the existence of intratumor heterogeneity in this type of cancer
Materials and methods: 51 ER positive breast cancer tumors were used to evaluate the intratumoral distribution of Ki-67
and Cyclin D1 expression. Image acquisition and visualization of the markers were performed by optical microscopy and
stereology sampling method.
Results: The mean Ki-67 labeling index was distributed heterogeneously in the same tumor, from 20.67±6.87 to 45.10±10.65.
The coefficient of variation (COV) revealed dispersion values between 13.4% and 42.9%. Associated with positive ER status,
all the tumors presented a Cyclin D1 expression with a COV varying between 19% and 28.5% and a mean labeling index
fluctuating between 19.40±4.42 and 41.64±10.08 within the same patient showing important intratumor heterogeneous
Conclusion: In this study, we have adopted a strictly quantitative approach to evaluate and demonstrate intratumor heterogeneity.
This establishes one of the main factors for poor response to cancer therapy. To achieve this, intratumor heterogeneity
should be usually definable and quantifiable but this domain awaits future progress and methods need to move towards
a better understanding of molecular and cellular mechanisms that initiate and maintain this tumor heterogeneity.
Breast cancer; Cyclin D1; ER+; Intra-tumoral heterogeneity; Ki-67.