On average, Invasive Ductal carcinoma accounts for about 75% of all diagnosed
breast cancers. The carcinoma usually starts from the ducts in mammalian tissue. It is often
related to Ductal Carcinoma in situ with the greatest difference being that invasive ductal
carcinoma has the ability to spread into other tissues and organs while ductal carcinoma in
situ is only limited to the ducts. The first site of development is usually the basement
membrane of the ducts. This is in the terminal lobular duct. Like any other cancer, invasive
ductal carcinoma is characterised by rapidly dividing and defective cells. In normal cells,
there is usually regulation in the cell division process. The regulation ensures that the cells
dividing are not defective, containing the required organelles and protein synthesis (Wu et al.,
2017). Cells that usually don’t meet these criteria usually undergo apoptosis which is a
programmed cell death or growth arrest. However, cancerous cells seem to defy these
regulators, speculatively owing to various gene mutations. The same is true for the cancerous
cells that begin in the basement membrane in invasive ductal carcinoma. Their fast and rapid
division limits their maturity, increasing the chances of them being defective (Marmor et al.,
2017). Their division is faster than that of surrounding cells in the terminal lobular duct unit
leading to their increasing numbers. Research has shown that these cancerous cells produce
exosomes which are membrane-bound vesicles containing DNA and RNA strands that may
lead to normal tissues becoming cancerous. A study on genetic mutations that results in this
rapid uncontrolled division of breast tissues indicates that P53, BRCA1 and BRCA2 gene
mutations are possible culprits. The p53 gene overexpression usually occurs as a means of
regulating cell division, tumour formation and responding to DNA damage. p53 promotes
apoptosis through transcription-dependent and -independent mechanisms that act in concert
Invasive Ductal Carcinoma 3
to ensure that the cell death program proceeds efficiently.
Invasive Ductal Carcinoma 4
Fig 1.0 A comparison between Normal and mutant p53. (Duffy et al., 2018)
Mutations in the p53 gene mean that these cancerous cells proceed with defective,
uncontrolled and rapid division unperturbed. BRCA1 and BRCA2 mutations are also thought
to be other causes that lead to the uncontrolled cell division witnessed in the ductal cells
(Duffy et al., 2018). The two acts as tumour suppressors and also play active roles in DNA
repair. Mutations in these genes mean reduced tumour inhibiting activity and limited DNA
repair resulting in cells with Damaged DNA, characteristic of cancerous cells. These gene
mutations are inheritable, presenting a familial element in cancer. Pesticides containing
carcinogenic compounds such as arsenic, ethylene-oxide and lindane which contribute to the
development of malignancies. Progesterone and oestrogen have also been discussed as
probable causes. Excessive exposure to these leads to induced expression of Cyclin G1. This
situation occurs in occasions such as early menarche, late pregnancy and late menopause.
Basing on the histological characteristics of the cancerous cells as compared to normal breast
epithelial cells and their ability to form glands, three classes of grading can be deduced
Invasive Ductal Carcinoma 5
(Zangouri et al., 2018). The grading focuses on three major aspects; tubule formation, mitotic
count and pleomorphism.
Fig 1.1 The different grades of Invasive Ductal Carcinoma. Pleomorphism becomes
more apparent from left to right. (Marmor et al., 2017)
Tumour formation in this case refers to the percentage of the tumour that is made up
of tubules which significantly decreases moving from grade 1 to grade 3. On the other hand,
nuclear pleomorphism refers to the degree of change in the nuclei size and shape as compared
to normal cells. As you move from grade 1 to grade 3, the size of the nuclei changes;
becoming larger than that of normal cells with the uniformity in size and shape decreasing
markedly. Lastly, the mitotic count is a simple count of the number of cells that are rapidly
dividing in which the rate of division increases as you proceed from grade 1 to grade 3.