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2.  Breast cancer (malignant
breast neoplasm) is cancer
originating from breast
tissue, most commonly
from the inner lining of milk
ducts or the lobules that
supply the ducts with milk.

3.  The breast is a glandular
organ.
 It is made up of a network
of mammary ducts.
 Each breast has about 15-
20 mammary ducts that
lead to lobes that are made
up of lobules.
 The lobules contain cells
that secrete milk that are
stimulated by estrogen and
progesterone which are
ovarian hormone.

4.  A. Breast Duct System
 B. Lobules
 C. Breast Duct System
 D. Nipple
 E. Fat
 F. Chest Muscle
 G. Ribs
 A. Cells lining duct
 B. Basement membrane
 C. Open central duct

5.  A. Breast Duct System
 B. Lobules
 C. Breast Duct System
 D. Nipple
 E. Fat
 F. Chest Muscle
 G. Ribs
 A. Cells lining duct
 B. Extra cancer like cells
 C. Intact basement
membrane
 D. Open central duct

6.  histopathological
 grade
 Stag
 Receptor statuse

7. Although breast cancer has many different histologies, the
considerable majority of breast cancers are derived from the
epithelium lining the ducts or lobules, and are classified as
mammary ductal carcinoma.
 Invasive ductal carcinoma
 Ductal carcinoma in situ
 Invasive lobular carcinoma

8.  Grading focuses on the appearance of the breast
cancer cells compared to the appearance of normal
breast tissue. Normal cells in an organ like the
breast become differentiated, meaning that they
take on specific shapes and forms that reflect their
function as part of that organ. Cancerous cells lose
that differentiation.

9.  Stage 0 is a pre-cancerous or marker condition, either ductal
carcinoma in situ (DCIS) or lobular carcinoma in situ (LCIS).
 Stages 1–3 are within the breast or regional lymph nodes.
 Stage 4 is metastatic cancer that has a less favorable
prognosis.

10. Breast cancer cells may or may not have many different types of
receptors.
 estrogen receptor (ER)
 progesterone receptor (PR)
 human epidermal growth factor receptor 2 (HER2) HER2/neu

11.  Cells with or without these receptors are called ER positive
(ER+), ER negative (ER-), PR positive (PR+), PR negative (PR-),
HER2 positive (HER2+), and HER2 negative (HER2-).
 Cells with none of these receptors are called basal-like or
triple negative.

12. ER receptors belong to a super-family of nuclear hormone
Receptors.
The main function of the estrogen receptor is as a DNA-binding
transcription factor that regulates gene expression when they
are bound to estrogens.
 ER is generally expressed at low levels in normal breast
epithelial cells.
 ER interactions with a number of other DNA-bound
transcription factors, such as the AP-1 complex or the SP-1
family of transcription factors.

14.  The progesterone receptor (PR) also known as NR3C3
(nuclear receptor subfamily 3, group C, member 3), is an
intracellular steroid receptor that specifically binds
progesterone.

15.  HER2/neu stands for "Human Epidermal growth factor
Receptor 2" and is a protein giving higher aggressiveness in
breast cancers. It is a member of the ErbB protein family,
more commonly known as the epidermal growth factor
receptor family.

16.  Inherited
 Risk Factors
 Environmental Factors

17.  Only 5-10% of breast cancers are inherited.
 Families that do have genetic defects in one of two genes,
breast cancer gene 1 (BRCA1) or breast cancer gene 2
(BRCA2), have a much greater risk of developing both breast
and ovarian cancer.
 Other inherited mutations – including the ataxia-
telangiectasia mutation gene, the cell-cycle checkpoint kinase
2 (CHEK-2) gene and the p53 tumor suppressor gene – also
make it more likely that will develop breast cancer.

18.  BRCA1 (Breast Cancer 1)
 BRCA2 (Breast Cancer 2)
 TP53 gene
 ATM gene

19.  BRCA1 is a human caretaker gene that produces a protein
called breast cancer type 1 susceptibility protein, responsible
for repairing DNA.

20.  BRCA2 (Breast Cancer 2 susceptibility protein) is a protein
that in humans is encoded by the BRCA2 gene and belongs to
the tumor suppressor gene family.
 The BRCA2 gene is located on the long (q) arm of
chromosome 13 at position 12.3 (13q12.3).

22.  BRCA1 and BRCA2 proteins are involved in control of
homologous recombination and double-strand break repair
in response to DNA damage .
 Modulation of chromatin and DNA structure
 Activation of DNA damage checkpoints.

24.  p53 (also known as protein 53 or tumor protein 53), is a
tumor suppressor protein that in humans is encoded by the
TP53 gene. p53 is crucial in multicellular organisms, where it
regulates the cell cycle and, thus, functions as a tumor
suppressor that is involved in preventing cancer.

26.  Cell Cycle Regulation
 Cell Senescence
 Apoptosis
 Autophagy
 Mitotic Catastrophe
 Angiogenesis

27.  Ataxia telangiectasia mutated (ATM) is a serine/threonine
protein kinase that is recruited and activated by DNA double-
strand breaks. It phosphorylates several key proteins that
initiate activation of the DNA damage checkpoint, leading to
cell cycle arrest, DNA repair or apoptosis.

28. Factors that Cannot be Lifestyle Risks
Prevented Oral Contraceptive Use
Gender Not Having Children
Aging Hormone Replacement
Genetic Risk Factors Therapy
(inherited) Not Breast Feeding
Family History Alcohol Use
Personal History Obesity
Race High Fat Diets
Menstrual Cycle Physical Inactivity
Estrogen Smoking

29.  Exposure to Estrogen
 Radiation
 Electromagnetic Fields
 Xenoestrogens
 Exposure to Chemicals

30. definitive surgery
adjuvant chemotherapy
adjuvant radiotherapy
adjuvant hormonal therapy

31.  Surgery is usually the first line of attack against breast cancer.
 Lumpectomy
 Mastectomy
 Lymph node removal
 Prophylactic mastectomy
 Prophylactic ovary removal
 Cryotherapy

32. Chemotherapy treatment uses medicine to weaken and destroy
cancer cells in the body, including cells at the original cancer
site and any cancer cells that may have spread to another part
of the body.
Chemotherapy is used to treat:
 early-stage invasive breast cancer to get rid of any cancer cells
that may be left behind after surgery and to reduce the risk of
the cancer coming back.
 advanced-stage breast cancer to destroy or damage the
cancer cells as much as possible.

33. Radiation therapy (radiotherapy) is a highly targeted, highly
effective way to destroy cancer cells in the breast.

34. Hormonal therapy medicines treat hormone-receptor-positive
breast cancers in two ways:
 by lowering the amount of the hormone estrogen in the body
 by blocking the action of estrogen on breast cancer cells

35. There are several types of hormonal therapy medicines,
including:
 aromatase inhibitors
 selective estrogen receptor modulators
 estrogen receptor downregulators.

36. Aromatase inhibitors stop the production of estrogen in post-
menopausal women
There are three aromatase inhibitors:
 Arimidex (chemical name: anastrozole)
 Aromasin (chemical name: exemestane)
 Femara (chemical name: letrozole)

37. SERMs work by sitting in the estrogen receptors in breast cells.
There are three SERMs:
 tamoxifen (also called tamoxifen citrate; brand name:
Nolvadex)
 Evista (chemical name: raloxifene)
 Fareston (chemical name: toremifene)

38. ERDs work in a similar way to SERMs.
ERDs also:
 reduce the number of estrogen receptors.
 change the shape of breast cell estrogen receptors so they
don't work as well.
There is one ERD available to treat hormone-receptor positive
breast cancer:
Faslodex (chemical name: fulvestrant)

39. 1)Roles of BRCA1 and BRCA2 in homologous recombination, DNA replication fidelity and
the cellular response to ionizing radiation.Simon N Powell*,1 and Lisa A Kachnic2
2)Pathology of hereditary breast cancer.Leonard Da Silva and Sunil R Lakhani.
3)TP53 Status and Response to Treatment in Breast Cancers.Mariana Varna,1, 2 Guilhem
Bousquet,1, 2 Louis-Franc¸ois Plassa,3 Philippe Bertheau,1, 2, 4and Anne Janin1, 2, 4.
4)The Role of Estrogen Receptors in Breast Cancer Metastasis.Suzanne A.W. Fuqua1.
5)New Molecular Classifications of Breast Cancer.Mary Cianfrocca, DO1 and William
Gradishar.