BREAST CANCER

Breast cancer is when cancer starts in the breast. A Breast cancer is when cancer starts in the breast. Breast cancer (malignant breast neoplasm) from breast tissue, most commonly from the inner lining of milk ducts or the lobules that supply the ducts with milk.     

TYPES OF BREAST CANCERS                

Tumours of the breast are believed to arise from terminal ductal lobular units and comprise two common morphological types (Russo & Russo, 1999). They are:

·                     Ductal Carcinoma

·                     Lobular Carcinoma

• Cancers originating from originating from lobules are known as lobular carcinomas; those from ducts are known as ductal carcinomas.
• In situ breast cancer- cancer cells remain confined within their place of origin and do not attack surrounding breast tissue. The term 'in situ' refers to pre-invasive breast cancer. This is breast cancer which has not yet penetrated ('invaded') through the basement membrane (the membrane at the base of the epithelial lining of ducts or glands).
• Invasive or metastatic breast cancer- cancer cells break free of their place of origin and spread to different parts of the body. In situ carcinoma has the potential to become invasive carcinoma, and so is treated as an early form of breast cancer. 

DUCTAL CARCINOMAS

About 80-90% of all breast cancers are ductal in origin. The ducts in the breast carry milk from the lobules or glands of the breast to the nipples.

There are two types of Ductal carcinomas. They are:

• Ductal carcinoma in situ (DCIS)
• Invasive Ductal Carcinoma (IDC)

 Ductal carcinoma in situ (DCIS)

Ductal carcinoma in situ (DCIS; also known as intraductal carcinoma) is the most common type of non-invasive breast cancer. DCIS means that the cancer cells are inside the ducts but have not spread through the walls of the ducts into the surrounding breast tissue.

A mammogram is often the best way to find DCIS early.

FIG-1: In the left-hand image above, the normal cells which line the ducts of the breast might look. In ductal carcinoma in situ (DCIS, the image to the right), the duct cells have developed the ability to multiply out of control - one of the characteristics of cancer. The cancerous cells are filling the duct but have not yet spread beyond the lining of the duct. This is known as DCIS.

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                   Cancer and Inflammations

Basics of cancer development

Cancer results from the outgrowth of a clonal population of cells from tissue. The development of cancer, referred to as carcinogenesis, can be modeled and characterized in many ways. Cancer development requires the acquisition of six fundamental properties: self-sufficient proliferation, insensitivity to anti-proliferative signals, evasion of apoptosis, unlimited replicative potential, the maintenance of vascularization, and, for malignancy, tissue invasion and metastasis.

 Cancer can also be considered regarding a step-wise development functionally grouped into three phases: initiation, promotion, and progression. Initiation is characterized by genomic changes within the “cancer cell,” such as point mutations, gene deletion and amplification, and chromosomal rearrangements leading to irreversible cellular changes. Tumour development is promoted by the survival and clonal expansion of these “initiated” cells. Progression encompasses a substantial growth in tumour size and either growth-related or mutually exclusive metastasis.

       Relation between Cancer and inflammation: -              

v Chronic infection in immunocompetent hosts such as human papilloma virus or hepatitis B and C virus infection leads to cervical and hepatocellular carcinoma, respectively.

v Microbes may cause cancer due to opportunistic infection such as in Kaposi’s sarcoma (a result of  human herpes virus (HHV)-8 infection) or inappropriate immune responses to microbes in certain  individuals, which may occur in gastric cancer, secondary to Helicobacter pylori colonization or  cancer because of long-standing inflammatory bowel disease precipitated by the intestinal  microflora.

v Conditions associated with chronic irritation and subsequent inflammation predispose to cancer, such   as the long-term exposure to cigarette smoke, asbestos, and silica.

v However, the tumour associated stroma may undergo selective pressure, as there have been recent reports of genetic changes in tumour associated stroma [51] and even loss of p53 in tumour-associated fibroblasts.

v The cell death and tissue injury that may occur right after initiation may induce tissue repair and homeostatic responses leading to tumour progression. In addition, signals derived from microbes also might activate innate microbial recognition pathways enhancing the development of tumours.

                   

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Cancer, Genomic Instability, Genetic factors and Epigenetic factors

Cancer is a group of diseases which involves polymorphisms and/or alterations in the expression of genes that confer undiminished proliferative and survival advantage to somatic or germinal cells.

Genomic Instability:

Clear distinction between cancerous and non-cancerous cell proliferation lies in genomic instability. Cancer cells contain multiple genetic and epigenetic alterations. As cancers progress, the numbers of alterations in their genome tend to increase. Cancers, even if outwardly homogeneous, usually consists of cell clones that differ at least slightly in their genetic constitution.

                                  The variant clones are continuously selected for those proliferating fastest, tolerating adverse conditions best, capable of evading immune responses etc.., with the best- adapted cell clone dominating growth

                                     Cancers with genomic instability will display greater variation and a higher risk of developing resistance.

Epigenetic factors: Methylation changes occur early and ubiquitously in cancer (Feinberg*., 2016)

     

Table.1 Hypomethylation and hypermethylation in cancer

	Hypomethylation	Hypermethylation
Frequency	Ubiquitous even in the earliest benign tumors	Some early hypermethylation, with increasing frequency with tumor progression
Targets	Repetitive sequences, coding regions, promoters	Promoters
Primary/ secondary change	Primary?	Can be secondary to gene silencing, chromatin changes
Possible effects in humans	Chromosomal instability, loss of imprinting, oncogene activation	Maintenance of tumor-suppressor-gene silencing
Effects in animal models	Lymphoma, Increased intestinal tumor initiation, Liver cancer	Increased intestinal tumor progression
Variation in the age of onset	Yes	Yes
Therapy	Inhibitor side effect?	Inhibition therapy

Genetic factors:

 Three main classes of genes:

a. (Proto) Oncogenes

b. Tumor Suppressor Genes and

c. DNA repair genes contribute to the development of cancer genotype and phenotype. These genes resist the natural and inherent death mechanism(s) embedded in cells (apoptosis and like processes), coupled with dysregulation of cell proliferation events.

Table.6: Genes which contribute to Cancer (Vogelstein et al., 2014)

Gene	Major heredity tumor types
Tumor –suppressor genes	Colon, thyroid, stomach, intestine
APC	Colon
CDH1 (E-cadherin)	Stomach
EXT1,2	Bone
TP53 (p53)	Breast, sarcoma, adrenal, brain
Stability genes
MUTYH	Colon
BRCA1, BRCA2	Breast, ovary
MSH2, MLH1, MSH6,PMS2	Colon, uterus
XPA, C; ERCC2-5; DDB2	Skin
Oncogenes
KIT	Gastrointestinal stromal tumors
MET	Kidney
PDGFRA	Gastrointestinal stromal tumors
RET	Thyroid, parathyroid, adrenal
15-LOX-1	Prostate, colorectal, breast
15-LOX-2	Prostate, colorectal
12-LOX	Breast, Ovarian, Colon
5-LOX	Breast, Ovarian, Colorectal

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                                  Biomarkers and Cancer Targets  

July 16-17, Dubai UAE

Cancer Targeted Therapy                                                               
                                                                                                                                                                                          
What are targeted cancer therapies?

Targeted malignancy treatments are drugs or different substances that piece the development and spread of disease by meddling with atoms ("sub-atomic focuses on") that are associated with the development, movement, and spread of growth. Directed disease treatments are infrequently called "molecularly focused on drugs," "molecularly focused on treatments," "exactness solutions," or comparable names.

Targeted malignancy  treatments differ from standard chemotherapy in several ways:

• Directed treatments follow up on particular atomic focuses on that are related with tumor, though most standard chemotherapies follow up on all quickly partitioning typical and dangerous cells.

• Targeted therapies are deliberately chosen or designed to interact with their target, whereas many standard chemotherapies were identified because they kill cells. 

• Directed treatments are regularly cytostatic (that is, they piece tumor cell multiplication), though standard chemotherapy operators are cytotoxic (that is, they execute tumor cells). 

Directed treatments are as of now the concentration of considerably anticancer medication improvement. They are a foundation of accuracy prescription, a type of drug that utilization data about a man's qualities and proteins to avoid, analyse, and treat ailment.

Many focused-on disease treatments have been affirmed by the Food and Drug Administration (FDA) to treat kinds of tumor. Others are being examined in clinical trials (inquire about investigations with individuals), and numerous more are in preclinical testing (consider ponders with creatures).

·     How are targeted therapies developed?

Once a candidate target has been identified, the next step is to develop a therapy that affects the target in a way that interferes with its ability to promote cancer cell growth or survival.

Most targeted therapies are either small molecules or monoclonal antibodies.

 Little atom mixes are commonly produced for focuses on that are situated inside the cell in light of the fact that such specialists can enter cells moderately effectively. Monoclonal antibodies are relatively large and generally cannot enter cells, so they are used only for targets that are outside cells or on the cell surface.

Applicant little atoms are normally distinguished in what are known as "high-throughput screens," in which the impacts of thousands of test mixes on a particular target protein are analysed. Compounds that affect the target are then chemically modified to produce numerous closely related versions of the lead compound. These related compounds are then tested to determine which are most effective and have the fewest effects on non target molecules.

Monoclonal antibodies are developed by injecting animals (usually mice) with purified target proteins, causing the animals to make many different types of antibodies against the target. These antibodies are then tested to find the ones that bind best to the target without binding to non target proteins.

Before monoclonal antibodies are used in humans, they are "humanized" by replacing as much of the mouse antibody molecule as possible with corresponding portions of human antibodies. Adapting is important to keep the human insusceptible framework from perceiving the monoclonal counter acting agent as "outside" and annihilating it before it has an opportunity to tie to its objective protein. Humanization is not an issue for small-molecule compounds because they are not typically recognized by the body as foreign.

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