This document discusses diagnostic options and evaluation for breast cancer including imaging modalities like mammography and sonography. Biopsy methods for palpable and non-palpable masses are described. Breast cancer diagnosis involves evaluating the glandular parenchyma, nipple-areolar complex, and breast skin for symptoms. Mammography findings and use of screening vs diagnostic mammograms is outlined. Biomarkers for prognosis and prediction are discussed. Surgical options for treatment of ductal carcinoma in situ include excisional biopsy with margins and additional radiotherapy depending on factors like size and histology.
It contains details about breast carcinoma-pathology,investigations and diagnosis,NACT,surgery and adjuvant therapy. Hope you will find it helpful.....
It contains details about breast carcinoma-pathology,investigations and diagnosis,NACT,surgery and adjuvant therapy. Hope you will find it helpful.....
cancer of breast , this slide cointains detailed information about the breast cancer that is definition, causes and risk factor, sign and symptoms, management of patient with cancer , giving psychological support .treatment
Cervical Cancer Symptoms, Causes, TreatmentsMedWorld India
Cervical cancer is the malignancy that starts in the cervix. Cervical cancer instigate from the cells located on the surface of the cervix. Cervical cancer occurs in several forms. The most common is squamous cell carcinoma, which accounts for 85 to 90 percent of cervical cancers.
Updated Information about inflammatory breast cancer (IBC) - how it is different from other locally advanced breast cancer, pathology, imaging, how it is treated, research directions, resources and contact info for the IBC Network
breast cancer is the malignent condition of breast and it is the 2nd most common cancer in females with needs to be special attention as it its a very private things for female for early detection and its treatment, and provide a brief knowledge regarding breast cancer to all the nursing students and for their application in their c
Understanding the pathophysiology of carcinoma of breast is essential for deciding the optimum treatment for this lethal disease. The bilogical behaviour of the disease should guide radical treatment of the disease. Radical surgery is still the gold standard for treatment. Chemotherapy,radiotherapy and hormonal manipulation are useful adjuncts to surgery.
High Blood Pressure or Hypertension is known as the silent killer. It is a condition that occurs without symptoms for many years and in most cases the cause is unknown. Genetic or environmental are the most explained reasons.
cancer of breast , this slide cointains detailed information about the breast cancer that is definition, causes and risk factor, sign and symptoms, management of patient with cancer , giving psychological support .treatment
Cervical Cancer Symptoms, Causes, TreatmentsMedWorld India
Cervical cancer is the malignancy that starts in the cervix. Cervical cancer instigate from the cells located on the surface of the cervix. Cervical cancer occurs in several forms. The most common is squamous cell carcinoma, which accounts for 85 to 90 percent of cervical cancers.
Updated Information about inflammatory breast cancer (IBC) - how it is different from other locally advanced breast cancer, pathology, imaging, how it is treated, research directions, resources and contact info for the IBC Network
breast cancer is the malignent condition of breast and it is the 2nd most common cancer in females with needs to be special attention as it its a very private things for female for early detection and its treatment, and provide a brief knowledge regarding breast cancer to all the nursing students and for their application in their c
Understanding the pathophysiology of carcinoma of breast is essential for deciding the optimum treatment for this lethal disease. The bilogical behaviour of the disease should guide radical treatment of the disease. Radical surgery is still the gold standard for treatment. Chemotherapy,radiotherapy and hormonal manipulation are useful adjuncts to surgery.
High Blood Pressure or Hypertension is known as the silent killer. It is a condition that occurs without symptoms for many years and in most cases the cause is unknown. Genetic or environmental are the most explained reasons.
A blood pressure measurement is always expressed in two numbers. The higher (systolic) number represents the pressure while the heart is beating, and the lower (diastolic) number represents the pressure when the heart is resting between beats.
Dr. Sachin Verma is a young, diligent and dynamic physician. He did his graduation from IGMC Shimla and MD in Internal Medicine from GSVM Medical College Kanpur. Then he did his Fellowship in Intensive Care Medicine (FICM) from Apollo Hospital Delhi. He has done fellowship in infectious diseases by Infectious Disease Society of America (IDSA). He has also done FCCS course and is certified Advance Cardiac Life support (ACLS) and Basic Life Support (BLS) provider by American Heart Association. He has also done a course in Cardiology by American College of Cardiology and a course in Diabetology by International Diabetes Centre. He specializes in the management of Infections, Multiorgan Dysfunctions and Critically ill patients and has many publications and presentations in various national conferences under his belt. He is currently working in NABH Approved Ivy super-specialty Hospital Mohali as Consultant Intensivists and Physician.
Current knowledge and state of the art about management of abnormal cervical Cancer screening tests and cancer precursors for health providers in low-income settings is presented.
Cervical cancer is usually a squamous cell carcinoma; less often, it is an adenocarcinoma. The cause of most cervical cancers is human papillomavirus infection. Cervical neoplasia is often asymptomatic; the first symptom of cervical cancer is usually irregular, often postcoital vaginal bleeding. Diagnosis is by a cervical Papanicolaou test and biopsy. Staging is clinical, combined with imaging and pathology results when available. Treatment usually involves surgical resection for early-stage disease or radiation therapy plus chemotherapy for locally advanced disease. If the cancer has widely metastasized, chemotherapy is often used alone.
Lecture on prenatal genetic diagnostic techniques and their value in detection of prenatal genetic anomalies. This lecture details techniques employed in the common diagnostic interventions used in prenatal period and their usefulness.
Breast cancer is the most common invasive cancer in women and the second leading cause of cancer death in women after lung cancer.
According to the American Cancer Society, more than 193,000 cases of breast cancer are diagnosed each year, with an estimated 40,000 deaths.
About 1% of these cancers occur in men.
This includes introduction its classification,etiology,clinical manifestations,diagnostic criteria,management.
http://cancer-treatment-madurai.com Breast cancer is a type of cancer that starts in the tissues of the breast. Dr.S.G.Balamurugan is one of the best cancer doctor in India, offers low cost breast cancer diagnosis, breast cancer treatments and breast cancer care at Guru Cancer Hospital, Madurai.
Tom Selleck Health: A Comprehensive Look at the Iconic Actor’s Wellness Journeygreendigital
Tom Selleck, an enduring figure in Hollywood. has captivated audiences for decades with his rugged charm, iconic moustache. and memorable roles in television and film. From his breakout role as Thomas Magnum in Magnum P.I. to his current portrayal of Frank Reagan in Blue Bloods. Selleck's career has spanned over 50 years. But beyond his professional achievements. fans have often been curious about Tom Selleck Health. especially as he has aged in the public eye.
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Introduction
Many have been interested in Tom Selleck health. not only because of his enduring presence on screen but also because of the challenges. and lifestyle choices he has faced and made over the years. This article delves into the various aspects of Tom Selleck health. exploring his fitness regimen, diet, mental health. and the challenges he has encountered as he ages. We'll look at how he maintains his well-being. the health issues he has faced, and his approach to ageing .
Early Life and Career
Childhood and Athletic Beginnings
Tom Selleck was born on January 29, 1945, in Detroit, Michigan, and grew up in Sherman Oaks, California. From an early age, he was involved in sports, particularly basketball. which played a significant role in his physical development. His athletic pursuits continued into college. where he attended the University of Southern California (USC) on a basketball scholarship. This early involvement in sports laid a strong foundation for his physical health and disciplined lifestyle.
Transition to Acting
Selleck's transition from an athlete to an actor came with its physical demands. His first significant role in "Magnum P.I." required him to perform various stunts and maintain a fit appearance. This role, which he played from 1980 to 1988. necessitated a rigorous fitness routine to meet the show's demands. setting the stage for his long-term commitment to health and wellness.
Fitness Regimen
Workout Routine
Tom Selleck health and fitness regimen has evolved. adapting to his changing roles and age. During his "Magnum, P.I." days. Selleck's workouts were intense and focused on building and maintaining muscle mass. His routine included weightlifting, cardiovascular exercises. and specific training for the stunts he performed on the show.
Selleck adjusted his fitness routine as he aged to suit his body's needs. Today, his workouts focus on maintaining flexibility, strength, and cardiovascular health. He incorporates low-impact exercises such as swimming, walking, and light weightlifting. This balanced approach helps him stay fit without putting undue strain on his joints and muscles.
Importance of Flexibility and Mobility
In recent years, Selleck has emphasized the importance of flexibility and mobility in his fitness regimen. Understanding the natural decline in muscle mass and joint flexibility with age. he includes stretching and yoga in his routine. These practices help prevent injuries, improve posture, and maintain mobilit
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Prix Galien International 2024 Forum ProgramLevi Shapiro
June 20, 2024, Prix Galien International and Jerusalem Ethics Forum in ROME. Detailed agenda including panels:
- ADVANCES IN CARDIOLOGY: A NEW PARADIGM IS COMING
- WOMEN’S HEALTH: FERTILITY PRESERVATION
- WHAT’S NEW IN THE TREATMENT OF INFECTIOUS,
ONCOLOGICAL AND INFLAMMATORY SKIN DISEASES?
- ARTIFICIAL INTELLIGENCE AND ETHICS
- GENE THERAPY
- BEYOND BORDERS: GLOBAL INITIATIVES FOR DEMOCRATIZING LIFE SCIENCE TECHNOLOGIES AND PROMOTING ACCESS TO HEALTHCARE
- ETHICAL CHALLENGES IN LIFE SCIENCES
- Prix Galien International Awards Ceremony
Ethanol (CH3CH2OH), or beverage alcohol, is a two-carbon alcohol
that is rapidly distributed in the body and brain. Ethanol alters many
neurochemical systems and has rewarding and addictive properties. It
is the oldest recreational drug and likely contributes to more morbidity,
mortality, and public health costs than all illicit drugs combined. The
5th edition of the Diagnostic and Statistical Manual of Mental Disorders
(DSM-5) integrates alcohol abuse and alcohol dependence into a single
disorder called alcohol use disorder (AUD), with mild, moderate,
and severe subclassifications (American Psychiatric Association, 2013).
In the DSM-5, all types of substance abuse and dependence have been
combined into a single substance use disorder (SUD) on a continuum
from mild to severe. A diagnosis of AUD requires that at least two of
the 11 DSM-5 behaviors be present within a 12-month period (mild
AUD: 2–3 criteria; moderate AUD: 4–5 criteria; severe AUD: 6–11 criteria).
The four main behavioral effects of AUD are impaired control over
drinking, negative social consequences, risky use, and altered physiological
effects (tolerance, withdrawal). This chapter presents an overview
of the prevalence and harmful consequences of AUD in the U.S.,
the systemic nature of the disease, neurocircuitry and stages of AUD,
comorbidities, fetal alcohol spectrum disorders, genetic risk factors, and
pharmacotherapies for AUD.
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TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Verified Chapters 1 - 19, Complete Newest Version.pdf
Pulmonary Thromboembolism - etilogy, types, medical- Surgical and nursing man...VarunMahajani
Disruption of blood supply to lung alveoli due to blockage of one or more pulmonary blood vessels is called as Pulmonary thromboembolism. In this presentation we will discuss its causes, types and its management in depth.
MANAGEMENT OF ATRIOVENTRICULAR CONDUCTION BLOCK.pdfJim Jacob Roy
Cardiac conduction defects can occur due to various causes.
Atrioventricular conduction blocks ( AV blocks ) are classified into 3 types.
This document describes the acute management of AV block.
The prostate is an exocrine gland of the male mammalian reproductive system
It is a walnut-sized gland that forms part of the male reproductive system and is located in front of the rectum and just below the urinary bladder
Function is to store and secrete a clear, slightly alkaline fluid that constitutes 10-30% of the volume of the seminal fluid that along with the spermatozoa, constitutes semen
A healthy human prostate measures (4cm-vertical, by 3cm-horizontal, 2cm ant-post ).
It surrounds the urethra just below the urinary bladder. It has anterior, median, posterior and two lateral lobes
It’s work is regulated by androgens which are responsible for male sex characteristics
Generalised disease of the prostate due to hormonal derangement which leads to non malignant enlargement of the gland (increase in the number of epithelial cells and stromal tissue)to cause compression of the urethra leading to symptoms (LUTS
Anti ulcer drugs and their Advance pharmacology ||
Anti-ulcer drugs are medications used to prevent and treat ulcers in the stomach and upper part of the small intestine (duodenal ulcers). These ulcers are often caused by an imbalance between stomach acid and the mucosal lining, which protects the stomach lining.
||Scope: Overview of various classes of anti-ulcer drugs, their mechanisms of action, indications, side effects, and clinical considerations.
Title: Sense of Taste
Presenter: Dr. Faiza, Assistant Professor of Physiology
Qualifications:
MBBS (Best Graduate, AIMC Lahore)
FCPS Physiology
ICMT, CHPE, DHPE (STMU)
MPH (GC University, Faisalabad)
MBA (Virtual University of Pakistan)
Learning Objectives:
Describe the structure and function of taste buds.
Describe the relationship between the taste threshold and taste index of common substances.
Explain the chemical basis and signal transduction of taste perception for each type of primary taste sensation.
Recognize different abnormalities of taste perception and their causes.
Key Topics:
Significance of Taste Sensation:
Differentiation between pleasant and harmful food
Influence on behavior
Selection of food based on metabolic needs
Receptors of Taste:
Taste buds on the tongue
Influence of sense of smell, texture of food, and pain stimulation (e.g., by pepper)
Primary and Secondary Taste Sensations:
Primary taste sensations: Sweet, Sour, Salty, Bitter, Umami
Chemical basis and signal transduction mechanisms for each taste
Taste Threshold and Index:
Taste threshold values for Sweet (sucrose), Salty (NaCl), Sour (HCl), and Bitter (Quinine)
Taste index relationship: Inversely proportional to taste threshold
Taste Blindness:
Inability to taste certain substances, particularly thiourea compounds
Example: Phenylthiocarbamide
Structure and Function of Taste Buds:
Composition: Epithelial cells, Sustentacular/Supporting cells, Taste cells, Basal cells
Features: Taste pores, Taste hairs/microvilli, and Taste nerve fibers
Location of Taste Buds:
Found in papillae of the tongue (Fungiform, Circumvallate, Foliate)
Also present on the palate, tonsillar pillars, epiglottis, and proximal esophagus
Mechanism of Taste Stimulation:
Interaction of taste substances with receptors on microvilli
Signal transduction pathways for Umami, Sweet, Bitter, Sour, and Salty tastes
Taste Sensitivity and Adaptation:
Decrease in sensitivity with age
Rapid adaptation of taste sensation
Role of Saliva in Taste:
Dissolution of tastants to reach receptors
Washing away the stimulus
Taste Preferences and Aversions:
Mechanisms behind taste preference and aversion
Influence of receptors and neural pathways
Impact of Sensory Nerve Damage:
Degeneration of taste buds if the sensory nerve fiber is cut
Abnormalities of Taste Detection:
Conditions: Ageusia, Hypogeusia, Dysgeusia (parageusia)
Causes: Nerve damage, neurological disorders, infections, poor oral hygiene, adverse drug effects, deficiencies, aging, tobacco use, altered neurotransmitter levels
Neurotransmitters and Taste Threshold:
Effects of serotonin (5-HT) and norepinephrine (NE) on taste sensitivity
Supertasters:
25% of the population with heightened sensitivity to taste, especially bitterness
Increased number of fungiform papillae
Title: Sense of Smell
Presenter: Dr. Faiza, Assistant Professor of Physiology
Qualifications:
MBBS (Best Graduate, AIMC Lahore)
FCPS Physiology
ICMT, CHPE, DHPE (STMU)
MPH (GC University, Faisalabad)
MBA (Virtual University of Pakistan)
Learning Objectives:
Describe the primary categories of smells and the concept of odor blindness.
Explain the structure and location of the olfactory membrane and mucosa, including the types and roles of cells involved in olfaction.
Describe the pathway and mechanisms of olfactory signal transmission from the olfactory receptors to the brain.
Illustrate the biochemical cascade triggered by odorant binding to olfactory receptors, including the role of G-proteins and second messengers in generating an action potential.
Identify different types of olfactory disorders such as anosmia, hyposmia, hyperosmia, and dysosmia, including their potential causes.
Key Topics:
Olfactory Genes:
3% of the human genome accounts for olfactory genes.
400 genes for odorant receptors.
Olfactory Membrane:
Located in the superior part of the nasal cavity.
Medially: Folds downward along the superior septum.
Laterally: Folds over the superior turbinate and upper surface of the middle turbinate.
Total surface area: 5-10 square centimeters.
Olfactory Mucosa:
Olfactory Cells: Bipolar nerve cells derived from the CNS (100 million), with 4-25 olfactory cilia per cell.
Sustentacular Cells: Produce mucus and maintain ionic and molecular environment.
Basal Cells: Replace worn-out olfactory cells with an average lifespan of 1-2 months.
Bowman’s Gland: Secretes mucus.
Stimulation of Olfactory Cells:
Odorant dissolves in mucus and attaches to receptors on olfactory cilia.
Involves a cascade effect through G-proteins and second messengers, leading to depolarization and action potential generation in the olfactory nerve.
Quality of a Good Odorant:
Small (3-20 Carbon atoms), volatile, water-soluble, and lipid-soluble.
Facilitated by odorant-binding proteins in mucus.
Membrane Potential and Action Potential:
Resting membrane potential: -55mV.
Action potential frequency in the olfactory nerve increases with odorant strength.
Adaptation Towards the Sense of Smell:
Rapid adaptation within the first second, with further slow adaptation.
Psychological adaptation greater than receptor adaptation, involving feedback inhibition from the central nervous system.
Primary Sensations of Smell:
Camphoraceous, Musky, Floral, Pepperminty, Ethereal, Pungent, Putrid.
Odor Detection Threshold:
Examples: Hydrogen sulfide (0.0005 ppm), Methyl-mercaptan (0.002 ppm).
Some toxic substances are odorless at lethal concentrations.
Characteristics of Smell:
Odor blindness for single substances due to lack of appropriate receptor protein.
Behavioral and emotional influences of smell.
Transmission of Olfactory Signals:
From olfactory cells to glomeruli in the olfactory bulb, involving lateral inhibition.
Primitive, less old, and new olfactory systems with different path
micro teaching on communication m.sc nursing.pdfAnurag Sharma
Microteaching is a unique model of practice teaching. It is a viable instrument for the. desired change in the teaching behavior or the behavior potential which, in specified types of real. classroom situations, tends to facilitate the achievement of specified types of objectives.
4. DIAGNOSISDIAGNOSIS
S/S involve three major compartement:S/S involve three major compartement:
Glandular parenchyma:Glandular parenchyma:
MassMass
Asymmetric NodularityAsymmetric Nodularity
PainPain
Nipple-Areolar Complex:Nipple-Areolar Complex:
DischargeDischarge
RashRash
Distortion of shapeDistortion of shape
Breast skin:Breast skin:
Erythema&EdemaErythema&Edema
5. MammographyMammography
Screening mammogram:Screening mammogram:
Annually after 40 yrs.Annually after 40 yrs.
In pts with known BRCA mutation annually after 25-30yrs.In pts with known BRCA mutation annually after 25-30yrs.
In pts with strong family history.In pts with strong family history.
Grading Breast lesion:Grading Breast lesion:
1=negative1=negative
2=Benign appearing2=Benign appearing
3=Probably benign lesion3=Probably benign lesion
4=Findings suspicious of CA breast biopsy recommended.4=Findings suspicious of CA breast biopsy recommended.
5=Highly suspicious of malignancy.5=Highly suspicious of malignancy.
Diagnostic mammogram:Diagnostic mammogram:
Indicated for:Indicated for:
a questionable breast massa questionable breast mass
To see other suspicious lesions& contralateral breast.To see other suspicious lesions& contralateral breast.
To search for an occult CA breast in pts with metastatic axillary LN.To search for an occult CA breast in pts with metastatic axillary LN.
To follow the females with CA breast undergoing BCT.To follow the females with CA breast undergoing BCT.
Mammographic findings suggestive of malignancy are spiculated masses & linearMammographic findings suggestive of malignancy are spiculated masses & linear
microcalcifications & architectural pattern.microcalcifications & architectural pattern.
6. SonographicSonographic
Differentiate between Solid and cysticDifferentiate between Solid and cystic
USG guided FNAC from the cyst wallUSG guided FNAC from the cyst wall
It is performed in relatively younger age group.It is performed in relatively younger age group.
7. Breast BiopsyBreast Biopsy
For palpable masses :For palpable masses :
F.N.A.B.F.N.A.B.
Sensitivity is >90%.Sensitivity is >90%.
It does not give information about grade & invasion of tumor.It does not give information about grade & invasion of tumor.
ER & PR can be determined by immunohistochemistry.ER & PR can be determined by immunohistochemistry.
Core Biopsy Indications include :Core Biopsy Indications include :
Lack of concordance b/w imaging findings & histology.Lack of concordance b/w imaging findings & histology.
ADHADH
Radial scar.Radial scar.
Excisional Biopsy.Excisional Biopsy.
Incisional Biopsy.Incisional Biopsy.
12. Evaluation of other Breast SymptomsEvaluation of other Breast Symptoms
Breast Pain :Breast Pain :
Uni-lateral.Uni-lateral.
Focal.Focal.
CBECBE
USG Breast.USG Breast.
Core tissue Biopsy.Core tissue Biopsy.
Secondary Mammogram.Secondary Mammogram.
Nipple Discharge.Nipple Discharge.
It is usually unilateral, spontaneous & Bloody.It is usually unilateral, spontaneous & Bloody.
Cytology.Cytology.
Subareolar Excisional Biopsy is indicated in :Subareolar Excisional Biopsy is indicated in :
When cytology reveals cellular atypia.When cytology reveals cellular atypia.
Inrtaductal lesion seen on USG.Inrtaductal lesion seen on USG.
Persistently discharging single duct.Persistently discharging single duct.
13. BREAST CA ;BREAST CA ;
CELLULAR,BIOCHEMICAL&MOLECULARCELLULAR,BIOCHEMICAL&MOLECULAR
BIOMARKERSBIOMARKERS..
Breast cancer progression is the result of cumulative effect of successiveBreast cancer progression is the result of cumulative effect of successive
discrete genetic alterations lead to a gradual transition from normal todiscrete genetic alterations lead to a gradual transition from normal to
Premalignant to malignant.Premalignant to malignant.
BRCA-1&2 .BRCA-1&2 .
5-10% cases are caused by cancer susceptibility genes.5-10% cases are caused by cancer susceptibility genes.
56-85% life time risk of developing breast ca.56-85% life time risk of developing breast ca.
15-45% life time risk of ovarian ca.15-45% life time risk of ovarian ca.
These are high grade,receptor negative and aneuploid.These are high grade,receptor negative and aneuploid.
Strategies for prevention of ca breast in BRCA carriers include :Strategies for prevention of ca breast in BRCA carriers include :
Prophylactic mastectomy & reconstruction.Prophylactic mastectomy & reconstruction.
Prophylactic oophorectomy and HRT.Prophylactic oophorectomy and HRT.
Intensive surveillance for breast ca .Intensive surveillance for breast ca .
Chemoprevention.Chemoprevention.
Screening mammogram.Screening mammogram.
14. Prognostic & Predictive BiomarkersPrognostic & Predictive Biomarkers
The biomarkers are biological alterations in tissue thatThe biomarkers are biological alterations in tissue that
occur b/w initiation & cancer developement.occur b/w initiation & cancer developement.
These are :These are :
Proliferative changes.Proliferative changes.
Histologic changes.Histologic changes.
Genetic alterations.Genetic alterations.
These include:These include:
Proliferative markers:PCNA,Ki-67.Proliferative markers:PCNA,Ki-67.
Apoptic indicators :bcl-2 and bax/bcl-2 ratio.Apoptic indicators :bcl-2 and bax/bcl-2 ratio.
Angiogenic indicators :VEGF.Angiogenic indicators :VEGF.
Growth Factor receptors :EGFr,HER-2/neu,p53.Growth Factor receptors :EGFr,HER-2/neu,p53.
15. cont.cont.
HER-2/neu Receptor:HER-2/neu Receptor:
HER-2/neu gene amplification carries poor prognosis.HER-2/neu gene amplification carries poor prognosis.
Anti-HER-2/neu antibodies in combination with Taxanes.Anti-HER-2/neu antibodies in combination with Taxanes.
Use of adenoviral E1A to suppress HER-2/neu gene transcription.Use of adenoviral E1A to suppress HER-2/neu gene transcription.
Angiogenic Factors:Angiogenic Factors:
VEGFVEGF
Extracellular matrix protein receptors-------integrins.Extracellular matrix protein receptors-------integrins.
Matrix metalloproteases.Matrix metalloproteases.
Antiangiogenic Factors:Antiangiogenic Factors:
Anti VEGF antibody.Anti VEGF antibody.
VEGF receptor inhibitor.VEGF receptor inhibitor.
MMP inhibitorsMMP inhibitors
Antiintegrin antibody.Antiintegrin antibody.
Vascular targeting agent-------Fixes complement and causes vasculitis.Vascular targeting agent-------Fixes complement and causes vasculitis.
16. Prognostic & Predictive Factors.Prognostic & Predictive Factors.
Tumour Factors.Tumour Factors. Host Factors.Host Factors.
Nodal statusNodal status AgeAge
Tumour sizeTumour size Menopausal statusMenopausal status
Cytologic/nuclear gradeCytologic/nuclear grade Family HistoryFamily History
Vascular invasionVascular invasion Previous breast ca.Previous breast ca.
Pathologic stagePathologic stage ImmunosuppressionImmunosuppression
HR statusHR status NutritionNutrition
DNA contentDNA content Prior chemotherapyPrior chemotherapy
Ext. Intraductal comp.Ext. Intraductal comp. Prior radiotherapyPrior radiotherapy
17. Cont.Cont.
Nottingham PrognosticNottingham Prognostic
index:index:
NPI=(Tumour size in cmNPI=(Tumour size in cm
x0.2)+Lymph nodex0.2)+Lymph node
stage(1=no node,2=1-3stage(1=no node,2=1-3
LN positive,3=4 or moreLN positive,3=4 or more
node involved)node involved)
+Grade(1,2 or 3).+Grade(1,2 or 3).
>5.4
2.4-5.4
<2.4
18. Ductal CA in situ.Ductal CA in situ.
>50% of breast cancers diagnosed with screening mammograph.>50% of breast cancers diagnosed with screening mammograph.
15-20% of all diagnosed female breast cancers.15-20% of all diagnosed female breast cancers.
Pathophysiology:Pathophysiology:
Pre-invasive cancer.Pre-invasive cancer.
Two broad categories:Two broad categories:
Comedo Type.:Comedo Type.:
Necrotic cellular debris within duct.Necrotic cellular debris within duct.
Numerous mitosis & large pleomorphic nuclei.Numerous mitosis & large pleomorphic nuclei.
Absence of specific architectural changesAbsence of specific architectural changes
Denser collection of microcalcification.Denser collection of microcalcification.
Non-Comedo Type :Non-Comedo Type :
Lack of central necrosis.Lack of central necrosis.
Low mitotic rate.Low mitotic rate.
ER-positive.ER-positive.
Fewer microcalcification.Fewer microcalcification.
Low ,medium & high grade.Low ,medium & high grade.
19. Prognostic Index for DCIS.Prognostic Index for DCIS.
ScoreScore 11 22 33
Size(cm)Size(cm) <1.5<1.5 1.5-41.5-4 >4>4
Margins(cm)Margins(cm) >1>1 1-0.11-0.1 <0.1<0.1
HistologyHistology Low withoutLow without
necrosisnecrosis
IntermediateIntermediate
With necrosisWith necrosis
HighHigh
gradegrade
20. DiagnosisDiagnosis
Screening mammogram:Microcalcification.Screening mammogram:Microcalcification.
P/C stereotactic core biopsy.P/C stereotactic core biopsy.
Vaccum assisted aspiration biopsy.Vaccum assisted aspiration biopsy.
Excisional biopsy:Excisional biopsy:
1 cm Margins of the excised lesion ,beyond the extent of1 cm Margins of the excised lesion ,beyond the extent of
disease indicated by pre-operative mammography, should bedisease indicated by pre-operative mammography, should be
free of disease.free of disease.
Excised lesions are marked at six surgical margins & shouldExcised lesions are marked at six surgical margins & should
be send for frozen-section.be send for frozen-section.
Small titanium clips are used to mark the margins of biopsySmall titanium clips are used to mark the margins of biopsy
cavity for subsequent radiotherapy & is helpful if the re-cavity for subsequent radiotherapy & is helpful if the re-
excisiopn is required.excisiopn is required.
Re-excision of the lesions with margins within 0.5cm of theRe-excision of the lesions with margins within 0.5cm of the
tumour.tumour.
21. Cont.Cont. Additional treatement.Additional treatement.
Lesions <0.5cm,favourable histology clear surgicalLesions <0.5cm,favourable histology clear surgical
margins.---------close surveillance.margins.---------close surveillance.
Lesions b/w 0.5-2.5cm, favourable histology, clear surgicalLesions b/w 0.5-2.5cm, favourable histology, clear surgical
margins.-------post op. radiotherapy.margins.-------post op. radiotherapy.
Lesions>2.5cmLesions>2.5cm
Wide excision with 1cm tumour free margins.+Post- op.Wide excision with 1cm tumour free margins.+Post- op.
radiotherapy.radiotherapy.
Risk factors contributing for consideration of simpleRisk factors contributing for consideration of simple
mastectomy.mastectomy.
Younger pts.Younger pts.
Multifocal disease.Multifocal disease.
Larger lesions relative to breast size.Larger lesions relative to breast size.
Strong family history.Strong family history.
Unfavourable histology.Unfavourable histology.
23. Lobular CA in situ.Lobular CA in situ.
Hormonal Influence.Hormonal Influence.
Higher frequency of ER-Higher frequency of ER-
positive tumours.positive tumours.
Diagnosis is purelyDiagnosis is purely
incidental.incidental.
Pre-malignant condition.Pre-malignant condition.
Close surveillance.Close surveillance.
Bilateral mastectomy.Bilateral mastectomy.
Prophylaxis with Tamoxefin.Prophylaxis with Tamoxefin.
Lobular hyperplasia
Atypical hyperplasia
Lobular ca in situ
25. Surgical TherapySurgical Therapy
Breast conservation.Breast conservation.
Tumours upto 5cm can be managed .Tumours upto 5cm can be managed .
Local recurrence rate after BCT & radiotherapy is less than 10%.Local recurrence rate after BCT & radiotherapy is less than 10%.
Pts with recurrence require mastectomy and less often re-excision.Pts with recurrence require mastectomy and less often re-excision.
Lumpectomy without radiation has higher recurrence but can be avoidedLumpectomy without radiation has higher recurrence but can be avoided
in low risk pts like:in low risk pts like:
Low grade.Low grade.
Small size.Small size.
Adequate resection margins.Adequate resection margins.
Special histologic Type.Special histologic Type.
Presence of good prognostic features in Primary cancers.Presence of good prognostic features in Primary cancers.
Negative SLNB.Negative SLNB.
26. Cont.Cont.
Contra-indications:Contra-indications:
Larger tumours in relatively small breast.Larger tumours in relatively small breast.
Females previously irradiated.Females previously irradiated.
Multifocal &Multicentric.Multifocal &Multicentric.
Pregnancy.Pregnancy.
Collagen vascular disease.Collagen vascular disease.
Positive resection margins.Positive resection margins.
Pts with BRCAI & II.Pts with BRCAI & II.
27. Cont.Cont.
BCT with radiotherapy:BCT with radiotherapy:
In all cases <45yrs.In all cases <45yrs.
>45yrs------tumour >1cm.>45yrs------tumour >1cm.
BCT without radiotherapy:BCT without radiotherapy:
>45yrs.>45yrs.
<1cm.<1cm.
Well differentiated.Well differentiated.
Tubular,Papillary,Mucinous.Tubular,Papillary,Mucinous.
Types of BCT :Types of BCT :
Wide local Excision.Wide local Excision.
Segmentectomy.Segmentectomy.
Quadrentectomy.Quadrentectomy.
Needle localization Excision for impalpable tumour.Needle localization Excision for impalpable tumour.
28. Axillary Surgery.Axillary Surgery.
Axillary LN status is important prognostic factor for survival.Axillary LN status is important prognostic factor for survival.
Clinically palpable LN.Clinically palpable LN.
F.N.A.C. to confirm.F.N.A.C. to confirm.
Neo-adjuvant chemotherapy.Neo-adjuvant chemotherapy.
Axillary clearance-upto level III.Axillary clearance-upto level III.
Complications.Complications.
Post op. radiotherapy .Post op. radiotherapy .
Clinically negative LN.Clinically negative LN.
No axillary evaluation is required in pts with low risk for axillaryNo axillary evaluation is required in pts with low risk for axillary
metastasis(<5%) which includes tumours <1cm,tubular,mucinous &metastasis(<5%) which includes tumours <1cm,tubular,mucinous &
papillary variety and elderly females with small cancer.papillary variety and elderly females with small cancer.
In all other pts with invasive carcinoma:SLNB & ALNS.In all other pts with invasive carcinoma:SLNB & ALNS.
31. Adjuvant Systemic TherapyAdjuvant Systemic Therapy
Pts. are at risk of developing either local or distant metastasis.Pts. are at risk of developing either local or distant metastasis.
Risk is assessed from different prognostic factors:Risk is assessed from different prognostic factors:
Size.Size.
LN status.LN status.
Estrogen Receptor status.Estrogen Receptor status.
Grade.Grade.
Lymphovascular invasion.Lymphovascular invasion.
Aim is to eliminate micrometastasis,thus reducing the risk ofAim is to eliminate micrometastasis,thus reducing the risk of
recurrence & metastasis.recurrence & metastasis.
Treatement can be given in the form of:Treatement can be given in the form of:
Adjuvant.Adjuvant.
Neo-adjuvant.Neo-adjuvant.
32. Currently available treatement optionsCurrently available treatement options..
ChemotherapyChemotherapy
Hormone therapyHormone therapy
Biological TherapyBiological Therapy
33. Cont.Cont.
Decision is based on:Decision is based on:
Disease related factors:Disease related factors:
Tumour size.Tumour size.
LN status.LN status.
Lymphovascu;ar invasion.Lymphovascu;ar invasion.
Receptor status.Receptor status.
Grade.Grade.
Pt related factors:Pt related factors:
AgeAge
Menopause.Menopause.
Fitness.Fitness.
34. ChemotherapyChemotherapy
Benefit is independent of nodal & menopausal status.Benefit is independent of nodal & menopausal status.
Absolute improvement is more for node positive pt.Absolute improvement is more for node positive pt.
Benefit is less for pts >70yrs.Benefit is less for pts >70yrs.
Combinations used:Combinations used:
CMF.CMF.
MF.MF.
CAF.CAF.
AC-----TAC-----T
Adverse effects.Adverse effects.
G.I. disturbance.G.I. disturbance.
Alopecia.Alopecia.
Hematological suppression.Hematological suppression.
Fertility and ovarian function is affected >40yrs in Cyclophosphamide containingFertility and ovarian function is affected >40yrs in Cyclophosphamide containing
regimens.regimens.
Induction of second cancers(hematological).Induction of second cancers(hematological).
Cardiac ToxicityCardiac Toxicity
36. Drugs Targeting Estrogen and It’sDrugs Targeting Estrogen and It’s
Receptor in Breast CancerReceptor in Breast Cancer
EstrogenEstrogen
CellCell
GrowthGrowth
andand
DivisionDivision
Estrogen
Receptor
SERMS (tamoxifen,SERMS (tamoxifen,
raloxifene), SERDSraloxifene), SERDS
(fulvstrant)(fulvstrant)
AromataseAromatase
inhibitors, ovarianinhibitors, ovarian
suppressionsuppression
37. Hormonal TherapyHormonal Therapy
Tamoxefin.Tamoxefin.
Beneficial in pts with ER+ve irrespective ofBeneficial in pts with ER+ve irrespective of
Age.Age.
LN status.LN status.
Menopausal.Menopausal.
For older pts adding CT is not helpful due to additionalFor older pts adding CT is not helpful due to additional
toxicity.toxicity.
Adverse effects:Adverse effects:
Vasomotor Symptoms.Vasomotor Symptoms.
Decrease cholesterol.Decrease cholesterol.
Increase thrombosis.Increase thrombosis.
Bone loss in pre-menopausal pts.Bone loss in pre-menopausal pts.
Bone protecting in post-menopausal pts.Bone protecting in post-menopausal pts.
38. Cont.Cont.
Ovarian ablation.Ovarian ablation.
In pre-menopausal pts.In pre-menopausal pts.
Benefit is independent of nodal status.Benefit is independent of nodal status.
Methods :Methods :
Surgery.Surgery.
Radiation.Radiation.
LHRH agonists.LHRH agonists.
It exists as an alternative to CT or as optimal endocrineIt exists as an alternative to CT or as optimal endocrine
therapy.therapy.
Treatement by LHRH agonist (Goserelin) in S/C depotsTreatement by LHRH agonist (Goserelin) in S/C depots
monthly.monthly.
Treatement is reversible with preservation of fertility.Treatement is reversible with preservation of fertility.
Menopausal symptoms.Menopausal symptoms.
39. Cont.Cont.
Aromatase inhibitor:(Anastrozole)Aromatase inhibitor:(Anastrozole)
Beneficial in post-menopausal females.Beneficial in post-menopausal females.
It inhibits the conversion of adrenal androgens into estradiolIt inhibits the conversion of adrenal androgens into estradiol
and estrone.and estrone.
Less severe side-effects.Less severe side-effects.
Increase risk of fractures due to effect in bone mineralIncrease risk of fractures due to effect in bone mineral
density.density.
Alternative first line therapy where potential risk forAlternative first line therapy where potential risk for
Tamoxefin is present.Tamoxefin is present.
Switching to aromatase inhibitor after 2-3 yr use ofSwitching to aromatase inhibitor after 2-3 yr use of
Tamoxefin.Tamoxefin.
41. Biological TherapyBiological Therapy
Target the factors which allow the cancer cells toTarget the factors which allow the cancer cells to
grow and survive and spreadgrow and survive and spread
. Adjuvant therapy containing Doxorubicin is. Adjuvant therapy containing Doxorubicin is
effective.effective.
Anti-HER-2/neu antibodies in combination withAnti-HER-2/neu antibodies in combination with
Taxanes.Taxanes.
Use of adenoviral E1A to suppress HER-2/neuUse of adenoviral E1A to suppress HER-2/neu
gene transcriptiongene transcription
42. The HER Family ofThe HER Family of
ReceptorsReceptors
HER1
EGFR
HER2 HER3
HER4
Tumor CellTumor Cell
•Trastuzumab (Herceptin)Trastuzumab (Herceptin)
•Pertuzumab (Omnitarg)Pertuzumab (Omnitarg)
•LapatinibLapatinib
•Erlotinib (Tarceva)Erlotinib (Tarceva)
•Gefitinib (Iressa)Gefitinib (Iressa)
•Cetuximab (Erbitux)Cetuximab (Erbitux)
43. Drugs Targeting HER-2 in Breast CancerDrugs Targeting HER-2 in Breast Cancer
HER-2
nucleus
cancer cell
cell division
Trastuzumab (Herceptin)
Anti-HER-2 Antibody (IV)
HER-2 Oncogene: overexpressed inHER-2 Oncogene: overexpressed in
20-25% of breast cancers20-25% of breast cancers
Lapatinib (Tykerb)
Dual HER-1/HER-2 (oral)
Tyrosine Kinase Inhibitor
44.
45. Multidisciplinary Cancer Breast Management
Natural History of DiseaseNatural History of Disease
• • Most cases of stage III breast cancer were onceMost cases of stage III breast cancer were once
stage I breast cancerstage I breast cancer
•• In poor countries, more than half of patients haveIn poor countries, more than half of patients have
locally advanced or metastatic disease at the time oflocally advanced or metastatic disease at the time of
diagnosisdiagnosis
–– Lack of educationLack of education
–– Lack of screeningLack of screening
46. Multidisciplinary Cancer Breast Management
Clinical Presentation ofClinical Presentation of
Stage III Breast CancerStage III Breast Cancer
Peau d’orange Large mass, edema, and erythema
47. Multidisciplinary Cancer Breast Management
Clinical Presentation of Stage III, Locally
Advanced (Inoperable) Disease
Large primary breast cancer Locally advanced breast cancer
48. Multidisciplinary Cancer Breast Management
Stage Classifications for Locally
Advanced Breast Cancer
Stage IIB T2 N1 M0
T3 N0 M0
Stage IIIA T0 N2 M0
T1 N2 M0
T2 N2 M0
T3 N1 M0
T3 N2 M0
49. Multidisciplinary Cancer Breast Management
Stage Classifications for Locally
Advanced Breast Cancer (cont.)
Stage IIIB T4 N0 M0
T4 N1 M0
T4 N2 M0
Stage IIIC Any T N3 M0
Stage IV Any T Any N M1
50. Locally Advanced CarcinomaLocally Advanced Carcinoma
Stage lll and Inflammatory breast Carcinoma.Stage lll and Inflammatory breast Carcinoma.
Combination CT (CAF)has dramatic regressionCombination CT (CAF)has dramatic regression
of breast lesion in 65-70% percent of cases.of breast lesion in 65-70% percent of cases.
With induction responses following 2-6 drugWith induction responses following 2-6 drug
cycles an extended simple mastectomy with levelcycles an extended simple mastectomy with level
l nodal dissection should be done.l nodal dissection should be done.
Peripheral lymphatics,skin flaps and central andPeripheral lymphatics,skin flaps and central and
apical LN group are treated with comprehensiveapical LN group are treated with comprehensive
radiation therapy.radiation therapy.
51. Cont.Cont.
Multimodal approach in stage lll decreases theMultimodal approach in stage lll decreases the
chest wall recurrence to 4-10%.chest wall recurrence to 4-10%.
And improve the 5 year survival to 45 %.And improve the 5 year survival to 45 %.
,and 10 year survival to 28 %.,and 10 year survival to 28 %.
52. Multidisciplinary Cancer Breast Management
Neoadjuvant Chemotherapy
•Concept developed concurrently with adjuvant
chemotherapy in the 1970s
•Treatment for locally advanced breast cancer
(stage III disease)
•Allows for immediate assessment of tumor response
•Allows for the evaluation of new and novel agents
53. Multidisciplinary Cancer Breast Management
Neoadjuvant Chemotherapy (cont.)
•Goals:
– Decrease tumor size
– Minimize surgery
– Establish tumor sensitivity
•Appropriate treatments:
– Chemotherapy
– Tamoxifen or aromatase inhibitors
– Radiation therapy
54. Multidisciplinary Cancer Breast Management
Clinical Rationale for Preoperative Chemotherapy:
•Excellent response rates for locally advanced breast cancer
• Efficacy of adjuvant chemotherapy for node- negative
breast cancer
• Equivalent survival for breast-conserving surgery and
mastectomy
55. Multidisciplinary Cancer Breast Management
Advantages of
Neoadjuvant Chemotherapy
•Increased rate of breast-conserving surgery
•Earlier treatment of micrometastases
•Treatment serves as in vivo chemosensitivity assay
•Improved rates of local control and disease-free survival
56. Multidisciplinary Cancer Breast Management
Factors Influencing Decision to Use
Neoadjuvant Chemotherapy in Operable Breast
Cancer
•Does the patient need adjuvant chemotherapy based
on information known prior to surgery?
•Would neoadjuvant chemotherapy potentially alter
the extent of resection?
•Does the patient desire breast preservation?
•Would treatment benefit from knowledge of in vivo
chemosensitivity?
57. Multidisciplinary Cancer Breast Management
Radiation Therapy after Mastectomy
According to Consensus Statement developed by
American Society for Therapeutic Radiology and
Oncology (ASTRO)
•Radiation therapy should be part of the treatment for stage
III breast cancers and for disease that involves four or more lymph
nodes
•At a minimum, the chest wall and the supraclavicular fossa should
be treated with doses of at least 50 Gy
58.
59. Oncoplastic Breast Surgery(OBS)Oncoplastic Breast Surgery(OBS)
It includes all approaches of plastic and Re-It includes all approaches of plastic and Re-
constructive surgery aimed at achieving tumourconstructive surgery aimed at achieving tumour
resection with satisfactory margins inresection with satisfactory margins in
conservative treatement.conservative treatement.
It attempted to minimize potential deformitiesIt attempted to minimize potential deformities
and to obtain best possible cosmeticand to obtain best possible cosmetic
results,without compromising resection marginsresults,without compromising resection margins
60. ClassificationClassification
Post-mastectomy breast re-constructionPost-mastectomy breast re-construction
ImmediateImmediate
DelayedDelayed
Conservative Post surgery Breast Re-Conservative Post surgery Breast Re-
constructionconstruction
ImmediateImmediate
DelayedDelayed
Re-construction of chest wall and soft tissueRe-construction of chest wall and soft tissue
deformities after surgical treatement of LABCdeformities after surgical treatement of LABC
and extensive local recurrence.and extensive local recurrence.
Editor's Notes
The human epidermal growth factor family of receptors consists of 4 transmembrane proteins with different properties (HER1-4), all involved in regulation of cell proliferation and survival.1-5
The prototype HER member HER1/EGFR (Erb-B1) binds a variety of growth factors, with ligand binding activating tyrosine kinase activity within the cytoplasmic domain and through various signal transduction intermediates.1
HER2 has no known ligand-binding activity, but its tyrosine-kinase activity is transactivated through HER2 interaction with other HER members (heterodimerization), usually following ligand binding to those receptors.3
The HER2 extracellular domains are fixed in an open conformation (exposed domain II loop) that resembles a ligand-activated state, and thus HER2 can constitutively interact functionally with other HER members.6
HER3 lacks inherent tyrosine kinase activity, but ligand binding promotes HER heterodimerization, resulting in complexes (eg, HER2/HER3) with highly proliferative signaling activity.2,4
The HER signaling network, mediated by these receptor interactions, stimulates and regulates not only cell proliferation, but also mobility, adhesion and survival.4,5 The activity of HER2/HER4 dimers is unclear, but may be implicated in providing survival signals to cardiomyocytes.4,5