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DEBJYOTI GHOSH
• Breast cancer with gross locoregional disease.
• Stage IIIa and IIIb tumors with:
 T3 tumors with N1, N2 and N3 nodes
 T4 tumors with any N nodes
 Any T tumors with N2 and N3 nodes
• Tumor characteristics: T3(Tumor > 5 cm), T4a, T4b, T4c,
T4d tumor
• Node characteristics: N2 or N3(Bulky and fixed nodes).
Clinically apparent internal mammary and supraclavicular
nodes.
CLINICAL FEATURES
Fungating mass and ulcer
over the swelling with
serous discharge
INVESTIGATIONS:
• Core biopsy from breast lump
• Mammography of both breasts
• Bone scan
• Chest X-Ray
• Liver Function Test
• USG/CT abdomen
• CT brain
TREATMENT:
• Pre-operative chemotherapy followed by surgery and
radiation
• Neoadjuvant chemotherapy results in downsizing of
tumor and easy resectability
• Hormonal therapy is also given depending on
hormone receptor status
• Surgery: Breast Conservation Surgery or Modified
Radical Mastectomy
• Post operative radiation therapy to breast flap and all
lymph node fields
• Recommended schedules:
 FAC
 AC
 AC followed by Taxane
• Newer drugs: Trastuzumab, Navelbine, Capecitabine and
Gemcitabine
NEOADJUVANT CHEMOTHERAPY
NEOADJUVANT ENDOCRINE THERAPY
• Tamoxifen
• Letrozole
SURGERY:
• Surgery after chemotherapy monitoring
• Treatment of primary tumor is surgical
• Breast Conservation Surgery or Modified Radical
Mastectomy
• Criteria for Breast Conservation Therapy
TREATMENT PATHWAYS FOR STAGE IIIA AND IIIB BREAST
CANCER
RECEPTOR STATUS
• Breast cancer cells may or may not have many different types
of receptors
• Three most important receptors are: Estrogen Receptor(ER),
Progesterone Receptor(PR), Human Epidermal Growth Factor
Receptor(HER2/neu)
• These receptors are present partially or absent totally called
TRIPLE NEGATIVE or BASAL-LIKE
• Presence of these receptors determine the chemotherapy and
the prognosis
ESTROGEN RECEPTORS
• Depend on estrogen hormone to grow
• 2 different forms – α and β , each encoded by a separate gene
• ERα – Endometrium, Breast Cancer cells, Ovarian stromal
cells, Hypothalamus and afferent ducts in males
• ERβ – Ovarian granulosa cells, Kidney, Brain, Bone, Heart,
Lungs, Intestinal mucosa and Prostate
• As per visualization research, small fraction of ERs reside in
cytoplasm, most in the nucleus
PROGESTERONE RECEPTORS
•The progesterone receptor (PR, also known as NR3C3 or
nuclear receptor subfamily 3, group C, member 3), is a
protein found inside cells.
• Activated by the steroid hormone progesterone
• In humans, PR is encoded by a single PGR gene residing on
chromosome 11q22
• Has 2 main forms, A and B, that differ in their molecular
weight
HER2 STATUS
• HER2 positive: Cancers that have too much HER2 protein
or extra copies of the HER2 gene. Respond
to drugs that target HER2
• HER2 negative: Cancers that don’t have excess HER2. Do
not respond to treatment by drugs that
target HER2
TRIPLE POSITIVE
• This term is used to describe cancers that are ER-positive,
PR-positive, and have too much HER2. These cancers can
be treated with hormone drugs as well as drugs that target
HER2.
• The medication tamoxifen helps stop cancer from coming
back by blocking hormone receptors, preventing hormones
from binding to them. It’s sometimes taken for upto 5 years
after initial treatment for breast cancer.
• A class of medicine called aromatase inhibitors actually
stops estrogen production. These include anastrozole,
exemestane, and letrozole. They’re only used in women
who’ve already gone through menopause.
TRIPLE NEGATIVE
• If the breast cancer cells don’t have estrogen or
progesterone receptors and don’t have too much HER2, they
are called triple-negative.
• Tend to occur more often in younger women
• Tend to grow and spread more quickly than most other
types of breast cancer.
• Hormone therapy or drugs that target HER2 are not
helpful in treating these cancers.
MOLECULAR SUBTYPE
• Newer approaches look at ER, PR, HER2 together, along
with the tumor grade, to categorize breast cancer into
several conceptual molecular classes that have
different prognoses and may have different responses to
specific therapies.
• DNA microarrays have assisted this approach.
• Proposed molecular subtypes include:
 Basal-like: ER-, PR- and HER2-; triple negative breast
cancer (TNBC) Most BRCA1 breast cancers are basal-like
 Luminal A: ER+ and low grade
 Luminal B: ER+ but often high grade
 Luminal ER-/AR+: Recently identified androgen
responsive subtype which may respond to antihormonal
treatment with bicalutamide
 Normal Breast like
 ERBB2/HER2+: Has amplified HER2/neu
 Claudin-low: A more recently described class; often
triple-negative, but distinct in that there is low expression
of cell-cell junction proteins including E-cadherin
AXILLARY LYMPH NODE DISSECTION
• Approximately 30% of patients with clinically non-
palpable lymph nodes have positive lymph nodes in ALND
specimen
• The presence and number of lymph nodes involved affect
staging, management and prognosis
• Precursor of ALND is SENTINEL LYMPH NODE BIOPSY
PRINCIPLES OF AXILLARY DISSECTION
It is removal of different levels of axillary lymph nodes with axillary fat and fascia
WHY AXILLARY
DISSECTION IS DONE?
WHICH LEVELS? TECHNICAL PRINCIPLES
• For staging • Level I – 60% • Any incision but caudal hair-
line is preferred
• To assess the prognosis –
number of nodes/size of
nodule
• Level I,II – 20-25%
• Level I,II,III – 15-20%
• Nerve to serratus anterior
should be safeguarded
• As a treatment – regional
control of the disease
• Medial & lateral pectoral nerves
should be retained when
dissection is done with
mastectomy
• To plan the adjuvant
therapy –
irradiation/chemo/hormone
•Level I and II
dissection
Low dissection has less
chances of
lymphoedema
• Drain should be kept
• All lymph nodes should be
labelled and sent for HPE. Usually
20-32 nodes are present in axilla.
Minimum of 10 nodes should be
dissected. Fat dissolving agents
used for node identification
THANK YOU

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Debjyoti locally advanced breast carcinoma

  • 2. • Breast cancer with gross locoregional disease. • Stage IIIa and IIIb tumors with:  T3 tumors with N1, N2 and N3 nodes  T4 tumors with any N nodes  Any T tumors with N2 and N3 nodes • Tumor characteristics: T3(Tumor > 5 cm), T4a, T4b, T4c, T4d tumor • Node characteristics: N2 or N3(Bulky and fixed nodes). Clinically apparent internal mammary and supraclavicular nodes.
  • 3. CLINICAL FEATURES Fungating mass and ulcer over the swelling with serous discharge
  • 4. INVESTIGATIONS: • Core biopsy from breast lump • Mammography of both breasts • Bone scan • Chest X-Ray • Liver Function Test • USG/CT abdomen • CT brain
  • 5.
  • 6. TREATMENT: • Pre-operative chemotherapy followed by surgery and radiation • Neoadjuvant chemotherapy results in downsizing of tumor and easy resectability • Hormonal therapy is also given depending on hormone receptor status • Surgery: Breast Conservation Surgery or Modified Radical Mastectomy • Post operative radiation therapy to breast flap and all lymph node fields
  • 7. • Recommended schedules:  FAC  AC  AC followed by Taxane • Newer drugs: Trastuzumab, Navelbine, Capecitabine and Gemcitabine NEOADJUVANT CHEMOTHERAPY NEOADJUVANT ENDOCRINE THERAPY • Tamoxifen • Letrozole
  • 8. SURGERY: • Surgery after chemotherapy monitoring • Treatment of primary tumor is surgical • Breast Conservation Surgery or Modified Radical Mastectomy • Criteria for Breast Conservation Therapy
  • 9. TREATMENT PATHWAYS FOR STAGE IIIA AND IIIB BREAST CANCER
  • 10. RECEPTOR STATUS • Breast cancer cells may or may not have many different types of receptors • Three most important receptors are: Estrogen Receptor(ER), Progesterone Receptor(PR), Human Epidermal Growth Factor Receptor(HER2/neu) • These receptors are present partially or absent totally called TRIPLE NEGATIVE or BASAL-LIKE • Presence of these receptors determine the chemotherapy and the prognosis
  • 11. ESTROGEN RECEPTORS • Depend on estrogen hormone to grow • 2 different forms – α and β , each encoded by a separate gene • ERα – Endometrium, Breast Cancer cells, Ovarian stromal cells, Hypothalamus and afferent ducts in males • ERβ – Ovarian granulosa cells, Kidney, Brain, Bone, Heart, Lungs, Intestinal mucosa and Prostate • As per visualization research, small fraction of ERs reside in cytoplasm, most in the nucleus
  • 12. PROGESTERONE RECEPTORS •The progesterone receptor (PR, also known as NR3C3 or nuclear receptor subfamily 3, group C, member 3), is a protein found inside cells. • Activated by the steroid hormone progesterone • In humans, PR is encoded by a single PGR gene residing on chromosome 11q22 • Has 2 main forms, A and B, that differ in their molecular weight
  • 13. HER2 STATUS • HER2 positive: Cancers that have too much HER2 protein or extra copies of the HER2 gene. Respond to drugs that target HER2 • HER2 negative: Cancers that don’t have excess HER2. Do not respond to treatment by drugs that target HER2
  • 14. TRIPLE POSITIVE • This term is used to describe cancers that are ER-positive, PR-positive, and have too much HER2. These cancers can be treated with hormone drugs as well as drugs that target HER2. • The medication tamoxifen helps stop cancer from coming back by blocking hormone receptors, preventing hormones from binding to them. It’s sometimes taken for upto 5 years after initial treatment for breast cancer. • A class of medicine called aromatase inhibitors actually stops estrogen production. These include anastrozole, exemestane, and letrozole. They’re only used in women who’ve already gone through menopause.
  • 15. TRIPLE NEGATIVE • If the breast cancer cells don’t have estrogen or progesterone receptors and don’t have too much HER2, they are called triple-negative. • Tend to occur more often in younger women • Tend to grow and spread more quickly than most other types of breast cancer. • Hormone therapy or drugs that target HER2 are not helpful in treating these cancers.
  • 16. MOLECULAR SUBTYPE • Newer approaches look at ER, PR, HER2 together, along with the tumor grade, to categorize breast cancer into several conceptual molecular classes that have different prognoses and may have different responses to specific therapies. • DNA microarrays have assisted this approach.
  • 17. • Proposed molecular subtypes include:  Basal-like: ER-, PR- and HER2-; triple negative breast cancer (TNBC) Most BRCA1 breast cancers are basal-like  Luminal A: ER+ and low grade  Luminal B: ER+ but often high grade  Luminal ER-/AR+: Recently identified androgen responsive subtype which may respond to antihormonal treatment with bicalutamide  Normal Breast like  ERBB2/HER2+: Has amplified HER2/neu  Claudin-low: A more recently described class; often triple-negative, but distinct in that there is low expression of cell-cell junction proteins including E-cadherin
  • 18. AXILLARY LYMPH NODE DISSECTION • Approximately 30% of patients with clinically non- palpable lymph nodes have positive lymph nodes in ALND specimen • The presence and number of lymph nodes involved affect staging, management and prognosis • Precursor of ALND is SENTINEL LYMPH NODE BIOPSY
  • 19. PRINCIPLES OF AXILLARY DISSECTION It is removal of different levels of axillary lymph nodes with axillary fat and fascia WHY AXILLARY DISSECTION IS DONE? WHICH LEVELS? TECHNICAL PRINCIPLES • For staging • Level I – 60% • Any incision but caudal hair- line is preferred • To assess the prognosis – number of nodes/size of nodule • Level I,II – 20-25% • Level I,II,III – 15-20% • Nerve to serratus anterior should be safeguarded • As a treatment – regional control of the disease • Medial & lateral pectoral nerves should be retained when dissection is done with mastectomy • To plan the adjuvant therapy – irradiation/chemo/hormone •Level I and II dissection Low dissection has less chances of lymphoedema • Drain should be kept • All lymph nodes should be labelled and sent for HPE. Usually 20-32 nodes are present in axilla. Minimum of 10 nodes should be dissected. Fat dissolving agents used for node identification