c






The main goal of surgical treatment is to eradicate the local presence of the cancer. The
procedures most often used for the local management of invasive breast cancer are mastectomy
with or without reconstruction and breast-conserving surgery combined with radiation therapy.
These procedures are described below. For patients who undergo total mastectomy for the
treatment of DCIS or as prophylactic surgery for the treatment for LCIS, the nursing care is
similar to that of a modified radical mastectomy (described later in the text). However, total
mastectomy does not involve the removal of axillary lymph nodes; therefore, mobility of the arm
on the affected side is regained much quicker, and there is no risk for lymphedema. Women still
face the same psychosocial issues involving the diagnosis of cancer and the loss of the breast,
and the nurse needs to address these in a similar manner.

  
     is removal of the entire breast
tissue, along with axillary lymph nodes. The pectoralis major and pectoralis minor muscles
remain intact. Before surgery, the surgeon plans an incision that will providemaximum
opportunity to remove the tumor and the affected nodes. At the same time, efforts are made to
avoid a scar that will be visible and restrictive. An objective of surgical treatment is to maintain
or restore normal function to the hand, arm, and shoulder girdle on the affected side. Skin flaps
and tissue are handled with great care to ensure proper viability, hemostasis, and drainage. If
reconstructive surgery is planned, a consultation is made with a plastic surgeon before the
mastectomy is performed. After the tumor is removed, bleeding points are ligated and the skin is
closed over the chest wall. Skin grafting is performed if the skin flaps are too small to close the
wound. A nonadherent dressing (Adaptic) may be applied and covered by a pressure dressing.
Two drainage tubes may be placed in the axilla and beneath the superior skin flap, and portable
suction devices may be used; these remove the blood and lymph fluid that collect after surgery.
The dressing may be held in place by wide elastic bandages or a surgical bra.

cBreast-conserving surgery consists of lumpectomy, wide excision,
partial or segmental mastectomy, or quadrantectomy (resection of the involved breast quadrant)
and removal of the axillary nodes (axillary lymph node dissection) for tumors with an invasive
component, followed by a course of radiation therapy to treat residual, microscopic disease.
The goal of breast conservation is to remove the tumor completely with clear margins while
achieving an acceptable cosmeticresult. The axillary lymph nodes are also removed through a
separate semicircular incision under the hair-bearing portion of the axilla. A drain is inserted into
the axilla through a separate stab wound to remove blood and lymph fluid. A dressing is applied
over the breast and under the arm and is secured with wide elastic bandages or a surgical bra.
Survival rates after breast-conserving surgery are equivalent to those after modified radical
mastectomy. The risk for local recurrence, however, is greater, at 1% per year after surgery
(Winchester & Cox, 1998). If the patient experiences a local recurrence, standard treatment is a
completion or salvage mastectomy, in which the rest of the breast tissue is removed. Survival
rates after this procedure are equivalent to those after mastectomy, but because the skin has been
irradiated, the choices for reconstruction remain limited, and the woman should be informed of
this possibility at the time of diagnosis and when considering her treatment options.


! c
Drugs used after and in addition to surgery are called adjuvant therapy. Chemotherapy prior to
surgery is called neo-adjuvant therapy. There are currently 3 main groups of medications used
for adjuvant breast cancer treatment:
y? Hormone Blocking Therapy
y? Chemotherapy
y? Vonoclonal Antibodies
One or all of these groups can be used.
þ"#$% Some breast cancers require estrogen to continue growing. They
can be identified by the presence of estrogen receptors (ER+) and progesterone receptors (PR+)
on their surface (sometimes referred to together as hormone receptors). These ER+ cancers can
be treated with drugs that either block the receptors, e.g. tamoxifen, or alternatively block the
production of estrogen with an aromatase inhibitor, e.g. anastrozole (Arimidex)
or letrozole (Femara). Aromatase inhibitors, however, are only suitable for post-menopausal
patients.
##$: Predominately used for stage 2-4 disease, being particularly beneficial in
estrogen receptor-negative (ER-) disease. They are given in combinations, usually for 3±6
months. One of the most common treatments is cyclophosphamide plus doxorubicin
(Adriamycin), known as AC; these drugs damage DNA in the cancer, but also in fast-growing
normal cells where they cause serious side effects. Damage to the heart muscle is the most
dangerous complication of doxorubicin. Sometimes a taxane drug, such as docetaxel, is added,
and the regime is then known as CAT; taxane attacks the microtubules in cancer cells. Another
common treatment, which produces equivalent results, is cyclophosphamide, methotrexate, and
fluorouracil (CVF). (Chemotherapy can literally refer to any drug, but it is usually used to refer
to traditional non-hormone treatments for cancer.)
 & % A relatively recent development in HER2+ breast cancer treatment.
Approximately 15-20 percent of breast cancers have an amplification of the þ
 gene or
overexpression of its protein product.This receptor is normally stimulated by a growth factor
which causes the cell to divide; in the absence of the growth factor, the cell will normally stop
growing. Overexpression of this receptor in breast cancer is associated with increased disease
recurrence and worse prognosis. Trastuzumab (Herceptin), a monoclonal antibody to HER2, has
improved the 5 year disease free survival of stage 1±3 HER2+ breast cancers to about 87%
(overall survival 95%).Trastuzumab, however, is expensive, and approx 2% of patients suffer
significant heart damage; it is otherwise well tolerated, with far milder side effects than
conventional chemotherapy.Other monoclonal antibodies are also undergoing clinical trials.
Finally, a recent article has claimed that Aspirin may reduce mortality from breast cancer.

 Radiotherapy is given after surgery to the region of the tumor bed, to destroy
microscopic tumors that may have escaped surgery. It may also have a beneficial effect on
tumour microenvironment.Radiation therapy can be delivered as external beam radiotherapy or
as brachytherapy (internal radiotherapy). Conventionally radiotherapy is given Ô
 the
operation for breast cancer. Radiation can also be given, arguably more efficiently, at the time of
operation on the breast cancer- intraoperatively. The largest randomised trial to test this approach
was the TARGIT-A Trialwhich found that targeted intraoperative radiotherapy was equally
effective at 4-years as the usual several weeks' of whole breast external beam
radiotherapy.Radiation can reduce the risk of recurrence by 50-66% (1/2 - 2/3rds reduction of
risk) when delivered in the correct doseand is considered essential when breast cancer is treated
by removing only the lump.
 #$Harnessing Infection to Fight Cancer by activating the immune
system (experimental). Conventional wisdom long held that the human immune system was no
match for cancer. Born of native cells, the logic went, cancer fooled the immune system into
concluding it was harmless. Thus protected from attack, cancer easily thrived until its host died.
A deeper understanding of our biological defenses has changed that. The human immune system
does battle cancer. But we could better optimize our defenses to fend off malignant disease.
That¶s clear from cancer treatments attempted in New York City and Germany as early as the
19th century. Those experiments and other undervalued evidence from the medical literature
suggest that acute infection²in contrast to chronic infection, which sometimes causes cancer²
can help a body fight tumors.
   #$ (Planned trial). A new clinical trial is designed around the use of QI's
proprietary dendritic cell therapy, which employs oncofetal antigen ("OFA") to recruit the
patient's own immune system to target and attack the cancer cells with the intent to improve
patient survivability and quality of life. Each patient will receive three monthly injections of the
patient's own dendritic cells that have been sensitized to OFA. It is anticipated that once the
sensitized cells are injected back into the patient, the patient's T-cells will locate the OFA found
on the patient's cancer cells, thereby generating an immune response with the goal of killing the
cancer cells and preventing further spread of the disease.
c'    # $ $ (phase III). Stimuvax is an investigational
therapeutic cancer vaccine designed to induce an immune response to cancer cells that express
V C1, a glycoprotein antigen widely expressed on common cancers. V C1 is over-expressed
on many cancers such as lung cancer, breast cancer, prostate cancer and colorectal cancer.
Stimuvax is thought to work by stimulating the body's immune system to identify and destroy
cancer cells expressing V C1.
Phase IIb study of 171 patients with inoperable stage IIIb NSCLC (lung cancer), in which
Stimuvax showed a trend towards extending median overall survival from 13.3 months for
patients receiving best supportive care (BSC) to 30.6 months for patients receiving Stimuvax
plus BSC.2,3 Reported side effects included mild-to-moderate flu-like symptoms,
gastrointestinal disturbances and mild injection-site reactions.
# #$ Vanipulating the immune system to recognize and eradicate breast
tumor cells is a highly attractive alternative approach to disease management. Active
immunization offers multiple theoretical advantages over all other therapies, including low
toxicity. The sustained antitumor effect due to immunological memory would obviate the
requirement for prolonged, repetitive cycles of therapy.
The objective of chemoimmunotherapy is to amplify natural pre-existing T cell responses
specific for any known or unknown tumor antigen and to recruit and amplify new tumor-specific
T cell responses resulting from the use of cytotoxic drugs. The direct cytolytic effect of some
cytotoxic drugs, such as paclitaxel, can enhance antigen presentation by inducing tumor cell
apoptosis. This mechanism of therapeutic synergy has been shown with cyclophosphamide,
doxorubicin, or paclitaxel when given with dendritic cell - based vaccines. ntil 9 years ago, it
was thought that the T cell depletion caused by chemotherapy would make immunotherapy
ineffective. However it has now been shown that, on the contrary, the vigorous T cell
repopulation following depletion can be directed against the tumor.
IVP321 induced both a sustained increase in the number and activation of APC (monocytes and
dendritic cells) and an increase in the percentage of NK and long-lived cytotoxic effector-
memory CD8 T cells. Clinical benefit was observed for 90 per cent of patients with only 3
progressors at 6 months. Also, the objective tumor response rate of 50 per cent compared
favorably to the 25 per cent rate reported in the historical control group. This form of chemo-
immunotherapy should be applicable to many chemotherapies.