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ESPAOLA, Mayreen M Medical Therapeutics
3A 23 July 2010
BREAST CANCER
INTRODUCTION
Carcinoma of the breast is the most common non-skin malignancy in women. A woman who
lives to age 90 has a one in eight chance of developing breast cancer. Needless to say, it is the leading
cause of cancer death among women.
Over the last two decades, breast cancer research has led to extraordinary progress in our
understanding of the disease, resulting in more efficient and less toxic treatments. Increased public
awareness and improved screening have led to earlier diagnosis at stages amenable to complete surgical
resection and curative therapies. Consequently, survival rates for breast cancer have improved
significantly, particularly in younger women.
Breast cancer incidence rates have risen globally, with the highest rates occurring in the
westernized countries. Reasons for this trend include change in reproductive patterns, increased
screening, dietary changes, and decreased activity. Although breast cancer incidence is on the rise
globally, breast cancer mortality has been decreasing, especially in industrialized countries.
Nevertheless, as the demographic bulge of the baby boomers continues to grow older, the number of
women with breast cancer is expected to increase by a third over the next 20 years.
The lifetime risk of acquiring breast cancer in all women, regardless of race, location, and age, is
approximately 12.7%. Asian and Pacific Islander women have an incidence rate which increases at 1.5%
per year or 89 out of 100 000 yearly. In the Philippines, 26 females out of 100 females and 1 male for
every 105 males may be diagnosed with breast cancer. Since the 1980s, breast cancer ranks first among
the top leading cancers afflicting women in the Philippines and ranks second to lung cancer if both sexes
are considered. Its incidence starts to peak at the age of 30 in women. In 2004, breast cancer cases
in the Philippines exceeded lung cancer by 685 cases for both sexes.
Recently, more women are presenting with a bilateral disease at an early age of 30-
40. Generally, the disease is still being diagnosed late in its course. Hence, the survival
rate of breast cancer in the Philippines is below 50%. Making the situation more difficult, an
estimated 70% of breast cancer patients in the Philippines are indigents. In addition, the
Philippines has the highest prevalence of breast cancer in all of Asia. Although the trend may
seem progressively alarming, the incidence rate is still relatively lower than the incidence rate among
female Westerners.
Since 1990, breast cancer death rates have steadily decreased. Approximately 40,610 breast
cancer deaths (40,170 women, 440 men) were projected in 2009. The largest decrease in mortality has
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been seen in women younger than 50 years (3.3% per year) versus those aged 50 years and older (2.0%
per year). This particular trend of breast cancer death rates is perceived as a representation of the
progress in both early detection and improved treatment modalities.
Risk factors which are highly sensationalized whenever dealing with carcinoma are, of course,
important points of discussion. In the case of carcinoma of the breast, the most important risk is gender.
Only 1% of breast cancer cases occur in men. Breast cancer is a predominantly female disease and will
continue to challenge women health care systems around the globe for the coming decades.
The Breast Cancer Risk Assessment Tool incorporates additional risk factors which can enable
physicians in accurately gauging the absolute risk of an individual woman developing invasive cancer
within the next 5 years or over a lifetime:
Age. The incidence rises throughout a womans lifetime, peaking at the age of 75-80 years, and
then, declining from thereafter. Sixty-one is the average age at diagnosis for white women, 56 for
Hispanic women, and 46 for African American women. In the Philippines, many breast cancers are
found among 35-50-year-old women. Breast cancer is very rare before the age of 25.
Age at Menarche. Women who reached menarche younger than 11 years have a 20% increased
risk of having this type of cancer compared with those who reached menarche older than 14 years. Late
menopause increases risk as well.
Age at First Live Birth. Women who experience a first full-term pregnancy at ages younger than
20 years have half the risk of nulliparous women or those who have had their first live birth at age 35.
This is supported by a hypothesis which explains that pregnancy enables terminal differentiation of milk-
producing luminal cells, eradicating their potential to be included in a possible pool of cancer precursors.
Atypical Hyperplasia. Women who have had previous breast biopsies especially if there is
evident atypical hyperplasia are at risk for having these histological changes as precursors for the
development of an invasive carcinoma.
First-Degree Relative with Breast Cancer.The number of affected first-degree relatives like a
mother, a sister, or a daughter is in direct proportion with the risk of breast cancer. This is especially
true in cases wherein the cancer occurred at a very young age. This is not a particularly strong risk
factor since only 13% of women with breast cancer have one affected relative and only 1% have two.
Over 87% of women with a family history will not get afflicted with breast cancer.
Estrogen Exposure.Postmenopausal hormone replacement therapy increases the risk of breast
cancer 1.2-1.7 fold. This increases even further upon the addition of progesterone. Reducing
endogenous estrogens via oophorectomy decreases the risk of acquiring breast cancer by up to 75%.
Drugs which block estrogenic effects as well as those which block estrogen formation offer lowered risks
for developing estrogen receptor (ER)-positive breast carcinoma.
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Other risk factors include: breast density, radiation exposure, carcinoma of the contralateral
breast or endometrium, geographic location, diet, obesity, exercise, environmental toxins, and tobacco.
Breastfeeding offers a reduction of breast cancer risk when prolonged. Lactation suppresses
ovulation and may trigger terminal differentiation of luminal cells. With this, breastfeeding should be
highly recommended to women of lactating age. It should be emphasized repeatedly that breastfeeding
benefits not only the infant but the nursing mother just as well.
Risk Factor Estimated
Relative Risk
Advanced Age >4
Family History
Two or more relatives (mother, sister)
One first-degree relative
Family history of ovarian cancer in women 5
>2
>2
Personal History
Personal History
Positive BRCA1/BRCA2 mutation
Breast biopsy with atypical hyperplasia
Breast biopsy with LCIS or DCIS
3-4
>4
4-5
8-10
Reproductive History
Early age at menarche (30y)/nulliparity
2
1.5-2
2
Use of combined estrogen/progesterone HRT 1.5-2
Current or recent use of oral contraceptives 1.25
Lifestyle Factors
Adult weight gain
Sedentary lifestyle
Alcohol consumption
1.5-2
1.3-1.5
1.5
ETIOLOGY AND PATHOGENESIS
Breast cancer is a malignant proliferation of epithelial cells lining the ducts or lobules of thebreast. It has been widely accepted for some time that breast cancer is a heterogeneous disease with a
wide array of histologic appearances. It has been confirmed that there are many types of cancer but
also show that most carcinomas cluster into several major groups with important biologic and clinical
differences. The majority of carcinomas are ER-positive and are characterized by a gene signature
dominated by the dozens of genes under the control of estrogen. Among the ER-negative tumors, many
fall into a distinctive basal-like group. The basal-like group has the characteristic of notable absence of
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estrogen and progesterone recepters and lack of overexpression of HER2/neuprotein. Indeed, ER-
positive and ER-negative carcinomas have always shown striking differences with regard to patient
characteristics, pathologic features, treatment response, and outcome.
Hormonal and genetic factors are the major risks for the development of breast cancer. Those
related with hormonal factors may be classified as sporadic cases while those related with genetic
factors may be classified as hereditary cases.
Hereditary Breast Cancer
Approximately 12% of breast cancer cases are caused by inheritance of some form of
susceptible gene/s. Mutations in BRCA1 and BRCA2 account for the majority of cancers attributable to
single mutations and about 3% of all breast cancers. Mutations in BRCA1 markedly increase the risk of
developing ovarian carcinoma in addition to breast cancer while BRCA2 mutations confers a smaller risk
for ovarian carcinoma but is most frequently related with male breast cancer.
BRCA1-associated breast cancers are commonly poorly differentiated, have a syncytial growth
pattern with pushing margins, have a lymphocytic response, and do not express hormone receptors or
overexpress them resulting in the so-called triple negative phenotype.This phenotype simply means that
there are breast cancers which do not express estrogen and progesterone receptors, and lack
overexpression of the HER2/neu protein. They are categorized as basal-like. These cancers are also
related with loss of the inactive X chromosome and reduplication of the active X which renders the Barr
body absent.
BRCA2-associated breast cancers are relatively poorly differentiated as well. Only, this type of
breast cancers more often expresses hormone receptors.
Other gene mutations associated with breast cancer are germline mutations in p53 (Li-Fraumeni
syndrome), germline mutations in CHEK2 (Li-Fraumeni variant syndrome), PTEN (Cowden syndrome),
LKBI/STK11 (Peutz-Jeghers syndrome), and ATM (ataxia telangiactasia). Germline mutations in p53 are
the most common mutations among sporadic cases. CHEK2 mutations, on the other hand, may increase
risk for breast cancer after radiation exporsure. These are all tumor suppressor genes which, along the
progress of carcinogenesis, have lost their normal function.
Sporadic Breast Cancer
Hormone exposure is the major risk factor for sporadic breast cancer cases. This is in relation
with several patient aspects: age, gender, age at menarche and menopause, reproductive history,
breastfeeding, and exogenous estrogens. Most of this type of breast cancer are ER-positive and occur
postmenopausally.
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Hormonal exposure increases the number of potential target cells by stimulating breast growth
during puberty, menstrual cycles, and pregnancy. It exposes cells for DNA damage via driving cycles of
proliferation. It can nourish premalignant or malignant cells once they appear. They can disrupt growth
of normal epithelium and stromal cells and allow for tumor development instead.
Carcinogenesis
Populations of cells that harbour some of the genetic and epigenetic changes required for
carcinogenesis give rise to morphologically recognizable breast lesions.These lesions are usually
proliferative changes which may be caused by loss of growth-inhibiting signals, aberrant changes in pro-
growth signals, or decreased apoptosis. Most early lesions express increased expression of hormone
receptors and abnormal proliferation regulation. Loss of heterozygosity is almost universally present in
carcinoma in situ. Profound DNA instability as represented by aneuploidy manifesting as nuclear
enlargement, irregularity, and hyperchromasia is seen only in high-grade ductal carcinoma in situ and
some invasive types. Malignant clones can sometimes achieve immortality and promote neo-
angiogenesis.
The stem cell hypothesis is a credible start in knowing how to determine the cell of origin of
breast cancer. This hypothesis reveals that malignant changes occur in a stem cell population that has
unique properties which define them from more differentiated cells. Although majority of tumor cells
would consist of non-stem cell progeny, only the malignant stem cells would contribute to tumor
progression or recurrence.
The ER-expressing luminal cell is the most likely type of cell origin for most carcinomas since
most are ER-positive. ER-negative cancers, on the other hand, may arise from ER-negative myoepithelial
cells and not luminal cells.
The transition of carcinoma in situ into an invasive one marks the final procedure for
carcinogenesis. It is the most crucial step yet it is not fully understood. Genetic markers specific for
invasive types have never been unearthed.The normal development of the breast in the human lifetime
is of special interest in the onset of carcinogenesis. Luminal, myoepithelial, and stromal cells are in a
complex interplay to render normal structure and function of the breast. Events involved in normal
formation of new ductal branch points and lobules during puberty and pregnancy are the events actually
repeated during carcinogenesis. These events include abrogation of the basement membrane,
increased proliferation, escape form growth inhibition, angiogenesis, and stromal invasion. In the case
of pregnancy, remodelling of the breast during and shortly after pregnancy involves inflammatory and
wound healing-like tissue reactions which give rise to an opportunity for the development of cancer.
Such changes could facilitate this final part of carcinogenesis.
THE CASE
General Data
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The patient is A.M., a 48-year-old Filipino female residing in Batangas City, Batangas. She is a
Roman Catholic and is presently an employee of the Batangas City government.
Chief Complaint
Right breast lump
History of Present Illness
Five years prior to admission, the patient first noticed changes in the contour of her right breast.
She had lumpectomy which revealed fibrocystic change in the right breast but no malignancy was noted.
Four years PTA,the patient followed up on unspecified breast exams and results reveal no
recurrence of the condition or malignancy. She had another unspecified breast exam,2 years PTA, and
this revealed no recurrence of the condition or malignancy.
Ten months PTA, the patient noticed a thickening and hardness in her right breast. She
described it as bumpy and irregularly-shaped beneath the areola. Breast ultrasound was done and
revealed multiple cystic masses of varying sizes noted in the retroareolar, periareolar, and inner zones
with the largest mass measuring 3.38 cm x 2.55 cm x 2.14 cm (LxWxAP). A fine-needle aspiration biopsy
(FNAB) was done but the specimen was too bloody that malignancy cannot be identified.
A month PTA, the patient described the mass as firm and growing and went to get advice
regarding options for operation. FNAB confirmed the diagnosis.
Past Medical History
Adult Illness. Medical: The patient already had urinary tract infection. Surgical: None
Health Maintenance. The patient regularly takes Moriami Forte, Fern Cee, Vitamin E 400 IU, and
Calcium.
Obstetrics-Gynecological History
The patient is G3P3 (3-0-0-3). All sons were delivered normally and were born in the hospital.
There were no complications in all pregnancies. She had her first live-birth delivery at the age of 23.
Menarche was at the age of 11 while Menopause was at 48 y/o with LMP during the second
cycle of her chemotherapy on 04 September 2008. The patient recalled using at least 3 napkins per day.
Menstrual period lasted for 7 days without accompanying signs and symptoms.
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DOB Place Age Sex Attendant
1. 24 June 1983 Hospital 27 M MD
2. 25 April 1988 Hospital 22 M MD
3. 05 January 1995 Hospital 15 M MD
Family History
The patients father has a heart disease while her mother and her brother both have diabetes.
There are no first-degree relatives who have breast cancer or any other type of cancer for that matter.
Personal and Social History
The patient is a local government employee. She is married and has three sons. She never
smokes. She does not take any alcoholic beverages. She has no history of illicit drug abuse.
Physical Examination
Head & Neck: HEENT normal. No palpable nodes or thyroid. Trachea is in the midline.
Respiratory: Clear to percussion and auscultation in all fields. Cardiovascular: Normal PMI. S1 & S2 are
normal. No murmurs or extra sounds. Peripheral pulses are present and equal bilaterally Breasts: There
is a firm, non-tender mass on the lower medial quadrant of the right breast. It has a measurement of 7
cm x 7 cm. There is no gross inflammatory response. There is no nipple discharge. Left breast is normal.
There are no axillary or supraclavicular nodes palpable bilaterally. Abdomen: Scaphoid, soft. No liver,
spleen, or kidneys palpable. No masses or tenderness. Bowel sounds normoactive. Pelvic Exam:
Normal. CNS: Grossly normal. Deep tendon reflexes present and equal bilaterally.
Course in the Wards
Fasting blood sugar, creatinine, sodium, and potassium were examined. The following results
were obtained:
TEST RESULT NORMAL RANGE
Fasting Blood Sugar 6.05 3.60-5.80 mmol/L
Creatinine 61.88 62.00-106.00 mmol/L
Sodium 139.00 137.00-145.00 mmol/L
Potassium 4.20 3.60-5.00 mmol/L
Complete blood count was also done with the following results:
TEST RESULT NORMAL RANGE
CBC
White Blood Cells 6.90 5-11 x 103/uL
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Red Blood CellsHemoglobinHematocritMCVMCHMCHCPlatelet
3.7710.332.385.727.331.9
256.0
4.2-5.4 x 106/uL12.0-16.0 g/dL
38-47%80-100 fL27-33 pg
31-36 g/dL150-400 x 103/uL
Differential Count:
NeutrophilLymphocyteMonocyteEosinophilsBasophilsBlastBand/Stabs
56.033.05.06.00.0
55-77%27-33%0-12%0-7%1-5%
Diagnosis
Correct staging of breast cancer patients is of extraordinary importance. It permits accurate
prognosis, and in many cases, is the basis of therapeutic decision-making. The TNM classification should
be used in accordance with the histologic classification in order to come up with a tailored management
for a particular cancer patient.
The TNM Classification
DISTANT METASTASIS (M)
M0 No distant metastasis
M1 Distant metastasis which includesspread to ipsilateral supraclavicular
nodes
Tumor Histological Grade (WHO Classification Standard)
GRADE 1 2 3
Duct formation >75% for 1min 10%~75% for2mins
2cm but 5cm
T3 Tumor>5cm
T4 Extension to chest wall, inflammation,satellite lesions, ulcerations
REGIONAL LYMPH NODES (N)
N0 No regional lymph nodes
N1 Metastasis to movable ipsilateralnodes
N2 Metastasis to matted or fixedipsilateral nodes
N3 Metastasis to ipsilateral internalmammary nodes
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same as a sub degree ofchange of 2points
significantchanges of 3points
Mitotic number(x400)
0~5/10HPF to 1pm.
6~10/10HPF for2 mins
>11/10HPF to 3points
The patient was diagnosed with invasive ductal carcinoma Stage I,
Grade 3. After the modified radical mastectomy was done,
immunohistochemistry tests were administered to determine
the following: (1) presence of estrogen and progesterone
receptors, (2) overexpression of HER2/neu protein, and (3)
presence of p53. All components mentioned above were absent
as revealed by the immunohistochemistry reports. The patient
reported no procedure with regards to radiation therapy after
her radical mastectomy. Mastectomy without further irradiation
was based on results from FNAB. Fine-needle aspiration cytology
may be sufficient enough to confirm malignancy.
TREATMENT
The diagnosis of invasive ductal carcinoma Stage 1, Grade 3 calls for immediate surgery of the
tumor. Breast-conserving treatments results in a survival that is as good as that after extensive
procedure like mastectomy or modified radical mastectomy with or without further irradiation. While it
is associated with a possibility of recurrence of the breast, 10-year survival is, at least, as good as that
after more radical surgery. Nevertheless, a great many women still undergo mastectomy who could
safely avoid this procedure. This could be because they fall under certain exclusions from breast-
conserving surgery: (1) it is not suitable for tumors>5 cm, (2) it is not suitable for tumor involving the
nipple areola complex, (3) it is not for tumors with extensive intraductal disease involving multiple
breast quadrants (4) it is not for women with history of collagen-vascular disease, and (4) it is not for
women who do not have motivation for breast conservation or do not have access to radiation therapy.
The patient in this case has an invasive ductal carcinoma which largely involves the nipple areola
complex. This is why, as primary treatment, she chose to undergo modified radical mastectomy of the
right breast. Radiation therapy may be indicated postmastectomy. But it is more regularly employed
after a breast-conservation surgery. In fact, for women with node-negative disease who have
undergone mastectomy like the patient, there was not a statistically significant reduction in 15-year
breast cancer mortality if further irradiation were to follow.
STAGE GROUPING
T N M
Stage 0 IS 0 0
Stage I 1 0 0
Stage IIA 0 1 0
1 1 0
2 0 0
Stage IIB 2 1 0
3 0 0
Stage IIIA 0 2 0
1 2 0
2 2 0
3 1,2 0
Stage IIIB 4 Any 0
Any 3 0
Stage IV Any Any 1
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Adjuvant systemic therapy can be immediately administered postmastectomy. This form of
therapy improves survival.However,estrogen receptor status of the carcinoma must be determined first.
Tamoxifen, a steroid hormonal chemotherapeutic drug, for example, is restricted to women with ER-
positive or ER-unknown breast tumors. The patient is ER-negative which is why Tamoxifen was no
longer administered. In addition, it is not effective in a high-risk node-negative disease like the case.
Risk Categories for Women with Node-Negative Breast Cancer
Low risk
(has all listed factors)Intermediate risk
(risk classified between theother categories)
High risk
(has at least one listedfactor)
Tumor size 1 cm 1-2 cm >2 com
ER- or PR- status + + -
Tumor grade Grade 1 Grade 1-2 Grade 2-3
Aromatase inhibitors like Anastrozole and Letrozole, can also be prescribed for survival
advantage. These have become first-line adjuvant therapy for postmenopausal women. However,
tamoxifen remains a more reasonable alternative. And since the use of aromatase inhibitors requires
hormone-receptor positive cancers, it is still not applicable to the patient. The same is true with
microtubule inhibitors which are essentially cytotoxic to cancer cells. Microtubule inhibitors like
Paclitaxel and Docitaxel both require hormone-receptor positive cancers. Both aromatase and
microtubule inhibitors are for metastatic cases which was not appreciated in the case. Monoclonal
antibodies like Trastuzumab, on the other hand, require overexpression of HER2/neu protein which was
also absent from the cancer discussed in the case.
The most plausible next step for the patient after having modified radical mastectomy is
chemotherapy. In women below age 50, chemotherapy, particularly polychemotherapy or multidrug
therapy may reduce the annual risk of disease relapse and death from breast cancer by 37% and 30%,
respectively. The 2005 Early Breast Cancer Trialists Collaborative Group has made numerous clinical
trials which attempt to determine which is superior between anthracycline-based regimens and
cyclophosphamide, methotrexate, fluorouracil (CMF)-type regimen alone. The usual anthracycline-
based regimens are mostly 6 months of fluorouracil, doxorubicin, cyclophosphamide (FAC) or
fluorouracil, epirubicin, cyclophosphamide (FEC). Compared to CMF, anthracycline-based regimens
were associated with a modest but a statistically significant 11% proportional reduction in the annual
risk of disease recurrence, and a 16% reduction in the annual risk of death. The absolute difference in
outcomes between anthracycline-based and CMF-type chemotherapy was about 3% at 5 years and 4%at 10 years. For the case, anthracycline-based regimens are hardly applicable. FAC as well as FEC
regimens are directed at cancers which overexpress the protein HER2/neu. The patient is negative for
HER2/neu overexpression as revealed by her immunohistochemistry report.
The CMF-type regimens, on the other hand, are more tailored in addressing the cancer of the
patient. CMF or the Bonadonna regimen can be used in both metastatic and non-metastatic cancer.
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And when it comes to node-negative breast cancer with an immunohistochemistry reading of negative
estrogen and progesterone receptors as well as absence of HER2/neu amplification, CMF regimen leads
the pack.
CMF Regimen
Cyclophosphamide is an alkylating agent which directs its action towards the DNA. It does not
discriminate between the cycling and resting cells and is actually most toxic for rapidly dividing cells. It
is mutagenic and carcinogenic. It is biotransformed by P450 cytochrome in the liver. Cyclophosphamide
actually has the strongest tendency to cause relative myelosuppression compared to the other drugs
included in the regimen. Other adverse reactions include: nausea, vomiting, alopecia, hemorrhagic
cystitis, sterility, and immunosuppression. Cyclophosphamide needs an assurance of adequate
hydration and diuresis during therapy. It is contraindicated for those with severe bone marrow
depression, and pregnancy and lactation.
Methotrexate is an antimetabolite which interferes with the availability of normal thymidine
nucleotide precursors. It is S-phase specific. It deprives cells of folate coenzymes needed for
biosynthesis. Although nucleotides adenine and guanine and amino acids methionine and serine
depend on folate coenzymes needed for their synthesis, the most prominent effect is on thymidine. It
becomes depressed which would result in depressed DNA, RNA, and protein synthesis. Administration
of leucovorin which bypasses the blocked enzyme replenishes the folate pool. Adverse reactions include
hematolic and GI effects, dermatologic reactions, renal dysfunction, allergic reactions, and ocular side
effects. It is contraindicated for those with serious anemia, leukopenia, thrombocytopenia, renal or
hepatic impairment, and pregnancy and lactation.
Fluorouracil is another antimetabolite which induces thymidine-less cell death among rapidly
dividing cells. Its anticancer effect takes place in S phase of the cell cycle. It is employed primarily in the
treatment of slowly growing solid tumors. It has to be administered intravenously because it is severely
toxic to the GI tract. Other adverse reactions are: hematotoxicity, leukopenia, thrombocytopenia,
stomatitis, anorexia, nausea, vomiting, diarrhea, maculopapular rash, alopecia, cerebellar dysfunction,
eye toxicity, and ECG changes. It is contraindicated for those with depressed bone marrow function,
poor nutritional state, pregnancy and lactation.
Safety Affordability Necessity Efficacy
Cyclophosphamide ++ ++ ++++ ++
Methotrexate +++ + ++++ ++
5-Fluorouracil +++ +++ ++++ ++
Methotrexate and 5-fluorouracil are safer drugs than cyclophosphamide because the latter has
the higher tendency to cause bone marrow depression compared to the former drugs. When it comes
to affordability, methotrexate emerges as the most expensive with a patient having to spend P5220.00
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for the duration of the 6 cycles. All drugs are essential part of the combination therapy which give all
rate of 4 +s. Efficacy of each drug may not be optimal if each would be used as a monotherapy.
Multidrug Therapy
When it comes to an invasive breast tumor with no involvement of axillary nodes and no distant
metastasis, breast-conserving surgery with consequent irradiation or mastectomy is considered the
primary treatment. After these procedures, it is most appropriate to follow up with chemotherapy for a
better survival and mortality rate for the patient. There are a lot of polychemotherapy which targets
this stage of invasive carcinoma (Stage I). But the most applicable are regimens which are anthracycline-
based and those which are of CMF-type. Anthracycline-based regimens highly depend on the
overamplification of HER2/neu protein. This specificity is not one with the case since the patient is
HER2/neu negative. Simply put, CMF-type regimen is the most appropriate.
Clinical trials show that CMF-type regimens are most applicable for Stage I breast carcinoma
which are estrogen-receptor and progesterone-receptor negative as well as p53 negative.
Overamplification of HER2/neu, which is absent from the case, is much needed to be able to utilize an
anthracycline-based therapy.
A clinical study involves the comparison of CMF regimen and a simple MF regimen among
female breast cancer patients with no axillary node involvement and no estrogen receptors. CMF
regimen gave recurrence-free survival benefit and most especially, overall survival benefit. Febrile
neutropenia was more frequent among CMF-treated patients. Menopausal women experience more
toxic effects in using the CMF regimen. Thus, methrotrexate followed by 5-fluoruracil is a reasonable
substitute for CMF for older women.
Safety Affordability Necessity Efficacy
CMF ++ ++ ++++ ++++
MF +++ ++++ +++ +++
The MF regimen seems safer because it does not include cyclophosphamide which has the
highest tendency among the 3 drugs to cause myelosuppression. Also, as shown in the previous study,
febrile neutropenia developed among CMF-treated patients. The MF regimen is more affordable
because of the absence of cyclophosphamide. For the 6 cycles, Ledoxan would cost P3787.80. Use of
the MF regimen requires no spending of such additional amount. The previous study revealed that CMF
has recurrence-free survival benefit as well as overall survival benefit. This means that although CMF
can be considered a regimen with risks, it is still the one that can render survival advantage and prolong
survival postmastectomy or after breast-conserving energy. The CMF regimen is chosen as the drug of
choice while the MF regimen is chosen as an alternative.
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PRESCRIPTIONS
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