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FINALS
PRINCIPLES OF
CANCER TREATMENT
Cancer growth
cancer mimics an organ attempting to regulate its
own growth
cancers have not set an appropriate limit on how
much growth should be permitted
NORMAL ORGANS
& CANCERS
PROBLEM
Cells that are reversibly not in cycle are capable
of replenishing tumor cells physically removed
or damaged by radiation and chemotherapy
which includes cancer stem cells
The stem cell fraction may define new targets
for therapies that will retard their ability to reenter the cell cycle.
c. Efforts to treat the tumor and reduce its size can result in an
increase in the growth fraction and an increase in growth
rate . TRUE.
ANSWER: C
Tumor size
increases slowly
goes through an exponential phase
slows again as the tumor reaches the size at
which limitation of nutrients or auto- or host
regulatory influences can occur
Growth rate
TRUE OR FALSE.
Tumors follow a Gompertzian growth curve.
ANSWER: TRUE
IT FOLLOWS A
GOMPERTZIAN GROWTH
CURVE
KILL
10^12 (1 kg).
GUIDING PRINCIPLE
PRIMUM SUCCERRERE
FIRST HASTEN TO HELP
SYSTEMIC
3. CHEMOTHERAPY- INCLUDES
HORMONAL AND MOLECULAR
TARGETED THERAPY
4. BIOLOGIC THERAPY- INCLUDES
IMMUNOTHERAPY & GENE
THERAPY
PRINCIPLES OF
CANCER SURGERY
CANCER PREVENTION
3. The presence of a
developmental anomaly
Prevention/Prophylaxis
Colectomy
the presence of a
developmental anomaly
Colectomy
thyroidectomy
bilateral
mastectomy or
oophorectomy
orchiectomy
Pancolonic involvement w/
ulcerative colitis
familial polyposis
MEN type 2
familial breast or
ovarian cancer syndromes
w/an undescended testis
PROPHYLAXIS
DIAGNOSIS
ANSWER: A
Core-needle biopsy usually obtains considerably less tissue,
but this procedure often provides enough information to
plan a definitive surgical procedure.
If an excisional biopsy cannot be performed, incisional biopsy
is the procedure of second choice. A wedge of tissue is
removed, and an effort is made to include the majority of
the cross- sectional diameter of the tumor in the biopsy to
minimize sampling error.
TREATMENT
4. Benefits of neoadjuvant
chemotherapy
a) Downgrade the tumor. FALSE. ONLY REDUCE THE SIZE NOT
DOWNGRADE.
b) Clinically control undetected metastatic disease. TRUE
c) Both A and B
*After an initial diagnostic biopsy, chemotherapy and/or radiation
therapy is delivered to reduce the size of the tumor and clinically
control undetected metastatic disease. Such therapy is followed
by a surgical procedure to remove residual masses; this is called
neoadjuvant therapy.
c) Patients with colon cancer who have fewer than five liver
metastases restricted to one lobe and no extrahepatic
metastases
ANSWER: C
Surgery may be curative in a subset of patients with
metastatic dis- ease.
Patients with lung metastases from osteosarcoma may
be cured by resection of the lung lesions.
In patients with colon cancer who have fewer than five
liver metastases restricted to one lobe and no
extrahepatic metastases
Hepatic lobectomy may produce long-term disease-free
survival in 25% of selected patients.
ANSWER: A
Surgery can also be associated with systemic antitumor effects. In
the setting of hormonally responsive tumors, oophorectomy
and/or adrenalectomy may eliminate estrogen production, and
orchiectomy may reduce androgen production, hormones that
drive certain breast and all prostate cancers, respectively; both
procedures can have useful effects on metastatic tumor growth.
If resection of the primary lesion takes place in the presence of
metastases, acceleration of metastatic growth has also been
described in certain cases, perhaps based on the removal of a
source of angiogenesis inhibitors and mass-related growth
regulators in the tumor.
ANSWER: B
Lymph node spread may be assessed using the sentinel node
approach, in which the first draining lymph node a spreading
tumor would encounter is defined by injecting a dye or
radioisotope into the tumor site at operation and then resecting
the first node to turn blue or collect label.
SURGERY
Most effective means of treating cancer.
about 40% of cancer patients are cured by surgery.
Unfortunately, a large fraction of patients with solid tumors have
metastatic disease that is not accessible for removal (60%)
Benefits even when the disease is not curable by surgery alone
local control of tumor,
preservation of organ function,
debulking that permits subsequent therapy to work better, and
staging information on extent of involvement
False
In patients with colon cancer who have fewer than five liver
metastases restricted to one lobe and no extrahepatic
metastases, hepatic lobectomy may produce long-term diseasefree survival in 25% of selected patients.
PALLIATION
Palliation
Insertion of central
venous catheters
Caval interruption
Stabilization
Palliation
Cord decompression
Splenectomy
Surgical placement of
appropriate infusion
portals
Correct other
treatment related
toxicities
PRINCIPLES OF
RADIATION THERAPY
26. Radiation:
A. Damage cause is dependent on the formation of radicals.
FALSE. DAMAGE IS DEPENDENT ON OXYGEN
B. Its selectivity for cancer cells may be due to defects in cancer
cells ability in repair defective RNA and other damage. FALSE. IT
IS REPAIR OF DEFECTIVE DNA NOT RNA.
C. A physical form of treatment that damages any tissue in its
path. TRUE.
D. Its selectivity for cancer cells may be due to defects in host
cells ability to repair sublethal RNA and other damage. FALSE. IT
IS THE CANCER CELLS ABILITY TO REPAIR, BUT NOT OF THE
HOST.
Augmentation of oxygen
presence is one basis for
radiation sensitization
Sulfhydryl
compounds
interfere with free radical
generation and may act as
radiation protectors.
Most radiation-induced cell
damage is due to the
formation of hydroxyl radicals
Exponential
component
Sensitive
Resistant
Hematopoietic
Heart
system
Skeletal muscle
Mucosal lining of
Nerves
the intestinal tract
Any bone marrow in
Organs with less
a radiation field will Organs with more
need for cell renewal
be eradicated by
self-renewal as a
*Bone is among the
therapeutic
part of normal
most radioresistant
irradiation.
homeostasis
organ
Acute toxicities
Often these can be alleviated by interruption of treatment:
Mucositis
Skin erythema (ulceration in severe cases)
Bone marrow toxicity
Effect
Can be affected
Threefold increase risk of fatal
myocardial infarction
Other effects/toxicities
Other late vascular effects
Chronic constrictive
pericarditis
Lung fibrosis
Viscus stricture
Spinal cord transection
Radiation enteritis
ANSWER: A
The selectivity of radiation for causing cancer cell
death may be due to defects in a cancer cells ability
to repair sublethal DNA and other damage.
Ionizing radiation causes breaks in DNA and
generates free radicals from cell water that may
damage cell membranes, proteins, and organelles.
Radiation damage is augmented by oxygen; hypoxic
cells are more resistant. Augmentation of oxygen
presence is one basis for radiation sensitization.
ANSWER: C
Radiation effect is influenced by three
determinants:
total absorbed dose (total rad)
number of fraction
time of treatment
RADIATION
QUANTITATED ON THE BASIS OF THE AMOUNT OF RADIATION
ABSORBED IN THE PATIENT; NOT BASED ON THE AMOUNT OF
RADIATION GENERATED BY THE MACHINE.
RAD(RADIATION ABSORBED DOSE)
DEF. 100 ERG OF ENERGY PER GRAM OF TISSUE.
COMPOUNDS THAT
DEPLETE THIOLS
BUTHIONINE
SULFOXIMINE
These are important adjuncts to the local treatment of certain tumors, such as
squamous head and neck, uterine cervix, and rectal cancers.
HYPOXIA-MAJOR FACTOR THAT INTERFERES W/ RADIATION EFFECTS
ANSWER: C
A serious late toxicity is the development of second solid tumors in or
adjacent to the radiation fields. Such tumors can develop in any organ
or tissue and occur at a rate of about 1% per year beginning in the
second decade after treatment. Some organs vary in susceptibility to
radiation carcinogenesis.
False
ANSWER: TRUE
X-rays and gamma rays are the forms of ionizing radiation
most commonly used to treat cancer.
They are both electromagnetic, nonparticulate waves that
cause the ejection of an orbital electron when absorbed.
This orbital electron ejection is called ionization.
X-rays are generated by linear accelerators; gamma rays
are generated from decay of atomic nuclei in radioisotopes
such as cobalt and radium.
These waves behave biologically as packets of energy, called
photons.
POWERPOINT
Electron beams have a very
low tissue penetrance and are
used to treat skin conditions
such as mycosis fungoides
Acute toxicities
Mucositis
skin erythema
(ulceration in severe cases)
bone marrow toxicity
Chronic toxicities
are more serious
Radiation of the head and neck region thyroid
failure.
Cataracts and retinal damage blindness.
Salivary glands stop making saliva dental caries
and poor dentition
Taste and smell can be affected
Mediastinal irradiation 3-fold risk of fatal MI
Often these can be
Other late vascular effects
alleviated by interruption of chronic constrictive pericarditis
treatment.
lung fibrosis
viscus stricture
spinal cord transection
radiation enteritis
RATIONALE:
RATIONALE
In radiation-resistant organs, the vascular endothelium
is the most sensitive component.
Organs with more self-renewal as a part of normal
homeostasis, such as the hematopoietic system and
mucosal lining of the intestinal tract, are more sensitive.
Acute toxicities include mucositis, skin erythema
(ulceration in severe cases), and bone marrow toxicity.
Often these can be alleviated by interruption of
treatment.
Radiation
Physical form of treatment that damages any tissue
in its path
Selectivity for cancer cells may be due to defects in a
cancer cell's ability to repair sublethal DNA and
other damage
Causes breaks in DNA and generates free radicals
from cell water that may damage cell membranes,
proteins and organelles.
Radiation
PRINCIPLES OF
CHEMOTHERAPY
d. Pancreatic carcinoma
Pediatric neoplasms
Wilms tumor
Embryonal rhabdomyosarcoma
Ewings sarcoma
Peripheral neuroepithelioma
Neuroblastoma
Ovarian carcinoma
Non-small-cell lung carcinoma
(stage III)
Lymphomascertain types
(pediatric/adult)
Gestational trophoblastic
neoplasia
Small-cell lung carcinoma
KARNOFSKY
Carefully quantitating its effect on tumor size
Using these measurements to objectively decide the basis for further
treatment of a particular patients or further clinical evaluation of a
drugs potential
PRINCIPLES OF DRUG
USE
RESPONSE
Defined as tumor shrinkage, is but the most immediate indicator of
drug effect
ANSWER: C
Apoptosis, or programmed cell death, refers to a highly ordered
process whereby cells respond to defined stimuli by dying, and it
recapitulates the necessary cell death observed during the
ontogeny of the organism. Cancer chemotherapeutic agents can
cause both necrosis and apoptosis. Apoptosis is characterized
by chromatin condensation (giving rise to apoptotic bodies),
cell shrinkage, and, in living animals, phagocytosis by
surrounding stromal cells without evidence of inflammation.
The antiapoptotic protein bcl2 attenuates mitochondrial
toxicity, while proapoptotic gene products such as bax
antagonize the action of bcl2.
APOPTOSIS
Programmed
Highly ordered process whereby cells respond to defined
stimuli by dying and it recapitulates the necessary cell
death observed during ontogeny of the organism
Chromatin condensation->apoptoic bodies
Cell shrinkage, phagocytosis by surrounding stroma
without evidence of inflammation(in living cells)
Signal transduction system or specific cell-surface
receptors
CELL DEATH
*
COMBINATION CHEMOTHERAPY
Refers to the use of regimens where different drugs are
combined with the goal of achieving at least an additive &
hopefully supra-additive effect
Component drugs in such regimens ideally have distinct,
nonoverlapping toxicities to the host
CHEMOTHERAPEUTIC
DRUGS
2. TARGETED AGENTS
Refer to small molecules or biologicals
- Generally macromolecules such as antibodies or cytokines
Designed & developed to interact with a defined molecular target
- Important in either maintaining the malignant state, or
- selectively expressed by the tumor cells
Targeted therapies seek to capitalize on the biology behind the aberrant
cellular behavior as a basis for therapeutic effects
4. BIOLOGIC THERAPIES
Are often macromolecules that have a particular target
e.g., antigrowth factor or cytokine antibodies
May have the capacity to regulate growth of tumor cells
Induce a host immune response to kill tumor cells
Include not only antibodies but cytokines & gene therapies
CONVENTIONAL
CHEMOTHERAPY
A. DIRECT DNA-INTERACTIVE
AGENTS- ALKYLATING
ALKYLATING AGENTS
CYCLOPHOSPHAMIDE
FOSFOMIDE
NITROGEN MUSTARD
CHLORAMBUCIL
MALPHALAN
PROCARBAZINE
DACARBAZINE
TEMOZOLAMIDE
CISPLATIN
CARBOPLATIN
OXALIPLATIN
ANTI-TUMOR ANTIBIOTICS OF
TOPOISOMERASE POISONS
DOXORUBICIN
DAUNORUBICIN
IDARUBICIN
BLEOMYCIN
MITOXANTRONE
ETOPOSIDE
CAMPTOTHECIN
TOPOTECAN
CPT-11/IRINOTECAN
ALKYLATING AGENTS
Alkylating agents as a class are cell cycle phasenonspecific agents.
They break down, either spontaneously or after normal organ or tumor
cell metabolism, to reactive intermediates that covalently modify bases
in DNA.
This leads to cross-linkage of DNA strands or the appearance of breaks
in DNA as a result of repair efforts.
Broken or cross-linked DNA is intrinsically unable to complete
normal replication or cell division; in addition, it is a potent activator of
cell cycle checkpoints and further activates cell-signaling pathways that
can precipitate apoptosis.
CYCLOPHOSPHAMIDE
An inactive drug unless
metabolized by the liver to
4-hydroxy-cyclophosphamide,
which decomposes into an
alkylating species, as well
as to chloroacetaldehyde
and acrolein. The latter
causes chemical cystitis;
therefore,
excellent
hydration
must
be
maintained while using
cyclophosphamide
Answer: C Rationale:
Letter A - it causes acute cardiotoxicity in the form of atrial
and ventricular dysrhythmias
Letter B - Cardiotoxicity has been related to iron-catalyzed
oxidation and reduction of doxorubicin, and not to
topoisomerase action
DOXORUBICIN
It can intercalate into DNA, thereby altering DNA structure,
replication, and topoisomerase II function.
It can also undergo reduction reactions by accepting
electrons into its quinone ring system, with the capacity to
undergo reoxidation to form reactive oxygen radicals after
reoxidation.
It causes predictable myelosuppression, alopecia, nausea,
and mucositis. In addition, it causes acute cardiotoxicity in
the form of atrial and ventricular dysrhythmias, but these
are rarely of clinical significance.
DOXORUBICIN
In contrast, cumulative doses >550 mg/m2 are associated with a
10% incidence of chronic cardiomyopathy.
The incidence of cardiomyopathy appears to be related to schedule
(peak serum concentration), with low-dose, frequent treatment or
continuous infusions better tolerated than intermittent higher-dose
exposures.
Cardiotoxicity has been related to iron-catalyzed oxidation and
reduction of doxorubicin, and not to topoisomerase action.
Cardiotoxicity is related to peak plasma dose; thus, lower doses and
continuous infusions are less likely to cause heart damage.
DOXORUBICIN
Doxorubicins cardiotoxicity is increased when given together with
trastuzumab (Herceptin), the anti-HER2/neu antibody. Radiation
recall or interaction with concomitantly administered radiation to
cause local site complications is frequent. The drug is a powerful
vesicant, with necrosis of tissue apparent 47 days after an
extravasation; therefore, it should be administered into a rapidly
flowing intravenous line.
Dexrazoxane is an antidote to doxorubicin-induced extravasation.
Doxorubicin is metabolized by the liver, so doses must be reduced
by 5075% in the presence of liver dysfunction.
MOA
TOXICITY
CISPLATIN
was discovered fortuitously by observing that bacteria
present in electrolysis solutions could not divide
Only the cisdiamine configuration is active as an antitumor
agent
Requires administration with adequate hydration
HYPOMAGNESEMIA can lead to hypocalcemia&tetany
Neurotoxicity with stocking-&-glove sensorimotor
neuropathy
Ototoxicity
Intensely emetogenic
Less evident myelosupression than with others
VESICANT DRUG
Doxorubicin
Daunorubicin
Vincristine
Vinblastine
Vinorelbine
Meclorethamine
Mitoxantrone(mild)
Dactinomycin
CISPLATIN
- Gradual decrease in kidney function is
common even with hydration
- HYPOMAGNESEMIA can lead to
hypocalcemia & tetany
- Neurotoxicity with stocking-and-glove
sensorimotor neuropathy
- Ototoxicity in 50% of patients treated
with conventional doses
- Intensely emetogenic, thus requiring
prophylactic antiemesis
-Myelosuppression less evident than
with other alkylating agents
--Chronic vascular toxicity (Raynauds
phenomenon, coronary artery disease)
is a more unusual toxicity.
Oxaliplatin
A platinum analogue with note- worthy
activity in colon cancers refractory to
other treatments. It is prominently
neurotoxic.
Carboplatin
Displays less nephro-, oto-, and
neurotoxicity. However,
myelosuppression is more frequent, and
because the drug is exclusively cleared
through the kidney, adjustment of dose
for creatinine clearance must be
accomplished through use of various
dosing nomograms.
DEOXYCOFORMYCIN
PEMETREXED
6-MERCAPTOPURINE (6-MP)
5-FU
LEUCOVORIN
6-THIOGUANINE
CYTOSINE ARABINOSIDE
2-CHLORODEOXYADENOSINE
GEMCITABINE
HYDROXYUREA
FLUDRABINE PHOSPHATE
AZATHIOPRINE
5FU
Oral bioavailability varies unreliably, but orally administered analogues
of 5FU such as capecitabine have been developed that allow at least
equivalent activity to many parenteral 5FU-based approaches.
Intravenous administration of 5FU leads to
bone marrow suppression after short infusions
stomatitis after prolonged infusions.
TAXANES
VINCRISTINE
DOCETAXEL
VINBLASTINE
PACLITAXEL
ANSWER: C
Vincristine (not docetaxel) binds to the tubulin dimer with the result that
microtubules are disaggregated. This results in the block of growing cells in
M-phase; however, toxic effects in G1 and S-phase are also evident,
Vincristine is metabolized by the liver, and dose adjustment in the presence
of hepatic dysfunction is required. It is a powerful vesicant, and infiltration
can be treated by local heat and infiltration of hyaluronidase.
The taxanes include paclitaxel and docetaxel. These agents differ from the
vinca alkaloids in that the taxanes stabilize microtubules against
depolymerization. The stabilized microtubules function abnormally and
are not able to undergo the normal dynamic changes of microtubule
structure and function necessary for cell cycle completion.
VINCRISTINE
VINBLASTINE
MOA:
1. Binds to the tubulin dimer with the result that microtubules are disaggregated
2. Block of growing cells in M-phase
(toxic effects in G1 & S-phase are also evident)
KINETICS
- Metabolized by the liver
o Dose adjustment in hepatic dysfunction is required
ADMIN
- Powerful vesicant
o Infiltration can be treated by local heat & infiltration of hyaluronidase
Clinically used IV doses neurotoxicity in the
MORE myelotoxic with more frequent
form of glove-and-stocking neuropathy is
thrombocytopenia
frequent
- MORE mucositis & stomatitis
- Acute neuropathic effects include jaw pain,
paralytic ileus, urinary retention, & the
syndrome of inappropriate antidiuretic hormone
secretion
- Myelosuppression is NOT seen
HORMONAL THERAPY
ESTROGEN
RECEPTOR
ANTAGONIST
PROGESTATIO
NAL AGENTS
AROMATASE
INHIBIOTRS
ANDROGEN
DEPRIVATION
TESTICULAR
ANDROGEN
SUPRESSION
TAMOXIFEN
MPA
ANDROGENS(
HALOTESTIN)
ESTROGENS
Answer: C
TARGETED THERAPY
Multikinase
inhibitors
Proteasome
Inhibitors
Histone
Deacetylase
Inhibitors
mTOR Inhibitors
IMATINIB
NILOTINIB
DASATINIB
BOSUTINIB
PONATINIB
GEFITINIB
SORAFINIB
&SUNITINIB
PAZOPANIB
REGORAFENIB
VANDETANIB
CABOZANTINIB
AXITINIB
BORTEZOMIB
CARFILZOMIB
VORINOSTAT
ROMIDEPSIN
TEMSIROLIMUS
EVEROLIMUS
ERLOTINIB
AFATINIB
CRIZOTINIB
VEMURAFENIB
DABRAFENIB
TRAMETINIB
HEMATOPOITEIC NEOPLASM
-IMATINIB
-NILOTINIB
-DASATINIB
-BORTEZOMIB
-VORINOSTAT
SOLID TUMORS
-GEFITINIB
-ERLOTINIB
-LAPATINIB
-SORAFINIB &SUNITINIB (MULTTITARGETED
KINASE ANTAGONISTS)
-TEMSIROLIMUS & EVEROLIMUS (mTOR)
d) Tratuzumab
SORAFENIB
- for solid tumors , Multitargetd kinase antagonist
-Drugs of this type with prominent activity against the vascular endothelial
growth factor receptor (VEGFR) tyrosine kinase have activity in renal cell
carcinoma.
- Sorafenib is a VEGFR antagonist with activity against the raf serinethreonine protein kinase, and regorafenib is a closely related drug with
value in relapsed advanced colon cancer.
Other Multitargted Kinase anatagonists
1. SUNITINIB-anti VEGFR, anti-PDGRF, anti-c-kit
Lapatinib
-targeted, solid tumors
HER2/NEU Combined EGF receptor & erbB2 tyrosine kinase
antagonist with activity in breast cancers refractory to
anti-erbB2 antibodies
Cetuximab -biologic, EGFR-directed antibodies
EGFR
-Colorectal cancers(refractory) with wild-type Ki-ras
oncoprotein;
-head and neck cancers treated with radiation;
MOA
-direct effects, antiproliferative, stimulated immune cell
or complement mediated response
Side effects
-rash, diarrhea, infusion reactions
Trastuzumab
HER2/NEU
Erlotinib
- For solid tumors
-EGF receptor tyrosine kinase antagonist
-With somewhat superior outcome in clinical trials in NonSmall Cell Lung Cancer (NSCLC)
- Even patients with wild-type EGF receptors may benefit from
erlotinib treatment
-The presence of EGF receptor tyrosine kinase mutations has
recently been shown to be a basis for recommending erlotinib
and afatinib for first-line treatment of advanced NSCLC.
SUNITINIB
IMATINIB
ERLOTINIB
TRASTUZUMAB
Renal cell
carcinoma
Pancreatic
neuroendocrine
tumor
GI stromal
tumor
Bcr-Abl fusion
protein (CML/ALL)
c-kit mutants
PDGFR
variants (GI
stromal tumor)
eosinophilic
syndromes
First-line
treatment of
NSCLC with ATP
site mutation of
EGFR;
second-line
treatment of
wild-type EGFR
NSCLC
HER2/neu
For breast cancer &
GI cancer
BIOLOGIC THERAPY
ANTIBODIES
CYTOKINES
ACUTE
COMPLICATIONS OF
CANCER TREATMENT
86. If indicated as primary prophylaxis, GCSF should be started agent against Her2
A. Right after chemotherapy
*in primary prophylaxis given shortly after completing chemo
B. 1 day after chemotherapy
*secondary prophylaxis -24-72hrs after
C. 1 day before chemotherapy
D. 1 hour prior to chemotherapy
*NOT SURE, PLEASCE CHECK
CASE
Answer: B
Most patients, however, receive regimens that do not have such a high
risk of expected febrile neutropenia, and therefore most patients
initially should not receive G-CSF or GM-CSF.
Special circumstancessuch as a documented history of febrile
neutropenia with the regimen in a particular patient or categories of
patients at increased risk, such as patients older than age 65 years with
aggressive lymphoma treated with curative chemotherapy regimens;
extensive compromise of marrow by prior radiation or chemotherapy;
or active, open wounds or deep-seated infectionmay support primary
treatment with G-CSF or GM-CSF.
FEBRILE NEUROPENIA
FEBRILE NEUROPENIA
THROMBOCYTOPENIA
THROMBOCYTOPENIA
THROMBOCYTOPENIA
ANEMIA
ANEMIA
OTHERS(NOT SURE IF
INCLUDED)
D. Gap 2
G1
first phase
preparations are made to replicate the genetic material
The cell stops before entering the DNA synthesis phase, or S phase, to take
inventory
Are we ready to replicate our DNA?
Is the DNA repair machinery in place to fix any mutations that are detected?
Are the DNA replicating enzymes available?
Is there an adequate supply of nucleotides?
Is there sufficient energy?
THANK YOU!
YANNIE SAN-ANTONIO
KAT KABIGTING
KIMPOY SEVILLA
FRECHELLE DY
FARA LUIS
JONATHAN DE LUNA