Tyrosine Kinase Inhibitors

TYROSINE KINASE INHIBITORS

Q. 1 Which teratogen causes deafness Imatinib is used in the treatment of ?
 A

Chronic myelomonocytic leukemia

 B

MDS

 C

ALL

 D GIST
Q. 1 Which teratogen causes deafness Imatinib is used in the treatment of ?
 A

Chronic myelomonocytic leukemia

 B

MDS

 C

ALL

 D GIST
Ans. A

Explanation:

Isotretinoin [Ref Williams obstetrics 22″4/e p 346, 347, 348; http//www.ijporlonline.com/article/50165-5876 (10)00264/abstract]

  • Isotretinoin can cause nzicrotia or anotia.
  • These defects are frequency associated with agenesis or stenosis of the external ear canal and may lead to deafness.

According to international journal of pediatrics otorhinolaryttgology

“Despite extensive precautions for its use, isotretinoin remains a cause of major birth defects including sensorieneural, conductive or mixed hearing loss”.

  • Isotretinoin is one of the most potent teratogene in common use.
  • Abnormalities commonly occur after 1st trimester.
  • Any organ system can be affected by isotretinoin exposure but malformations typically involve the cranium, face, heart, central nervous system and thymus.
  • Facial defects include cleft palate and maldevelopment of the facial bones and cranium.
  • Cardiac anomalies include conotruncal or outflow tract defects.
  • Hydrocephalus is the most common central nervous defect.
  • Thymic abnormalities include aplasia, hypoplasia or malposition.

Features of Fetal Alcohol syndrome

  • Behaviour disturbances
  • Brain defects
  • Cardiac defects
  • Spinal defects
  • Craniofacial anomalies

Absent or h)poplastic philtrum – Broad upper lip

– Flattened nasal bridge

– Hypoplastic upper lip vermilion – Micrognathia

– Microphthalmia

– Short nose

– Short palpebral tissues

Warfarin

  • First trimester            –           Hypoplastic nasal bridge, chondrodysplasia
  • Second trimester        –           C.N.S. malformation
  • Third trimester           –           Risk of bleeding, Discontinue the use one month before delivery

Q. 2

Imatinib is used in the treatment of ?

 A Chronic myelomonocytic leukemia
 B

MDS

 C

ALL

 D GIST
Q. 2

Imatinib is used in the treatment of ?

 A Chronic myelomonocytic leukemia
 B

MDS

 C

ALL

 D GIST
Ans. A

Explanation:

Chronic myelomonocytic leaukemia (d) GIST [Ref ]

  • Imatinib is a competitive inhibitor of tyrosine kinase.
  • Tyrosine kinase is a signal transducer i.e. it transmits growth signals from outside of the cell or from the cytoplasm to nucleus.
  • Let’s step aside from the question for a while and discuss the growth cycle.
  • The pathway for normal cell growth starts with growth factor
  • Growth factors act on growth factor receptors
  • These growth factor receptors are turned on and off by growth factor signals.
  • The signals from the growth factor receptors in turn is sent to the cell nucleus by signal transduction pathways.
  • These are the intermediate pathways between the growth factor receptor and the cell nucleus where the signal is received.
  • In the nucleus the signal is received by transcription factors.
  • These are the final molecules in the chain that tell the cell to divide.

Now let’s come back to signal transduction pathways

Signal transduction pathways:-

  • There are various types of signal transduction pathways
  • Protein kinases are one of the important signal transduction pathways

Protein kinase pathways

  • There are of three types

(i)   Tyrosine kinase pathway

(ii)  Threonine/serine kinase pathway

(iii) Other pathways

The important Tyrosine kinase pathways are RAS/ABL and the growth factors which are associated withTyrosine kinases pathway are

  • EGF
  • TGF
  • HGF
  • POGF
  • VEGF
  • FGF
  • c-KIT
  • The components of the cell proliferation pathways are also called protoncogenes. Normally they regulate cell proliferation and differentiation.
  • But mutations in them are a frequent cause of cancers.
  • Mutations in any one of the component may lead to specific cancer. Mutation turn them into oncogenes from protoonc ogenes.
  • Newer anticancer drugs are targetted at these components. These anticancer drugs target specific component of the cell proliferations pathways and thus act specifically against the cancer produced by the gene.
  • Imatinib is targetted at tyrosine kinase (signal transducer) thus it will act against tyrosine kinase (ABL, BCR), and all the growth factors involved in the tyrosine kinase pathways.

Thus Imatinib shows remarkable therapeutic benefit in patients with :

  • CML (BCR-ABL)
  • GIST (KIT mutation positive)
  • CMML
  • HES
  • Dermatofibrosarcoma protuberans

Q. 3

Imatinib used in CML acts by

 A

inhibiting Bcr/abl translocation via tyrosine kinase

 B Blocking the action of P-glycoprotein
 C

Competitive inhibition of ATP binding site of Abl kinase

 D

C-kit kinase inhibition

Q. 3

Imatinib used in CML acts by

 A

inhibiting Bcr/abl translocation via tyrosine kinase

 B Blocking the action of P-glycoprotein
 C

Competitive inhibition of ATP binding site of Abl kinase

 D

C-kit kinase inhibition

Ans. C

Explanation:

Competitive inhibition _of ATP binding site of ABL kinase [Ref. Harrison 16thie p 4781

  • CML is characterized by the presence of a distinctive molecular abnormality namely philadelphia chromosome.
  • Philadelphia chromosome in formed as a result of reciprocal translocation between long arm of chromosome 22 and chromosome 9 i.e. t (9 ; 22).
  • ABL protooncogene from chromosome 9 is translocated to chromosome 22 where BCR is present and results in formation of BCR-ABL fusion chimeric gene.

 The drug imatinib mesylate is a BCR-ABL tyrosine kinase signal transduction inhibitor. This drug acts as a inhibitor of the ATP binding site on the protein and prevents its phosphorylation and thus its activity.

An important point

  • CML is caused by reciprocal translocation between BCR and ABL gene located on chromosome 9 and 22.
  • Imatinib mesylate does not block this translocation i.e., BCR ABL translocation.

– Instead, it blocks the constitutive abnormal tyrosine kinase, BCR-ABL that is created by the Philadelphia chromose (BCR-ABL).

– The drug inhibits the proliferation and induces apoptosis in BCR-ABL positive cells.

Also know

Protein tyrosine kinase inhibitors

  • Protein kinases are ubiquitous and critical components of signal transduction pathways that transmit information concerning extra cellular or cytoplasmic conditions to the nucleus, thereby influencing gene transcription and/or DNA synthesis.

The protein kinases can be classified into three categories:

(i)   Tyrosine kinase

(ii)  Serine threonine kinase

(iii) Kinases with activity for all three residues

  • Abnormal activation of specific tyrosine kinase has been demonstrated in many human neoplasms. Thus they can be targeted in certain cancer therapies.
  • There currently are three small-molecular weight protein tyrosine kinase inhibitors that are FDA approved and many others are in clinical trials.

i) Imatinib

  • Imatinib has efficacy in diseases in which the ABL, KIT or PDGFR have dominant roles in driving the proliferation of the tumour.
  • Thus, imatinib shows remarkable therapeutic benefits in patients with

– CML (BCR-ABL)

– GIST (KIT mutation positive)

– CMML (EVT6-PDGFR)

ii) Gefitinib

  • The epidennal growth factor receptor (EGFR) belongs to the family of tyrosine kinase.
  • Gefitinid is a specific inhibitor of the EGFR tyrosine kinase that competitively inhibits ATP binding.
  • EGFR is overexpressed in non-small cell carcinoma of lung, thus Gefitinib has been approved for use in non-small cell carcinoma.

iii) Erlotinib

  • It is a human HERI/EGFR tyrosine kinase inhibitor.
  • It is indicated for patients with locally advanced or metastatic non-small cell lung cancer.

Quiz In Between


Q. 4 Imatinib acts on:
 A NMYC
 B Tyrosine kinase
 C PDGF
 D VEGF
Q. 4 Imatinib acts on:
 A NMYC
 B Tyrosine kinase
 C PDGF
 D VEGF
Ans. B

Explanation:

Tyrosine kinase


Q. 5

The drug imatinib acts by inhibiting which of the following enzyme?

 A

Tyrosine kinase

 B

Glutathione reductase

 C

Thymidine synthase

 D

Protein kinase

Q. 5

The drug imatinib acts by inhibiting which of the following enzyme?

 A

Tyrosine kinase

 B

Glutathione reductase

 C

Thymidine synthase

 D

Protein kinase

Ans. A

Explanation:

Imatinib is a tyrosine kinase inhibitor domain of BCR-ABL oncoprotein and prevents phosphorylation of the kinase substrate by ATP. It is indicated for the treatment of chronic myelogenous leukemia and gastrointestinal stromal tumors. 
 
5 Fluorouracil inhibits thymidylate synthase thereby interfering with synthesis of DNA to lesser extent RNA. Its effect is more marked on atypical, rapidly proliferating cells. It is used topically for the treatment of multiple actinic keratoses.
 
Ref: Chu E., Sartorelli A.C. (2012). Chapter 54. Cancer Chemotherapy. In B.G. Katzung, S.B. Masters, A.J. Trevor (Eds), Basic & Clinical Pharmacology, 12e.

Q. 6

Sorafenib a tyrosine kinase inhibitor is used to treat which of the following?

 A

Myeloproliferative disorder

 B

Follicular lymphoma

 C

Medullary carcinoma thyroid

 D

Hepatocellular carcinoma

Q. 6

Sorafenib a tyrosine kinase inhibitor is used to treat which of the following?

 A

Myeloproliferative disorder

 B

Follicular lymphoma

 C

Medullary carcinoma thyroid

 D

Hepatocellular carcinoma

Ans. D

Explanation:

Sorafenib is used to treat hepatoma which are not resectable as a palliative measure.

Ref: arrisons Principles of Internal Medicine, 18th Edition, Page 783.

 

Quiz In Between


Q. 7

Imatinib used in CML acts by –

 A

Inhibiting BCR/ABL translocation via tyrosine kinase

 B

Blocking the action of P glycoprotein

 C

Competitive inhibition ofATP binding site ofABL kinase

 D

C-Kit kinase inhibition

Q. 7

Imatinib used in CML acts by –

 A

Inhibiting BCR/ABL translocation via tyrosine kinase

 B

Blocking the action of P glycoprotein

 C

Competitive inhibition ofATP binding site ofABL kinase

 D

C-Kit kinase inhibition

Ans. C

Explanation:

Ans. is ‘c’ i.e. Competitive inhibition of ATP binding site of ABL kinase

o In CML, there is Bcr-Abl translocation which leads to unregulated activation of intracellular (non-receptor)

tyrosine kinase, Le., Bcr-Abl tyrosine kinase.

o Imatinib is a Bcr-Abl tyrosine kinase (intracellular-nonreceptor tyrosine kinase) inhibitor.

o This drug block the activity of nonreceptor tyrosine kinase by acting as a inhibitor of the ATP binding site on the protein and prevents its phosphorylation.

About option ‘a’

o Imatinib does not inhibit Bcr-Abl translocation, it inhibits overactive tyrosine kinase after Bcr-Abl translocation has already occured.


Q. 8

Imatinib is used in the treatment of

 A

CML

 B

MDS

 C

ALL

 D

All

Q. 8

Imatinib is used in the treatment of

 A

CML

 B

MDS

 C

ALL

 D

All

Ans. A

Explanation:

Ans. is `a’ i.e., CML


Q. 9

Treatment of chronic phase of CML is?

 A

Imatinib

 B

Hydroxyurea

 C

Interferon

 D

Cytarabine

Q. 9

Treatment of chronic phase of CML is?

 A

Imatinib

 B

Hydroxyurea

 C

Interferon

 D

Cytarabine

Ans. A

Explanation:

Ans. is ‘a’ i.e., Imatinib

o Imatinib is the first line therapy for newly diagnosed CML patients.

Quiz In Between


Q. 10

All are true regarding Sunitinib except –

 A

It inhibits tyrosine kinase receptors

 B

It is used for renal cell carcinoma

 C

It is used for the treatment of GIST

 D

It is excreted primarily in urine

Q. 10

All are true regarding Sunitinib except –

 A

It inhibits tyrosine kinase receptors

 B

It is used for renal cell carcinoma

 C

It is used for the treatment of GIST

 D

It is excreted primarily in urine

Ans. D

Explanation:

Ans. is ‘d’ i.e., It is excreted primarily in urine

  • Sunitinib inhibits multiple Tyrosine kinase receptors. It inhibits PDGF, VEGF and c-kit.

o Sunitinib and sorafinib are used in renal cell carcinoma (in RCC there is overexpression of VEGF) and GIST (in GIST there is over expression of C-Kit & PDGF).

o It is eliminated primarily by hepatic route with excretion in faeces.


Q. 11

Tyrosine kinase inhibitors are used in the treatment of-

 A

Gastrointestinal stromal tumors (GIST)

 B

Acute myeloid leukemia

 C

Neurofibromatosis

 D

Small cell carcinoma lung

Q. 11

Tyrosine kinase inhibitors are used in the treatment of-

 A

Gastrointestinal stromal tumors (GIST)

 B

Acute myeloid leukemia

 C

Neurofibromatosis

 D

Small cell carcinoma lung

Ans. A

Explanation:

Ans. is `a’ i.e., Gastrointestinal stromal tumors (GIST)

Tyrosine kinase inhibitors imatinib and sunitinib are approved for the treatment of Gastrointestinal Stromal Tumors (GIST).


Q. 12

Which of the following agents is recommended for treatment of Gastrointestinal Stromal Tumors (GIST) –

 A

Sorafenib

 B

Imatinib

 C

Gefitinib

 D

Erlotinib

Q. 12

Which of the following agents is recommended for treatment of Gastrointestinal Stromal Tumors (GIST) –

 A

Sorafenib

 B

Imatinib

 C

Gefitinib

 D

Erlotinib

Ans. B

Explanation:

Ans. is ‘b’ i.e., Imatinib

Tyrosine kinase inhibitors imatinib and sunitinib are approved for the treatment of Gastrointestinal Stromal Tumors (GIST)

Quiz In Between


Q. 13

All of the following statements about Erlotinib are true, except:

 A

Tyrosine kinase inhibitor

 B

Food decreases its absorption

 C

Rashes may occur

 D

Used in Non small cell lung carcinoma

Q. 13

All of the following statements about Erlotinib are true, except:

 A

Tyrosine kinase inhibitor

 B

Food decreases its absorption

 C

Rashes may occur

 D

Used in Non small cell lung carcinoma

Ans. B

Explanation:

Ans is ‘b’ i.e. Food decreases its absorption

Erlotinib

o Erlotinib is a human HER1/EGFR tyrosine kinase inhibitor.

o It is indicated for treatment of patients with locally advanced or metastatic non small cell lung cancer. It is also used in carcinoma of pancreas, head & neck cancer, hepatocellular carcinoma and carcinoma of unknown primary.

o Erlotinib is about 60% absorbed after oral administration and its bioavailability is substantially increased to almost 100% by food The time to peak concentrations is approximately 4 hours after a dose. The half life of erlotinib is about 36 hours and it is eliminated predominately by CYP450 3 A4. Smoking increases the clearance of erlotinib by 24% which may result in treatment failure.

o The most common adverse reaction in patients receiving erlotinib are diarrhea and rash. Other side effects are intersitital lung disease, anorexia, pruritis, conjunctivitis, elevated livers enzymes and bleeding.


Q. 14

Initial treatment recommended for newly diagnosed patient with CML is:

 A

Allogenic Bone Marrow Transplantation

 B

Imatinib Mesylate Therapy

 C

TNF-a

 D

IFN-a

Q. 14

Initial treatment recommended for newly diagnosed patient with CML is:

 A

Allogenic Bone Marrow Transplantation

 B

Imatinib Mesylate Therapy

 C

TNF-a

 D

IFN-a

Ans. B

Explanation:

Answer is B (Imatinib Mesylate Therapy)

Harrison’s 18th edition recommends starting treatment of newly diagnosed CML with TK inhibitors (Imatinib) and reserving alloginic transplantation for those who develop Imatinib resistance.

The therapy of CML is changing rapidly because we have a proven curative treatment (allogenic transplantation) that has significant toxicity and a new targeted treatment (imatinib) with outstanding outcome based on 8 year follow up data. We recommend starting with TK inhibitors (Imatinib) and reserving allogenic transplantation for those who develop imatinib resistance’

Note:

  • The only curative treatment for CML is Allogenic stem cell Transpintation
  • The treatment of choice in CML is Allogenic BMTe
  • The drug treatment of choice in CML is ImatinibQ
  • Initial treatment recommended for newly diagnosed patient with CML is Imatinib.

Treatment of CML MEW

  • The only curative treatment for CML is Allogenic Stem Cell Transplantation (SCT) (Allogenic bone marrow transplantation)Q
  • The treatment of choice for CML is also Allogenic Stem Cell Transplantation (SCT) (Allogenic bone marrow transplantation)e
  • The drug treatment of choice for CML is Imatinibe
  • Interferon alpha (IFN a ) used to be the drug treatment of choice for CML when Imatinab was not available

Q. 15

Chemotherapeutic Agent of Choice for the treatment of CML is:

 A

Imatinib

 B

Vincristine

 C

Cyclophosphamide

 D

Methotrexate

Q. 15

Chemotherapeutic Agent of Choice for the treatment of CML is:

 A

Imatinib

 B

Vincristine

 C

Cyclophosphamide

 D

Methotrexate

Ans. A

Explanation:

Answer is A (Imatinib): 

Tyrosine Kinase Inhibitors (Imatinib) are the chemotherapeutic agents for choice in the management of CML. Tyrosine Kinase inhibitors target the ‘constitutively active tyrosine kinase’ implicated in the pathogenesis of CML. Although they do not cure the disease, these agents are able to achieve long term control of CML in the majority of patients. Most recent texts (Including Harrisons) recommend Tyrosine Kinase Inhibitors (Imatinib) as the initial treatment of choice for newly diagnosed CML reserving Allogeneic Stem Cell Transplantation (SCT) for those who develop Imatinib Resistance.

Quiz In Between


Q. 16

All of the following statements about Non Small Cell Carcinoma of Lung (NSCCL) are true, Except:

 A

Contralateral mediastinal nodes are a contraindication to surgical resection

 B

Single Agent Chemotherapy is preferred for patient > 70 years with advanced disease

 C

Squammous Cell Carcinoma is the most common NSCCL amongst Asian population

 D

Gefitinib is most effective for female smokers with adenocarcinoma on histology

Q. 16

All of the following statements about Non Small Cell Carcinoma of Lung (NSCCL) are true, Except:

 A

Contralateral mediastinal nodes are a contraindication to surgical resection

 B

Single Agent Chemotherapy is preferred for patient > 70 years with advanced disease

 C

Squammous Cell Carcinoma is the most common NSCCL amongst Asian population

 D

Gefitinib is most effective for female smokers with adenocarcinoma on histology

Ans. D

Explanation:

Answer is D (Gefitinib is most effective for female smokers with adenocarcinoma on histology):

Gefitinib is an oral ‘small molecule Tyrosine kinase Inhibitor’ (that inhibit signalling via EGFR) approved for the treatment of patients with NSCCL. Data to support the use of Gefitinib in NSCCL are however diminishing and Gefitinib is most effective in females who have never smoked with adenocarcinoma on histology.

Single agent cgemotherapy is prefered for elderly patients (> 70 years)

American Society of Clinical Oncology (ASCO) recommends the use of single agent chemotherapy for elderly patients (> 70 years) with a poor performance status (2003 Guidelines)

It has however now been stressed (2009 Guidelines) that age alone should not be used to select chemotherapy for patients with advanced NSCLC. Physiological Age (not chronological age) and performance status should be considered when selecting the chemotherapy regimen.

Chemotherapy for Advanced (Stage IV) NSCLC

Young patient

Good performance status (PS < 2)

  • Double agent chemotherapy is preferred for first line therapy
  • Platinum based combinations are preferred over non platinum based combinations

Elderly patient

Poor performance status (PS 2)

  • Single Agent Chemotherapy is preferred to reduce
    potential toxicity from chemotherapeutic agents.
  • Vinorelbine or docetexal are often used for single agent chemotherapy in the elderly with a poor PS.

 

Gefitinib is most effective for females with adenocarcinoma histology who have never smoked

Gefitinib is an acceptable second line agent for treatment of patients with advanced NSCLC with adequate performance status when the disease has progressed during or after first line platinum based chemotherapy.

 

Clinical Features that correlate with responsiveness to Gefitinib (Harrison)

 

  • Female Sex
  • Never smoking status
  • Adenocarcinoma Histology
  • Asian Ethinicity

Contralateral Mediastinal nodes are a contraindication to Surgical Resection

ALB. In otherwise fit individual, direct extension of tumour into the chest wall, diaphragm, mediastinal pleura or pericardium or to within 2 cm of the main carina does not exclude surgery. Though surgically resectable, patients with N2 (ipsilateral mediastinal) nodes may require neoadjuvant or adjuvant therapy.

Contraindication to surgical resection in NSCLC (Davidson)

  • Distant metastasis (M1)
  • Invasion of central mediastinal structures including heart, great vessels. trachea and oesophagus (T4)
  • Malignant pleural effusion (T4)
  • Contralateral mediastinal nodes (N3)
  • FEV, < 0.8L
  • Severe or unstable cardiac or other medical condition

Squammous Cell Carcinoma is the most common histological subtype of Lung Cancer in Asia (Including India)

 

  • Most common lung cancer worldwide is adenocarcinoma
  • Most common lung cancer in India (Asia) is squammous cell carcinoma
  • Most common lung cancer in women is adenocarcinoma
  • Most common lung cancer in smokers is squammous cell carcinoma
  • Most common lung cancer in nonsmokers is adenocarcinoma
  • Most common lung cancer in young patients is adenocarcinoma
  • Most common lung cancer to metastasize is small cell carcinoma

 

 


Q. 17

Which of the following anticancer drugs are competitive inhibitors of tyrosine kinase ‑

 A

Imatinib and suntinib

 B

Letrozole

 C

Bicalutamide

 D

Fulvestrant

Q. 17

Which of the following anticancer drugs are competitive inhibitors of tyrosine kinase ‑

 A

Imatinib and suntinib

 B

Letrozole

 C

Bicalutamide

 D

Fulvestrant

Ans. A

Explanation:

Ans. is ‘a’ i.e., Imatinib and suntinib

Molecular targeted agents

  • Tyrosine kinase inhibitors
  • Competitive inhibitors → Imatinib, Nilotinib, Sunitinib, Dasatinib, Erlotinib, Gefitinib, Lapitinib, Sorafinib (Remember all ends with ‘ nib’).
  • Monoclonal antibodies → Cetuximab, panitumomab.
  • HER2/neu (ERB B2) inhibitors Monoclonal antibody – Transtuzumab.
  • Targeted antibody → Gemtuzomab (anti CD-33), Rituximab (anti – CD20), Alemtuzumab (anti CD-52).
  • Vascular endothelial growth factor (VEGF) inhibitor → Monoclonal antibody – Bevacizumab.
  • Proteosome inhibitors → Bortezomib.
  • Histone deacylase inhibitor → Vorinostat
  • DNA – methyl transferase inhibitor → 5-azacytidine, 2-deoxy-5 azacytidine.
  • All – trans – retinoic acid.
  • Biological response modifier – Recombinant IL-2 (aldesleukin, denileukin).

Q. 18

The drug used in the management of medullary carcinoma thyroid is

 A

Cabozantinib

 B

Rituximab

 C

Tenofovir

 D

Anakinra

Q. 18

The drug used in the management of medullary carcinoma thyroid is

 A

Cabozantinib

 B

Rituximab

 C

Tenofovir

 D

Anakinra

Ans. A

Explanation:

Ans.is ‘a’ i.e., Cabozantinib

Medullary thyroid cancers (MTCs) are neuroendocrine tumors of thyroid paraf011icular cells that do not concentrate iodine.

  • The primary treatment for MTC is extensive and meticulous surgical resection.
  • There is a limited role for external-beam radiotherapy.

For patients with asymptomatic metastatic tumors generally less than 1 to 2 cm in diameter, growing in  diameter less than 20 percent per year

  • Systemic therapy is not required
  • Such patients should be monitored for disease progression. Known sites of metastatic disease should be imaged by CT or MRI every 6 to 12 months, and potential new sites of disease should be imaged every 12 to 24 months.
  • For patients with metastatic tumors at least 1 to 2 cm in diameter, growing by at least 20 percent per year, or Or patients with symptoms related to multiple metastatic foci that cannot be alleviated with surgery or external beam radiotherapy
  • Administer systemic treatment as part of a clinical trial.

 

  • Forpatients with metastatic tumors at least I to 2 cm in diameter, growing by at least 20 percent per year, or

for patients with .symptoms related to multiple metastatic foci who cannot participate in a clinical trial

 

  • An oral tyrosine kinase inhibitor (TKI) is suggested, rather than traditional cytotoxic chemotherapy.
  • For initial TKI therapy
  • Cabozantinib or vandetanib rather than sorafenib or sunitinib.
  • Cytotoxic chemotherapy, of which dacarbazine-based regimens such as cyclophosphamide-vincristine­dacarbazine are preferable, is an alternative option for patients who cannot tolerate or who fail multiple TKIs

Drugs used in medullary carcinoma thyroid

Tyrosine kinase inhibitors

Cvtotoxic chemotherapy

Cabozanitib

Cyclophosphamide
Vandetanib Vincristine
Sorafenib Dacarbazine
Sunitinib  

Q. 19

Erlotinib is used in ‑

 A

Colon cancer

 B

Pancreatic cancer

 C

Gall bladder cancer 

 D

GIST

Q. 19

Erlotinib is used in ‑

 A

Colon cancer

 B

Pancreatic cancer

 C

Gall bladder cancer 

 D

GIST

Ans. B

Explanation:

Ans. is ‘b’ i.e., Pancreatic cancer

Quiz In Between



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