Targeted Therapy for Cancer in Bangalore

  • Home
  • Targeted Therapy for Cancer in Bangalore
Introduction

Targeted Therapy for Cancer in Bangalore

For most of the twentieth century, cancer drugs were chosen by where a cancer started. Targeted therapy changed that logic. It selects a drug based on what a tumour is doing at a molecular level — which gene is altered, which protein is overactive, which signal is stuck in the on position.

01

The National Cancer Institute describes targeted therapy as acting on specific proteins that control how cancer cells grow, divide and spread. Different agents work in different ways: blocking the signals that tell a cell to multiply, cutting off the blood supply a tumour needs, triggering the process by which a damaged cell destroys itself, or flagging cancer cells so the immune system can find them.

02

The condition attached to all of this is testing. The NCI puts it directly: most of the time, your tumour will need to be tested before a targeted drug can be used. A drug designed to block a particular protein has nothing to act on if that protein is not there.

03

Athira's precision oncology commitment exists for this reason. Genomic profiling and molecular characterisation are used to establish whether a target exists in your tumour, and whether a drug for it is available. Results are interpreted alongside the full clinical picture at the multidisciplinary tumour board — because a molecular finding only becomes useful when it is read in context.

Athira Precision Oncology

Athira's precision oncology commitment exists for this reason. Genomic profiling and molecular characterisation are used to establish whether a target exists in your tumour, and whether a drug for it is available. Results are interpreted alongside the full clinical picture at the multidisciplinary tumour board — because a molecular finding only becomes useful when it is read in context.

Understanding Targeted Therapy

Understanding Targeted Therapy

01

The idea of a driver.

Cancers grow because something in the cell's control machinery has gone wrong.

Cancers grow because something in the cell's control machinery has gone wrong. Sometimes a single altered gene produces a protein that keeps signalling growth regardless of the normal checks — a driver alteration. A targeted drug is built to interfere with that specific protein.

The main mechanisms (National Cancer Institute):

01

Blocking growth signals.

Many targeted drugs sit on or inside a receptor and prevent the message to divide being passed on.

02

Cutting off blood supply.

Tumours need new blood vessels to keep growing. Anti-angiogenic drugs interfere with the signals that build them.

03

Triggering cell death.

Some agents restore the cell's own self-destruct process, which cancer cells often disable.

04

Flagging cells for immune attack.

Certain antibody drugs bind to a protein on the cancer cell surface, marking it for the immune system.

Drug Forms

Small molecules

Broadly, targeted drugs come in two forms. Small-molecule inhibitors are usually tablets or capsules taken at home, and can enter the cell to act on proteins inside it.

Drug Forms

Monoclonal antibodies

Monoclonal antibodies are larger and given by infusion, acting mainly on the cell surface.

Understanding Treatment

Why side effects are different.

Because targeted drugs act on specific proteins rather than on all fast-dividing cells, they generally avoid the classic chemotherapy pattern. But the proteins they target often exist in healthy tissue too — which is why skin rash, diarrhoea, mouth soreness, blood pressure changes, liver enzyme changes and altered wound healing are seen with various agents. These are usually manageable with dose adjustment and supportive treatment.

Resistance.

Cancers can adapt. A tumour that responds well may eventually find a way around the blocked pathway. Repeat testing at progression sometimes identifies a new alteration and a next-line option.

When Is Targeted Therapy Recommended?

Targeted therapy may be recommended when testing has identified an actionable alteration in your tumour, and depending on the cancer type and stage.

Your oncologist may consider it when:

01

Genomic or biomarker testing has found a specific mutation, gene fusion, amplification or protein overexpression for which an approved drug exists

02

The cancer type is one where molecular testing is routine at diagnosis — several lung, breast, colorectal, gastric, thyroid and ovarian cancers, and a number of blood cancers, among others

03

HER2 status, hormone receptor status or a similar marker points to a specific drug class

04

Targeted therapy is being combined with chemotherapy, hormonal therapy or immunotherapy as part of a defined regimen

05

Disease has progressed on earlier treatment and repeat profiling identifies a new option

06

A targeted maintenance approach is appropriate after an initial response

When it is not the answer.

If no actionable alteration is found, targeted therapy is not an option — and a negative result is genuinely useful information, because it prevents time being spent on a treatment that could not have worked. Your oncologist will then discuss the alternatives.

Diagnosis and Evaluation

Targeted therapy depends more completely on diagnostics than any other part of medical oncology.

01

Adequate tumour tissue.

Molecular testing needs sufficient, well-preserved material. Where the original biopsy is inadequate, a repeat biopsy may be recommended.

02

Genomic profiling.

Testing on the tumour to identify gene alterations. Depending on the cancer, this may be a single-gene test, a focused panel, or comprehensive next-generation sequencing across many genes at once.

03

Immunohistochemistry.

Immunohistochemistry, to assess protein expression such as HER2.

04

FISH or similar techniques.

FISH or similar techniques, to detect gene amplifications and rearrangements that other methods may miss.

05

Liquid biopsy, where appropriate.

The American Cancer Society notes biomarker testing may be performed on blood or another body fluid as well as on tissue — useful when a tissue biopsy is difficult, or to look for resistance alterations at progression.

06

Germline considerations.

The American Cancer Society also notes that biomarker testing can reveal inherited risk mutations. Where a result has implications for family members, genetic counselling should be discussed.

07

Baseline organ function.

Baseline organ function, including cardiac assessment for agents known to affect heart function, and liver function for drugs metabolised there.

08

Medication review.

Many oral targeted drugs interact with other medicines, and some with specific foods. Bring a full list, including supplements.

Treatment and Care Approaches

01

Oral targeted therapy.

Many small-molecule inhibitors are taken daily at home. Adherence matters — these drugs work by maintaining continuous suppression of a pathway, so consistency is part of the treatment.

02

Infused monoclonal antibodies.

Infused monoclonal antibodies, given in the day care unit at set intervals.

03

Combination regimens.

Targeted agents are frequently given with chemotherapy, with hormonal therapy, or with immunotherapy, depending on the cancer.

04

Maintenance targeted therapy.

Maintenance targeted therapy, continued after an initial response to hold the disease stable.

05

Treatment at progression.

Where a cancer stops responding, repeat molecular testing may identify a resistance mechanism and a subsequent option.

06

Side-effect management.

Dermatological care for rash, antidiarrhoeal protocols, blood pressure monitoring, and dose modification. Managing toxicity well is often what allows a patient to stay on an effective drug.

07

Structured monitoring.

Structured monitoring with periodic bloods, imaging, and organ-specific tests appropriate to the agent.

Precision Oncology

Personalised Cancer Care at Athira

Targeted therapy is the clearest expression of what precision oncology means in practice — and Athira treats it that way.

01

The starting question is not which drug, but which test.

Choosing the right panel matters: comprehensive sequencing is valuable in some situations and unnecessary in others, and the decision is made based on what could realistically change the plan.

02

Interpretation is where experience shows.

A sequencing report may list many variants, most of which are not clinically meaningful. Distinguishing an actionable driver from background noise is a judgement made at the tumour board, with pathology input, rather than by reading a report in isolation.

03

Delivery is individualised too.

Oral therapy means the patient is managing treatment at home — so dosing instructions, food and drug interactions, what to do about a missed dose, and how to recognise a side effect that needs attention are covered explicitly, not assumed.

04

And the plan is revisited.

Response is monitored, toxicity is managed rather than tolerated, and at progression the question of repeat profiling is raised again.

Athira Healthcare

Why Athira

Precision oncology as a stated commitment. Genomic profiling and molecular-targeted therapy are named among the centre's four core commitments and one of its three pillars.

01

Testing before prescribing.

This follows the NCI's own position that a tumour generally has to be tested before a targeted drug can be used.

02

Molecular findings read in a clinical context.

Reports are reviewed at the multidisciplinary tumour board alongside pathology and imaging, so a result becomes a decision rather than a data point.

03

Research-informed practice.

Dr. Niti Krishna Raizada's involvement as Principal Investigator or Co-Investigator on more than 60 global multicentric trials means direct familiarity with how molecularly selected therapies are studied and applied.

04

Coordination across specialties.

Targeted therapy rarely stands alone. Surgical and radiation oncology are part of the same team.

05

Support for oral therapy at home.

Patients on oral targeted drugs are followed actively rather than simply handed a prescription.

Targeted Therapy

Frequently Asked Questions

How is targeted therapy different from chemotherapy?

+

Chemotherapy acts broadly on fast-dividing cells. Targeted therapy acts on a specific protein that a particular cancer depends on. That is why targeted drugs require testing first — without the target present, the drug has nothing to act on.

Do I need genomic testing before starting?

+

In most cases, yes. The National Cancer Institute states that most of the time your tumour will need to be tested before a targeted drug can be used. Some cancers have routine markers tested at diagnosis; others require a broader panel.

What happens if no target is found?

+

It means targeted therapy is not an option for you at present, and your oncologist will discuss other approaches — chemotherapy, immunotherapy or hormonal therapy, depending on the diagnosis. A negative result still has value: it prevents an ineffective treatment being tried.

Is targeted therapy a tablet or an injection?

+

Both exist. Small-molecule inhibitors are usually taken orally at home; monoclonal antibodies are given by infusion at the centre. Which applies depends on the drug.

Does targeted therapy have side effects?

+

Yes, though they differ from chemotherapy. Skin rash, diarrhoea, mouth soreness, blood pressure changes and liver enzyme changes are among the more common, varying by drug. Most are manageable, and dose adjustment is often enough.

What if I miss a dose of my oral medication?

+

Follow the specific instruction you were given for your drug, as the advice differs between agents. If you are unsure, contact the team rather than guessing or doubling up.

Can targeted therapy be combined with other treatments?

+

Yes. It is frequently given alongside chemotherapy, hormonal therapy or immunotherapy, and may be used before or after surgery or radiation depending on the plan.

How long does targeted therapy continue?

+

Often for as long as it keeps working and remains tolerable. Some regimens run for a defined period; many continue until progression or unacceptable side effects.

What does it mean if the drug stops working?

+

Cancers can develop resistance by adapting around the blocked pathway. Repeat testing — sometimes on blood rather than tissue — may identify the resistance mechanism and point to a further option.

Can genomic testing tell me if my family is at risk?

+

Sometimes. The American Cancer Society notes biomarker testing can reveal inherited mutations that raise cancer risk. If your results suggest this, genetic counselling should be discussed so that testing for relatives can be considered properly.