Prostate Cancer Treatment in Delhi and Gurgaon

prostate cancer information

Prostate is an accessory gland of male reproductive system situated in the pelvis beneath the urinary bladder and anterior to the rectum. It is about the size of a walnut in young males. Its size increases with age, with most rapid increase occurring after puberty (under the influence of androgenic hormones, especially testosterone) until the age of 30 years, approximately.

It provides the passage for urethra through its center and contributes about 25% to the volume of the ejaculate. It also provides a passage for the ejaculatory ducts of the seminal vesicles (a pair of glands situated behind the prostate), which drain their secretions (that make-up most of the semen volume) into the prostatic urethra.

prostate anatomy diagram

It consists of mainly 3 zones: a transition zone (surrounding the urethra and constituting about 10% of the prostate); a central zone (surrounding the ejaculatory ducts and constituting around 25% of the prostate); and a peripheral zone (incompletely covering the other two zones and constituting bulk of the prostate).

Adenocarcinoma (affecting secretory cells of the prostate) is the most commonly encountered (more than 95% of all cases) prostate cancer.

Prostate Cancer Risk Factors

Age

older age

  • Prostate cancer is a disease of old age. Older age men are generally at increased risk of developing prostate cancer.
  • More and more people are being diagnosed with the disease due to increasing life expectancy
  • By 90 years of age 50 to 60% of will have the disease.
  • About 60% of all the incidence of prostate cancer is observed in men older than 65 years of age.

Smoking

tobacco smoking

  • May be a risk factor.
  • Source of cadmium exposure
  • Associated with more advanced stage at diagnosis and increased prostate cancer–related mortality (Bostwick et al, 2004).
  • No clear dose-response relationship

Family history

family history of prostate cancer

Individuals with a history of prostate cancer in close relatives are considered to be at increased risk of developing prostate cancer. Number of people previously affected with the disease increases the risk in other family members.

Family History Relative Risk Absolute Risk (%)
None 1 8
Father or brother 2 15
Father or brother affected < 60 years 3 20
Father and brother 4 30
Hereditary prostate cancer 5 35-45

Genetic alterations

genetic cancer predisposition syndromes

  • Some inherited genetic alterations have been reported to be associated with a high risk of prostate cancer, e.g., Lynch syndrome or hereditary non-polyposis colorectal cancer (HNPCC, generally caused by mutation in the MLH1 or MSH2 gene), mutations in RNASELMSR1HOXB13, and BRCA2 genes, etc.
  • Has both a familial and genetic component.
  • Most prostate cancer is likely to be polygenic in origin
  • The existence of true hereditary prostate cancer is suggested by three epidemiologic observations:
      • relatives of patients younger than 55 years are at higher risk for prostate cancer than are those with older affected relatives;
      • there is stronger familial clustering in families with early-onset prostate cancer
      • the number of affected family members and their age at onset are the most important determinants of risk among relatives.
  • Hereditary prostate cancer accounts for 43% of early-onset disease (55 years of age or younger) but only 9% of all cancers occurring by the age of 85 years (Carter et al, 1992).

Inflammation/Infection

  • Chronic inflammation contributes to the development of infection-associated cancer (Coussens and Werb, 2002 ; Platz and De Marzo, 2004 ).
  • Similar process may underlie the development of prostate cancer.
  • Two meta-analyses examining 34 case-control studies reported statistically significant associations of prostate cancer with a history of sexually transmitted infection (relative risk = 1.4) or prostatitis (odds ratio = 1.57) (Dennis and Dawson, 2002 ; Dennis et al, 2002).
  • Proliferative inflammatory atrophy –characterized by epithelial atrophy, low apoptotic index, and increased proliferative index (Putzi and Marzo, 2000).

Race/Ethnicity

race and ethnicity

  • Western countries has the highest incidence of this disease, highest being in the African American.
  • African-American and Caribbean men are generally at higher risk of developing and dying of prostate cancer.
  • Asian migrated to the western countries have higher incidence than the native.

Overweight or Obese males

obese overweight males

  • Sedentary lifestyle with increasing obesity also increases the risk of prostate cancer. Regular physical activity decreases the mortality and improves outcome in patients with the disease.
  • They are at higher risk of developing an aggressive form of prostate cancer.
  • Severe obesity (BMI ≥ 35) associated with higher grade tumors and higher rates of biochemical failure after radical prostatectomy (Freedland et al, 2004).
  • Higher BMI is associated with lower serum PSA concentration ( Baillargeon et al, 2005 ),

Diet

diet rich in red meat and fats

  • It has been reported that a diet rich in red meat and fats may increase the risk of prostate cancer, while an adequate consumption of vegetables and antioxidants such as vitamin E and selenium may reduce the risk of prostate cancer.
  • Dietary factors may contribute to prostate cancer development ( Bostwick et al, 2004 ).
  • Asians having the lowest rates of clinical prostate cancer.

Alcohol

excessive alcohol consumption

  • No increased risk for prostate cancer among light to moderate drinkers (Breslow and Weed, 1998).
  • A dose-dependent increase in prostate cancer risk highest in those imbibing more than three hard liquor drinks per day (relative risk, 1.85) during a period of 11 years (Sesso et al, 2001).
  • There was no association with wine or beer consumption and prostate cancer risk
  • Conclusion -prostate cancer risk was NOT associated with total alcohol consumption
  • Consumption of one to three glasses of red wine per week had a protective effect (relative risk, 0.82), (Marieke Schoonen et al, 2005).

Vitamin D, Calcium

  • An essential vitamin that is a part of the steroid hormone superfamily
  • Vitamin D as a determinant of prostate cancer risk comes from several epidemiologic observations ( Peehl et al, 2003 ):
      • Men living in northern latitudes -higher mortality rate from prostate cancer.
      • Prostate cancer occurs in older men vitamin D deficiency is more common.
      • African Americans-highest worldwide incidence and mortality rates for prostate cancer.
      • Dietary intake of dairy products rich in calcium- higher risk
      • Native Japanese, whose diet is rich in vitamin D derived from fish, have a low incidence of prostate cancer.

Androgens

  • Androgens influence the development, maturation, and maintenance of the prostate
  • Variable exposure of the prostate to androgens plays an important role in prostate carcinogenesis.
  • Higher incidence of prostate cancer observed in African Americans may be related to elevated levels of circulating androgen.
  • Long-term absence of androgen exposure to the prostate appears to protect against the development of cancer
  • A dose-response relationship between androgen levels and cancer risk has not been established.
  • Androgen concentrations are associated with risk of prostate cancer remains unclear (Hsing, 2001 ; Chen et al, 2003 ; Parsons et al, 2004 ; Platz et al, 2005).

Estrogens

  • Estrogens protect against prostate cancer by inhibition of prostate epithelial cell growth
  • Alternatively, they increase risk by eliciting inflammation in concert with androgens (Naslund et al, 1988) or by the production of mutagenic metabolites.
  • Estrogens receptor-β may play an important role in initiation of prostate cancer.
  • Age-related prostatic disease parallels increases in serum estrogens levels.

Sexual Activity

  • Frequent ejaculation has a protective effect against prostate cancer (RR 0.66 to 0.89), (Giles et al, 2003; Leitzmann et al, 2004). Men reporting 21 or more ejaculations per month in their 20s and 40s, in the previous year, and as a lifetime average -a protective effect (Leitzmann ). The biologic basis for this effect is not known.
  • Men who underwent vasectomy at an early age had a higher risk.
  • 10% increase risk for each additional 10 years since vasectomy (Dennis et al, 2002)

Signs and Symptoms of Prostate Cancer

Symptoms of Local spread

  • Not able to maintain the flow of the urine.
  • Trouble starting urination
  • Increased frequency of urination
  • Blood in urine or semen.
  • Pain while urinating.

Symptoms of Distant spread

  • Pain at one or more bony sites
  • Cough, breathlessness
  • Jaundice

Most common sites of spread of prostate cancer are adrenal gland, bone, liver and lung.

First Sign and Symptom of Prostate Cancer

Initial symptoms of prostate cancer are caused due to interruption of urinary stream leading to incomplete emptying of bladder. This usually leads to symptoms such as-

  • Increased frequency of urination
  • Need to get up at night multiple times to urinate
  • Sense of incomplete voiding
  • Not able to control the flow of urine
  • Dribbling of urine

Also urinary retention may cause infection in urine leading to-

  • Burning sensation in urine
  • Increased frequency of urination
  • Episodes of fever

Symptoms of Advanced Stage Prostate Cancer

Symptoms of advanced disease may be caused due to local involvement of nearby structures and metastasis to distant sites.

Local spread may cause:

  • Increased frequency of micturition
  • Getting up at night multiple times for urination
  • Sense of incomplete emptying of bladder
  • Interrupted steam of urine flow
  • Painful urination
  • Blood in urine or semen

Distant spread may cause:

  • Back pain or pain at bony sites
  • Chest discomfort, cough, breathlessness
  • Yellowish discoloration of eyes and/or urine

Where does it spread? What are the symptoms of metastatic disease?

More commonly prostate cancer metastasis can occur in bones, lymph nodes, lungs, liver, brain, etc. The symptoms of metastatic disease depend on the site of metastasis, along with local symptoms discussed above. These may be one or more of the following-

  • metastasis is most often asymptomatic
  • back pain
  • breathlessness, cough, chest discomfort
  • yellowish discoloration of eyes and/or urinr
  • altered sensorium, headache, vomiting
  • Enlarged lymph nodes, usually pelvic, but rarely supraclavicular or axillary (left-sided)
  • Ascites and pleural effusion are rare
  • Locally extensive cancer -may present with pelvic pain, rectal bleeding or obstruction

How does it feel when you have prostate cancer? Does it make you feel tired?

In addition to the symptoms discussed above, prostate cancer may lead to deep seated, dullness and stiffness in pelvis and lower back, loss of weight and appetite, fatigue, nausea and vomiting. Back pain may be caused due to metastasis or spread of disease to bones of back.

Prostate Cancer Staging Investigations

Digital Rectal Exam (DRE)

digital rectal examination for prostate

  • It is a type of physical examination performed to find any abnormality (bumps or hard areas) in the prostate or nearby structures.
  • In this test, a doctor inserts a lubricated, gloved finger into the rectum via the anus to physically examine the prostate and nearby internal structures.
  • In case of an abnormality, detailed investigations are required to establish the diagnosis of prostate cancer.
  • But it is not very sensitive, and further testing may be required even if it is normal if there is a suspicion of the disease.

PSA (Prostate Specific Antigen) Assay

prostate specific antigen

  • Prostate-specific antigen or PSA is the biomarker for prostate cancer. PSA may be falsely elevated in conditions other than prostate cancer. Most commonly seen are urinary tract infection, bladder catheterization, needle biopsy of prostate and transurethral resection of the prostate.
  • Normal PSAs levels also vary with the age of a person. It is less than 2.5 in 40 to 49 years, less than 3.5 in 50 to 59 years, less than 4.5 in 60 to 69 years and less than 6.5 in 70 to 79 years of age.
  • But we can never be 100% sure just based on PSA. It guides us for further investigations and confirms the disease by DRE, biopsy, and imaging.
  • So to understand it better we come to the free to total PSA ratio. PSA levels of 4 to 10 are overlapping for benign hypertrophy of prostate and prostate cancer, so free to total PSA ratio will help us to differentiate these two conditions. If the ratio is less than 10%, it goes in the favor of cancer. If the ratio is less than 10%, it goes in the favor of cancer.
  • Along with other factors (age, race, and family history), it may help to indicate whether further investigations are required. It can help in determining the overall stage of disease and in determining the appropriate treatment option. It can also be used to assess the efficacy of treatment and disease progression/recurrence.

Transrectal ultrasound (TRUS)

  • TRUS of the prostate, first described by Wantanabe and colleagues (1968)
  • Should be performed in both the transverse and the sagital planes.
  • 39% of all cancers are isoechoic and up to 1% of tumors may be hyperechoic. A hypoechoic lesion is malignant in 17% to 57% of cases ( Frauscher et al, 2002a ),
  • This helps the doctor to examine the prostate along with the nearby structures for any abnormality.
  • This test can measure the size of the prostate or the presence of any abnormalities and can guide a biopsy needle to take biopsy samples from the affected areas.

Prostate Biopsy (TRUS Guided)

TRUS guided prostate biopsy

Indications of TRUS-guided prostate biopsy-

  • Diagnosis of suspected symptomatic prostate cancer (i.e., bone metastasis, cord compression).
  • Screening for prostate cancer in asymptomatic patient > age 50 with > a 10-year life expectancy (if strong family history or if African American, consider screening at age 45).
  • Prostate nodule or significant prostate asymmetry regardless of PSA level.
  • PSA > 4.0 ng/dL regardless of age. In men < age 60-65 years, consider biopsy if PSA > 2.5 ng/dL. If PSA > 0.6 ng/dL at age 40.
  • Increased PSA velocity (>0.75-1.0 ng/dL/yr)
  • Prior to intervention in symptomatic benign prostatic hyperplasia (e.g., surgical therapy or initiation of 5α-reductase inhibitors)
  • Prior to cystoprostatectomy or orthotopic urinary diversion
  • To diagnose failed radiation therapy before use of second-line therapy
  • Follow-up biopsy (3-6 mo) after diagnosis of high-grade PIN or ASAP

Imaging Tests

One or more of the following imaging investigations are required to stage the disease and reassess following treatment-

Computed tomography (CT) scan and Magnetic Resonance Imaging (MRI)

CT Scan

  • not routinely recommended
  • low sensitivity
  • may be appropriately reserved for high-risk patients (those with locally advanced disease by DRE, a PSA greater than 20 ng/mL, or men with poorly differentiated cancer on needle biopsy).
  • Intravenous urography is rarely obtained to stage prostate cancer
  • chest radiograph is a low-yield examination

PSMA (Prostate Specific Membrane Antigen) Positron emission tomography (PET) scan

  • This is useful for staging of prostate cancer.
  • Better sensitivity and specificity compared to FDG-PET, in cases of prostate cancer.

Bone Scan

bone scan

  • In this test, a radioactive material is injected into the vein of the patient, which gets accumulated in the areas of bones affected by the disease, which are then detected with the help of radioactivity detectors. In this way, it may help to detect the spread of cancer to bones.
  • Most sensitive modality for the detection of skeletal metastases (Schaffer and Pendergrass, 1976 ; Gerber and Chodak, 1991 ; Terris et al, 1991).
  • Skeletal radiography is obtained only to confirm a positive bone scan in men at low risk for bone metastases.
  • Bone metastases at diagnosis are rare in men without bone pain  the routine use of bone scans in this population may not be useful.
  • Bone scans are not routinely obtained for patients with PSA levels less than 10 ng/mL and no bone pain.

Stages of Prostate Cancer

We will start with the normal prostate anatomy. It lies in the pelvic region below the urinary bladder and urethra passes through it, causing an obstruction on enlargement.

Below the prostate lies the perineal body which acts as the urethral sphincter and controls the passage of urine.

Above lies, the urinary bladder and rectovesical pouch and rectum and anal canal lie behind the prostate.

applied anatomy of prostate

TNM is the most commonly used staging system for prostate cancer. It uses mainly 5 parameters: “T” stands for “Tumor”; “N” for “Lymph Nodes”; and “M” for “Metastasis”. the PSA level; and the Grade group (based on the Gleason score). Numbers and/or letters after T (0, 1a, 1b, 1c, 2a, 2b, 2c, 3a, and 3b), N (0 and 1), and M (0 and 1) provide more details about each of these parameters.

PSA level is indicated in nanograms per milliliter (ng/mL). Grading (1 to 5) is assessed based on Gleason score (as described below).

T Staging

T1 – It is clinically inapparent disease with no abnormality on palpation or imaging. It maybe an incidental finding on excision of prostate done for some other reason or it maybe diagnosed after biopsy of prostate done for elevated PSA.

 
T2 disease is localized to the prostate. It may be diagnosed with palpation or imaging. It is called as T2a when it occupies less than half of one lobe of the prostate.
T2a stage-localised to less-than-half of one lobe of prostate
 
T2b if it occupies more than 50% of one lobe of the prostate.
T2b stage-occupies more than half of one lobe of prostate
 
Remember that all cases of the T2 disease are confined to the prostate.
 
Extracapsular extension of the tumor without any external organ infiltration is called as T3a.
T3a stage - extracapsular extension
And an extracapsular extension to involve seminal vesicles is called as T3b.
T3b stage-extracapsular extension to seminal vesicles
T4 disease is infiltration of the adjacent organs. In this figure, the tumor infiltrates the perineal body.
 
T4 - tumor infiltrates the perineal body Here it extends posteriorly to involve the rectum.
 
T4 stage involves the rectum And here it extends superiorly to infiltrate the urinary bladder.
 
T4, extends posteriorly to urinary bladder It may also extend laterally to involve the pelvic wall.
 

T4, extends to pelvic wall

N Staging

N0 – No spread of tumor to nearby lymph nodes

N1 – Tumor has spread to regional lymph nodes

M Staging

M0 – No spread of tumor to distant body parts

M1 –  Spread to a distant body parts such as bones, lungs, liver, brain, etc.

Gleason’s Scoring and Grading for Prostate Cancer

Gleason scoring system involves scoring of prostate cancer based on the extent of abnormality observed in the collected biopsy samples (usually the Gleason score ranges from 3 to 5 for a single biopsy sample).

Since prostate cancer is a multifocal disease, the score for different biopsy samples collected from the same patient may differ. Thus, score of specimen with most predominant Gleason score is added to the highest Gleason score observed, to give overall Gleason score (that may range from 6 to 10). Further, Gleason grade groups (1 to 5) are derived according to the following table:
 
Gleason Grade Group Gleason Score Gleason Pattern
1 </=6 </=3+3
2 7 3+4
3 7 4+3
4 8 4+4, 5+3, 3+5
5 9 or 10 4+5, 5+4, 5+5

What are the 4 Stages of Prostate Cancer?

Once T, N, M, PSA, and grade group are determined through different diagnostic techniques, this information is combined to assign an overall stage (from 0 to IV) to the disease.

Stage TNM Score, PSA (ng/mL), Grade Group (GG)
I T1a-2 N0 M0 PSA<10 GG=1
IIA T1a-2a N0 M0 PSA>/=10,<20 GG=1
  T2b-2c N0 M0 PSA<20 GG=1
IIB T1-2 N0 M0 PSA<20 GG=2
IIC T1-2 N0 M0 PSA<20 GG=3-4
IIIA T1-2 N0 M0 PSA>/=20 GG=1-4
IIIB T3-4 N0 M0 Any PSA GG=1-4
IIIC Any T N0 M0 Any PSA GG=5
IVA Any T N1 M0 Any PSA Any GG
IVB Any T Any N M1 Any PSA Any GG

Survival according to Stage of Prostate Cancer

It is calculated based on whether the disease is Localised, Regional or Dstant.

Localised

  • Cancer is limited to the prostate.
  • 5 year survival nearly 100%.

Regional

  • Cancer has spread to nearby structures or lymph nodes
  • 5 year survival nearly 100%.

Distant

  • Cancer has spread to distant body parts.
  • 5 year survival 31%

Treatment of Prostate Cancer

This is the prostate cancer natural history. As you can see in the figure it progresses very slowly and the patient may survive for years after diagnosis. prostate cancer natural history The first peak correlates with localized disease and is treated with local therapy in most of the cases. We will discuss this in detail later.

The second peak correlates with recurrence after local therapy or metastatic disease. It is treated with local or systemic therapy.

The third peak correlates with the castrate-resistant prostate cancer, that is the disease which has progressed on hormonal therapy. It is usually treated with chemotherapy but other agents may also be used.

Androgen Deprivation Therapy or Hormonal Therapy for Prostate Cancer

Hormonal therapy, also known as androgen suppression therapy or androgen deprivation therapy (ADT), is one of the most effective and most widely used therapy option for Prostate cancer. Hormonal therapy consists of various drugs that act by decreasing the concentration of androgens in the blood or by inhibiting the stimulatory action of androgens on the prostate cancer cells.

ADT is the most commonly used primary systemic therapy for the management of localized or advanced prostate cancer. It can be employed as neoadjuvant (prior to surgery or radiation), concomitant (in combination with surgery or radiation), or adjuvant (after surgery or radiation) therapy for the management of locally advanced or metastatic (that has spread to distant body parts like bones, liver, lungs, or brain) prostate cancers.

Androgen deprivation therapy The pituitary gland releases LH and FSH, which directly acts on the testis to release testosterone. ACTH released from the pituitary gland acts on the adrenal gland to release DHEA, which subsequently gets converted into testosterone.

The testosterone released from testis and adrenal gland enters the prostate cell and gets converted into DHT which causes the growth and survival of prostate cancer cells.

GnRH agonists/antagonists (Leuprolide, Goserelin, Dagarelix)

These act on the pituitary gland and prevent the release of LH/FSH and ACTH as shown in the figure below.

GnRH agonists or antagonists

Cytochrome 17P Inhibitors

These prevent the release of testosterone from testes and adrenal gland as shown below. Cytochrome P450 type 17(CYP17), an enzyme required for the secretion of androgen from the adrenal glands.

Cytochrome 17P Inhibitors prevent the release of testosterone from testes and adrenal gland as shown below.

cytochrome 17P inhibitor

Abiraterone has been approved, in combination with low-dose prednisone, for the treatment of the asymptomatic patients with metastatic CRPC who have not received prior chemotherapy or patients with metastatic CRPC who have initially received the docetaxel-containing chemotherapy. abiraterone

Androgen Receptor Blockers (Bicalutamide, Nilutamide, Enzalutamide)

These prevent the binding of testosterone on androgen receptors on prostate cancer cells, thereby reducing their growth and survival. androgen receptor blockers

Enzalutamide has been approved as the first-line treatment for the asymptomatic patients with metastatic CRPC who have not received prior chemotherapy or subsequent-line treatment for patients who have received prior docetaxel-containing chemotherapy. enzalutamide Another method for androgen deprivation is surgical castration in which both testes are removed. Unlike medical construction, it is a one-time procedure.  

Treatment of Hormone Sensitive Prostate Cancer

The prostate cancer treatment depends on patient’s performance status, life expectancy, comorbidities,  stage of the disease, along with other factors. For hormone naive disease, the treatment decision is taken based on the risk of the disease.

Very Low to Low-Risk Disease

T1a-2 N0 M0, PSA<10, GG=1

Active surveillance is the preferred treatment approach in such cases.

Intermediate-Risk Disease

T2b-2c N0 M0 PSA<20 GG=1  TO  T1-2 N0 M0 PSA<20 GG=3-4

Active surveillance is the preferred treatment for elderly, comorbid patients with less than 10 years of life expectancy. Whereas, radical prostatectomy and/or radiotherapy is recommended for younger patients with good performance status and better life expectancy. Androgen deprivation therapy may also be required in some cases. Chemotherapy is also an option for some cases.

High-Risk Disease

T1-2 N0 M0 PSA>/=20 GG=1-4 TO Any T N0 M0 Any PSA GG=5

In high risk disease, radical prostatcetomy or radiotherapy is the standard treatment. Androgen deprivation therapy may be added. Chemotherapy is also an option for some cases. In case of an elderly patient with poor life expectancy, androgen deprivation therapy or active surveillance may be considered.

Metastatic Disease

Low volume metastasis can be treated with androgen deprivation therapy with or without radiotherapy. Chemotherapy may also be considered. For high volume metastatic disease with a vast spread of disease to distant organs, chemotherapy plus androgen deprivation therapy is the standard treatment.

Difference between Observation and Active Surveillance

These are the options mainly in early stages of disease. Observation is preferred when the life expectancy of the patient is less than 10 years. PSA is done every 6 to 12 months for an initial 5 years, and then annually. Active surveillance is done when the life expectancy of the patient is more than 10 years. In this, PSA is done every 6 months and DRE, prostate biopsy and MRI pelvis are done annually.

Treatment of Castrate Resistant Prostate Cancer

After some years of starting androgen deprivation therapy, PSA may start rising, or there may be a disease progression on scans. This state is called as castrate-resistant prostate cancer.

If the patient has localized CRPC, then the treatment options are the observation or androgen deprivation therapy with a different agent that used previously.

And for metastatic CRPC, the treatment options are androgen deprivation therapy, chemotherapy, cancer vaccine or bone-directed therapy.

CRPC is the disease which has progressed on GnRH analogs, so non-GnRH analogs are used for the treatment, such as androgen receptor blockers or 17 hydroxylase inhibitors.

Treatment of Recurrent Prostate Cancer

The second peak correlates with recurrence after local therapy or metastatic disease. We will discuss it one by one. Recurrence after surgery may be in the form of PSA persistence, that is a failure to fall to normal, or PSA recurrence, that is, rising after becoming undetectable.

And recurrence after radiation therapy may be in the form of rise in PSA or positive DRE. For localized recurrence, the treatment options are observation, surgery if initially treated with radiotherapy, radiotherapy if initially treated with surgery and androgen deprivation therapy.

And for metastatic recurrence, androgen deprivation therapy is the mainstay of treatment. The patients who present directly with metastatic disease are treated directly with hormonal therapy and chemotherapy may be added in some patients who present with high volume disease.

When we use androgen deprivation therapy for the first time for localized, metastatic or recurrence after local therapy, it may be in form of medical or surgical castration. GnRH agonists or antagonists are used for medical castration, and for surgical castration, both the testes are removed, called as bilateral orchiectomy.

Immunotherapy for Prostate Cancer

Immunotherapy act by stimulating the immune system to kill and destroy cancer cells. It is a type of cancer treatment that enhances the body’s own immune system to fight effectively against cancer. Following are the immunotherapeutic agents which are approved for the treatment of advanced-stage prostate cancer.

Sipuleucel-T

It is the only approved cancer vaccine for the treatment of prostate cancer. Similar to conventional vaccines that stimulate the immune system to fight against specific infections, Sipuleucel-T stimulates the immune system to attack the prostate cancer cells. It is an autologous vaccine, that is, it is made from man’s own immune cells.

The patient’s white blood cells are first removed using a process called leukapheresis. The cells are then exposed to prostatic acid phosphatase (PAP), a glycoprotein enzyme normally produced by the prostate cells, which is usually elevated in patients with metastatic prostate cancer and is generally associated with poor prognosis. The cells are then infused back to the patient.

This process is generally repeated 2 more times, 2 weeks apart, to deliver a total of 3 doses. The modified white blood cells attack and kill the prostate cancer cells. Sipuleucel-T has been approved for the treatment of asymptomatic or minimally symptomatic patients with metastatic CRPC with no liver metastases, life expectancy >6 months, and ECOG performance status 0-1 (overall in good health).

Pembrolizumab

pembrolizumab

It is an anti-PD1 antibody or commonly known as an immune-checkpoint inhibitor. It acts by preventing the interaction of immune-checkpoint with its ligands and thereby removing the breaks from the immune cells that attack and kill the cancer cells.

It has been approved for the treatment of patients with unresectable or metastatic microsatellite instability-high (MSI-H) or mismatch repair (MMR)-deficient solid tumors (including prostate cancer) who have progressed on prior treatment and who do not have a satisfactory alternative treatment option available.

Role of Radiopharmaceuticals in the treatment of Prostate cancer

Various radiopharmaceuticals (e.g. Radium-223, Strontium-89, and Samarium-153) are used for the palliation of pain due to bone metastasis that commonly occurs in the case of advanced-stage prostate cancer.

Radium-223

It is an alpha particle-emitting radioactive agent, which is preferentially taken up by rapidly growing bone cells within the metastatic bone lesions due to its chemical similarity with calcium. Within the metastatic bone lesions, Ra-223 kills cancer cells by emitting alpha-rays and inducing double-strand DNA breaks.

Thus, Ra-223 has a specific action against bone metastases resulted from prostate cancer and helps in improving the survival of patients with CRPC and bone metastasis. It has been approved for treatment of metastatic CRPC in patients with symptomatic bone metastases and no known visceral metastases. It can be safely combined with secondary hormonal therapy drugs approved for the treatment of metastatic CRPC, e.g. abiraterone or enzalutamide.

Strontium-89 (89Sr) and Samarium-153 (153Sm)

These are beta-emitting radiopharmaceuticals that specifically target bone metastases in prostate cancer. The beta-emitters do not have a survival advantage as that of Ra-223 but can be used for the palliation of pain associated with wide-spread bone metastases. These agents provide significant pain relief with minimum side effect compared to other palliative treatments in patients with multifocal bone pain and who are not the candidate for chemotherapy.

Best Prostate Cancer Specialist in Delhi

Dr Sunny Garg is a renowned Medical Oncologist in New Delhi with an experience of around 10 years of treating prostate cancer patients. He has treated prostate cancer patients with Chemotherapy, Androgen Deprivation Therapy, Hormonal Therapy, Cytochrome 17p Inhibitors, Androgen Receptor Blockers, Targeted Therapy, Immunotherapy and Personalized Cancer Treatment. He is currently practicing at Manipal Hospital, Dwarka.

Diagnostic modalities available at our hospital include Whole Body PSMA PET CT Scan, Transrectal Ultrasound Guided Prostate Biopsy, Prostate Specific Antigen, etc. Other treatment facilities for Prostate Cancer available are Radical Prostatectomy, Transurethral Resection of the Prostate, Pelvic Lymphadenectomy, Laproscopic Prostatectomy, Retropubic Prostatectomy, etc.

Call +91 9686813020 for appointment.