Tumor markers are substances produced by tumor cells or the body's response to tumors that can be detected and measured in bodily fluids or tissues. They can help diagnose certain cancers, distinguish between benign and malignant tumors, monitor treatment response and detect recurrence. However, no single tumor marker is perfect as tumor marker levels can also be elevated in some non-cancerous conditions.
A wonderful slide for tumor markers in GI surgery. Cancer biomarkers are often used in monitoring response in cancer.
Tumor marker, biomarkers in common practice.
Tumour Markers are substances present in the tumour, produced by the tumour or by the host as a response to the presence of the tumour, providing information about biological characteristics of the tumour. these tumour markers may specific for the tissue but often get elevated in neoplastic as well non-neoplastic lesions, further Various analytical platforms available for serum tumour markers lack standardisation. These factors add to interpretative challenges in serum tumour markers
A wonderful slide for tumor markers in GI surgery. Cancer biomarkers are often used in monitoring response in cancer.
Tumor marker, biomarkers in common practice.
Tumour Markers are substances present in the tumour, produced by the tumour or by the host as a response to the presence of the tumour, providing information about biological characteristics of the tumour. these tumour markers may specific for the tissue but often get elevated in neoplastic as well non-neoplastic lesions, further Various analytical platforms available for serum tumour markers lack standardisation. These factors add to interpretative challenges in serum tumour markers
Tumor markers
Many cancers are associated with the abnormal production of some molecules which can be measured in plasma. These molecules are known as tumor markers.
A good tumor maker should have those properties:
1. A tumor marker should be present in or produced by tumor itself.
2. A tumor marker should not be present in healthy tissues.
3. Plasma level of a tumor marker should be at a minimum level in healthy subjects and in benign conditions.
4. A tumor marker should be specific for a tissue, it should have different immunological properties when it is synthesized in other tissues.
5. Plasma level of the tumor marker should be in proportion to the both size of the tumor and the activity of the tumor.
6. Half-life of a tumor should not be very long
7. A tumor marker should be present in plasma at a detectable level, even though tumor size is very small
Tumor Biomarkers For Screening, Progression and Prognosis Vivek Misra
Tumor markers are substances that can be found in the body (usually in the blood or urine) when cancer is present. Along with other tests, tumor markers can be used to help show if cancer is present, to determine the type of cancer, and in some cases to help show if treatment is working. Some of the more common tumor markers are discussed here.
Tumor markers are substances, such as proteins, biochemicals, hormones or enzymes, produced by tumor cells or by the body in response to tumor cells. As tumor cells multiply, cancer spreads, and tissue is damaged, these substances increase and leak into the bloodstream. Tumor marker levels in blood help physicians evaluate people for certain types of cancer
Tumor markers
Many cancers are associated with the abnormal production of some molecules which can be measured in plasma. These molecules are known as tumor markers.
A good tumor maker should have those properties:
1. A tumor marker should be present in or produced by tumor itself.
2. A tumor marker should not be present in healthy tissues.
3. Plasma level of a tumor marker should be at a minimum level in healthy subjects and in benign conditions.
4. A tumor marker should be specific for a tissue, it should have different immunological properties when it is synthesized in other tissues.
5. Plasma level of the tumor marker should be in proportion to the both size of the tumor and the activity of the tumor.
6. Half-life of a tumor should not be very long
7. A tumor marker should be present in plasma at a detectable level, even though tumor size is very small
Tumor Biomarkers For Screening, Progression and Prognosis Vivek Misra
Tumor markers are substances that can be found in the body (usually in the blood or urine) when cancer is present. Along with other tests, tumor markers can be used to help show if cancer is present, to determine the type of cancer, and in some cases to help show if treatment is working. Some of the more common tumor markers are discussed here.
Tumor markers are substances, such as proteins, biochemicals, hormones or enzymes, produced by tumor cells or by the body in response to tumor cells. As tumor cells multiply, cancer spreads, and tissue is damaged, these substances increase and leak into the bloodstream. Tumor marker levels in blood help physicians evaluate people for certain types of cancer
A tumor marker is a substance present in or produced by a tumor or by the tumor’s host in response to the tumor’s presence that can be used to differentiate a tumor from normal tissue or to determine the presence of a tumor based on measurement in the blood or secretions.
Tumor markers (also known as biomarkers) are substances found at higher than normal levels in the blood, urine, or body tissue of some people with cancer. Although cancer cells often produce tumor markers, other healthy cells in the body produce them as well.
Concept: reannealing nucleic acids to identify sequence of interest.
Separates DNA/RNA in an agarose gel, then detects specific bands using probe and hybridization.
Hybridization takes advantage of the ability of a single stranded DNA or RNA molecule to find its complement, even in the presence of large amounts of unrelated DNA.
Allows detection of specific bands (DNA fragments or RNA molecules) that have complementary sequence to the probe.
Size bands and quantify abundance of molecule.
Biomarkers have a diversified role in diagnosis, prognostication and risk stratification. This presentation aims to compile the basic information and new literature on various biomarkers pertaining to cancer care.
The presentation aims to be of introductory level. Classification of tumor markers along with brief description of selected tumor markers are provided.Applications and methods are listed but not discussed at length.
PREDICTIVE AND DIAGNOSTIC BIOMARKERS FOR OVARIAN CANCERDr. Girija Wagh
OVARIAN CANCER HAS ELUDED SCREENING AND EARLY DETECTION . SEVERAL BIOMARKERS ARE PROPOSED AND HERE IS A AN UPDATED REVIEW OF WHAT EXISTS IN THE CURRENT CLIMATE FOR THE SAME Ovarian carcinomas relate to highest death rate in gynecologic malignancies as absence of symptoms shield the disease in the early stage. Current evidences have been devoted to discovering early effective screening mechanism prior to the onset of clinical symptoms.Serum biomarkers may aid in the diagnosis of Early ovarian cancer
Distinguish malignant from benign disease
Prevent unnecessary surgery
Improve rates of early detection. Prof Girija Wagh is the Head of the Department of OBG at Bharati University Medical College and Hospital and a well acknowledged teacher and a researcher.This overview will certainly help the learners to approach this condition with more promise
Instructions for Submissions thorugh G- Classroom.pptxJheel Barad
This presentation provides a briefing on how to upload submissions and documents in Google Classroom. It was prepared as part of an orientation for new Sainik School in-service teacher trainees. As a training officer, my goal is to ensure that you are comfortable and proficient with this essential tool for managing assignments and fostering student engagement.
Operation “Blue Star” is the only event in the history of Independent India where the state went into war with its own people. Even after about 40 years it is not clear if it was culmination of states anger over people of the region, a political game of power or start of dictatorial chapter in the democratic setup.
The people of Punjab felt alienated from main stream due to denial of their just demands during a long democratic struggle since independence. As it happen all over the word, it led to militant struggle with great loss of lives of military, police and civilian personnel. Killing of Indira Gandhi and massacre of innocent Sikhs in Delhi and other India cities was also associated with this movement.
A Strategic Approach: GenAI in EducationPeter Windle
Artificial Intelligence (AI) technologies such as Generative AI, Image Generators and Large Language Models have had a dramatic impact on teaching, learning and assessment over the past 18 months. The most immediate threat AI posed was to Academic Integrity with Higher Education Institutes (HEIs) focusing their efforts on combating the use of GenAI in assessment. Guidelines were developed for staff and students, policies put in place too. Innovative educators have forged paths in the use of Generative AI for teaching, learning and assessments leading to pockets of transformation springing up across HEIs, often with little or no top-down guidance, support or direction.
This Gasta posits a strategic approach to integrating AI into HEIs to prepare staff, students and the curriculum for an evolving world and workplace. We will highlight the advantages of working with these technologies beyond the realm of teaching, learning and assessment by considering prompt engineering skills, industry impact, curriculum changes, and the need for staff upskilling. In contrast, not engaging strategically with Generative AI poses risks, including falling behind peers, missed opportunities and failing to ensure our graduates remain employable. The rapid evolution of AI technologies necessitates a proactive and strategic approach if we are to remain relevant.
2024.06.01 Introducing a competency framework for languag learning materials ...Sandy Millin
http://sandymillin.wordpress.com/iateflwebinar2024
Published classroom materials form the basis of syllabuses, drive teacher professional development, and have a potentially huge influence on learners, teachers and education systems. All teachers also create their own materials, whether a few sentences on a blackboard, a highly-structured fully-realised online course, or anything in between. Despite this, the knowledge and skills needed to create effective language learning materials are rarely part of teacher training, and are mostly learnt by trial and error.
Knowledge and skills frameworks, generally called competency frameworks, for ELT teachers, trainers and managers have existed for a few years now. However, until I created one for my MA dissertation, there wasn’t one drawing together what we need to know and do to be able to effectively produce language learning materials.
This webinar will introduce you to my framework, highlighting the key competencies I identified from my research. It will also show how anybody involved in language teaching (any language, not just English!), teacher training, managing schools or developing language learning materials can benefit from using the framework.
Francesca Gottschalk - How can education support child empowerment.pptxEduSkills OECD
Francesca Gottschalk from the OECD’s Centre for Educational Research and Innovation presents at the Ask an Expert Webinar: How can education support child empowerment?
Acetabularia Information For Class 9 .docxvaibhavrinwa19
Acetabularia acetabulum is a single-celled green alga that in its vegetative state is morphologically differentiated into a basal rhizoid and an axially elongated stalk, which bears whorls of branching hairs. The single diploid nucleus resides in the rhizoid.
The Roman Empire A Historical Colossus.pdfkaushalkr1407
The Roman Empire, a vast and enduring power, stands as one of history's most remarkable civilizations, leaving an indelible imprint on the world. It emerged from the Roman Republic, transitioning into an imperial powerhouse under the leadership of Augustus Caesar in 27 BCE. This transformation marked the beginning of an era defined by unprecedented territorial expansion, architectural marvels, and profound cultural influence.
The empire's roots lie in the city of Rome, founded, according to legend, by Romulus in 753 BCE. Over centuries, Rome evolved from a small settlement to a formidable republic, characterized by a complex political system with elected officials and checks on power. However, internal strife, class conflicts, and military ambitions paved the way for the end of the Republic. Julius Caesar’s dictatorship and subsequent assassination in 44 BCE created a power vacuum, leading to a civil war. Octavian, later Augustus, emerged victorious, heralding the Roman Empire’s birth.
Under Augustus, the empire experienced the Pax Romana, a 200-year period of relative peace and stability. Augustus reformed the military, established efficient administrative systems, and initiated grand construction projects. The empire's borders expanded, encompassing territories from Britain to Egypt and from Spain to the Euphrates. Roman legions, renowned for their discipline and engineering prowess, secured and maintained these vast territories, building roads, fortifications, and cities that facilitated control and integration.
The Roman Empire’s society was hierarchical, with a rigid class system. At the top were the patricians, wealthy elites who held significant political power. Below them were the plebeians, free citizens with limited political influence, and the vast numbers of slaves who formed the backbone of the economy. The family unit was central, governed by the paterfamilias, the male head who held absolute authority.
Culturally, the Romans were eclectic, absorbing and adapting elements from the civilizations they encountered, particularly the Greeks. Roman art, literature, and philosophy reflected this synthesis, creating a rich cultural tapestry. Latin, the Roman language, became the lingua franca of the Western world, influencing numerous modern languages.
Roman architecture and engineering achievements were monumental. They perfected the arch, vault, and dome, constructing enduring structures like the Colosseum, Pantheon, and aqueducts. These engineering marvels not only showcased Roman ingenuity but also served practical purposes, from public entertainment to water supply.
Welcome to TechSoup New Member Orientation and Q&A (May 2024).pdfTechSoup
In this webinar you will learn how your organization can access TechSoup's wide variety of product discount and donation programs. From hardware to software, we'll give you a tour of the tools available to help your nonprofit with productivity, collaboration, financial management, donor tracking, security, and more.
Macroeconomics- Movie Location
This will be used as part of your Personal Professional Portfolio once graded.
Objective:
Prepare a presentation or a paper using research, basic comparative analysis, data organization and application of economic information. You will make an informed assessment of an economic climate outside of the United States to accomplish an entertainment industry objective.
2. Tumor markers are the substances that can be
detected in higher than normal amounts in the
serum, urine, nipple aspirate fluid or tissues of
patients with certain types of cancer
Poduced either by cancer cells themselves or by
the body as a response to the cancer.
3. Tumor markers are indicators of cellular,
biochemical, molecular or genetic
alterations by which neoplasia can be
recognized.
A substance, released in to the circulation
by tumor tissue, whose detetion in the
serum indicates the presence of tumor.
4. Three defining characteristics
1. Expressed exclusively by the tumor
2. Collection of specimen for the tumor
marker assay is easy
3. The assay itself is
Reproducible
Rapid
Inexpensive
Currently there is no one tumor marker fulfills all these criteria
5. Diagnostic
Distinguish benign from malignant disease
Correlate with the amount of tumor
(Tumor burden)
Allow subtype classification
Allow accurate staging
Prognostic
Guide choice of therapy
Predict response to therapy
7. Protein tumor markers
First type of tumor markers identified
Called as classic tumor markers
Poor sencitivity & specificity
Serum/plasma concentrations correlate
with tumor burden as they are shed from
the expanding neoplasm.
8. DNA Base tumor markers
Single nucleotide polymorphisms (SNPs)
Chromosomal translocations bcr-abl 9:22 (philadelphia) (CML)
Changes in DNA copy number
Microsatellite instability
Epigenetic changes (e.g., differential promotor region methylation
RNA Based markers
Overexpressed/ underexpressed transcripts
Regulatory RNA (e.g., micro-RNA
11. Tumor marker Cancer Non-neoplastic
condition
Prostate specific antigen
(PSA)
Prostate cancer Prostatis
Prostatic hypertrophy
Neuron – specific enolase Small cell cancer of lung
Neuroblastoma
Lactate dehydrogenase Lymphoma
Ewing’s Sarcoma
Hepatitis
Hemolytic anemia
Many others
12. Tumor marker Cancer Non-neoplastic conditions
Prostate specific antigen Prostatic cancer Prostatitis
Prostatic hypertrophy
Monoclonal immunoglobulin Myeloma Infection
MGUS
CA – 125 Ovrian cancer
Some Lymphomas
Menstruation
Peritonitis
Pregnancy
CA – 19-9 Ca Colon
Ca Pancreas
Ca Breast
Pancreatitis
Ulcerative colitis
CA 15-3 Ca Breast
Ca 72-4 Ca stomach
CD 30 Hodgkin’s disease
Anaplastic large cell lymphoma -
CD 25 Hairy cell leukemia
13. Most studied tumor marker
Onco-fetal protein
Normally present during fetal life
Low concentrations in healthy adults
Structurally
• Glyco-protein
• Molecular weight – 200 kd
• Component of the glycocalyx in cell membrane, located on the luminal
side of the normal intestinal epithelial cells
14. Secreted in to the circulation
Found in mucous secretions of
Exact function unknown
Involved in inhibition of apoptosis
• By anchoring the cell to the ECM
Stomach
Small intestine
Biliary tree
15. Testing Immunoassay
Normal serum levels
• Non smokers 0.0 to 3.4 ng/ml
• Smokers 5 ng/ml
Borderline
2.5 ng/ml – 5 ng/ml
• Benign disorders
Inflammatory bowel disease
Pancreatitis
Cirrhosis
COPD
Elevated >5 ng/ml
• Carcinome colon, pancreas, lung, breast, ovary
• 75 % of the patients with recurrent colo rectal cancers elevate CEA levels before developing
the symptoms
16. Screening
low sensitivity
• early stage diseases – elevated CEA – 5% - 40 %
Prognosis
• Reflect burden of tumor
• Stage of the disease
• Elevated Pre-op level - Predictor of poor survival
& recurrence
17. Monitoring
Recurrent disease
Metastasis
• Hepatic
• Retroperitoneal
• Local
• Pulmonary
• peritoneal
Sensitive
Less sensitive
75 % of the patients with recurrent colo rectal cancers elevate CEA levels
before developing the symptoms
18. Oncofetal antigen
Single chain poly-peptide
Molecular weight – 700 kd
Elevated levels in fetus, pregnancy
decrease sharply after birth
Synthesized by Hepatocytes
Endodermally derived GI tissue
19. Testing
Immuno assay/ RIA
Normal
< 15 ng/ml
Elevated
• HCC
• non-seminiferous testicular cancer
10 to 20% HCC do not have detectable AFP levels
Elevated in non cancer conditions
• Hepatitis
• Inflammatory bowel disease
• cirrhosis
20. Screening
Sensitivity 25% to 75%
Specificity 76% to 94%
Positive predictive value 9% to 50%
Combination of AFP & USG improves the efficacy of the
screening
In combination with β-HCG useful in classification &
monitoring therapy of non-seminiferous testicular carcinomas
22. Monitoring
AFP level drop < 10 ng/ml, after complete resection
If AFP does not drop below 20 ng/ml potoperatively
suspect early recurrence.
AFP levels decline in response to effective
chemotherapy.
Ineffective chemotherapy can be avoided with AFP
monitoring
23. Mucin type glycoprotein expressed on the surface of
the pancreatic cells
Normally present within the biliary tree
Both acute/ chronic biliary tract disease can elevate CA
19-9 levels.
Widely used Serum tumor marker for Ca pancreas
Not a diagnostic marker
Limited use in monitoring the response to therapy
24. Testing
Immunoassay
Normal 37 U/ml
Pancreatic cancer
• Sensitivity 67% to 92%
• Specificity 68% to 92%
Limitations
Patients with –ve Lewis blood group antigen (10% of the population) can not synthesize CA
19-9
Benign biliary tract disease can have up to 400 U/ml (significant number of acute/ chronic
pancreatitis)
Elevated in other cancers Biliary tree - 95%
Stomach – 5%
Colon – 15%
HCC – 7%
Lung – 13%
25. Screening
Not a useful screening modality
Low sensitivity in early stage disease
With increasing levels diagnosis of pancreatic cancer
becomes more accurate
> 1000 U/ml almost diagnostic of pancreatic cancer
Not useful in distinguishing benign from malignant
distal CBD strictures.
26. Prognosis
Levels correlate with the tumor burden
> 95% of unresectable have > 1000 U/ml
Whose levels returned to normal after
curative resection survived longer than those
whose levels fell but never normalized.
27. Monitoring
Serial monitoring
Raised levels after curative resection precede
clinical/ CT evidence of recurrence by 2 to 9
months
Failure of CA 19-9 levels to fall with chemotherapy
reflects poor tumor response.
28. Serine protease – formed in the prostatic
epithelium and secreted in to the prostatic
ducts
Function
• To digest the gel that is formed in seminal fluid after
ejaculation
Under normal circumstances - only small
amount of PSA leak in to the circulation
29. • There are 2 major circulating forms of
PSA:
Free
Complexed:
Complexed to 1-antichymotrypsin or 2-macroglobulin
30. Serum PSA increase
• With enlargement of the gland (BPH)
• Distortion of its architecture
PSA is considered as a tissue specific marker than
prostate cancer specific marker.
Useful marker
• Curative radical prostatectomy
31. Testing
Normal range – increase with age
• 2.5 ng/ml – 40 to 49 yr
• 3.5 ng/ml - 50 to 59 yr
• 4.5 ng/ml - 60 to 69 yr
• 6.5 ng/ml – 70 yr or older
• Rate of PSA increase in a normal 60 yr old – 0.04 ng/ml/yr
Intermediate
• 4 to 10 ng/ ml
Suspicious for malignancy
• . 10 ng/ ml
33. PSA Density
Higher PSA densities are more suggestive
of malignancy than BPH
PSA
Prostatic volume
=
34. PSA Velocity (PSA slope)
Rate of change in the concentration of PSA over time
Individuals with initial levels lower than 4 ng/ml a PSA
slope greater than 0.75 ng/ml/yr is significant
Individuals with initial levels higher than 4 ng/ml a PSA
slope greater than 0.4 ng/ml/yr is significant
35. Screening
Widely used as screening tool for Ca Prostate
Enables early detection & diagnosis
Risk of over diagnosis
• Autopsy studies
Ca prostate found in 55% of men in their 5th decade
Ca prostate found in 64% of men in their 7th decade
Indicating that significant proportion of these cancers are not lethal
Only 1 in 8 screening detected cancers is likely to kill its host if left
untreated.
36. Screening
Annual PSA for screening of prostate cancer:
• in men over 50 years old
• in younger men at high risk: e.g.,
Those with a family history of prostate cancer
• Total PSA: Screening for and in monitoring of
prostate cancer
• Free PSA:
Differentiate levels of PSA that are in the grey zone
Patient with cancer prostate have a lower % of free PSA
.
37. Monitoring
Response to therapy
• After radical prostatectomy
PSA level expected to normalize in 2 to 3 weeks
If PSA remained elevated for 6 months – recurrent disease developed eventually
• Radiotherapy
Takes 3 to 5 months for normalize PSA
Failure to normalize predicts relapse
• A rise in PSA is usually a first sign of
Recurrence
Metastatic progression
38. Carbohydrate epitope on a glycoprotein carcinoma antigen
Present in fetus & its derivatives of coelomic epithelium
• peritoneum
• pleura
• pericardium
• amnion
Normal adults – CA 125 found in the epithelium of
• fallopian tubes
• endometrium
• endocervix
Neithe fetal nor adult ovarian epithelium expresses CA 125
39. Testing
Immunoassay
Normal
• Serum < 35U/ml
• Peritoneal fluid < 200 U/ml
Elevated levels in 80% of ovarian cancer
Ovarian masses with elevated CA 125 has a sensitivity of 75% & specificity of 90% for
malignancy
Also detected in other malignancies
• Gynaecological
Fallopian tube
Endometrium
cervix
• Non gynaecological
Pancreas
Colon
Lung
liver
40. Testing
Benign conditions with elevated CA 125
• endometriosis
• adenomyosis
• uterine fibroids
• PID
• cirrhosis
• Ascitis
CA 125 is adjunt to diagnos Ca Pancreas
rather diagnostic iself
41. Screening – post menopausal women
Poor specificity
Alone is not useful in diagnosing ovarian
cancer
Positive cases are further screened with
transvaginal USG
42. Prognosis
At the time of diagnosis elevated CA 125
have worst prognosis
Percentage of patients with elevated levels
• 50% of Stage I
• 70% of Stage II
• 90% of Stage III
• 98% of Stage IV
43. Monitoring
> 95% of patients levels decrease with partial/ complete
response therapy
Recurrent cases levels elevated 3 months before
clinical/imaging evidence.
Rising level is an indication for second look laparotomy – 95%
times recurrent disease found
Peritoneal fluid level is more sensitive than serum level
44. • Beta HCG is a hormone normally secreted by
trophoblasts in the placenta during pregnancy
• It is a glycoprotein consisting of - and -
subunits
• Detection and follow-up of gestational trophoblastic
diseases (GTDs)
• GTDs include:
Hydatiform mole (vesicular mole)
Choriocarcinoma
45. Non-seminomatous testicular cancers
• β-HCG
> 90% choriocarcinomas
• AFP
90 to 95% yolk sac tumors
20% of teratomas
10% of embryonal carcinomas
46. Diagnosis
Non-seminiferous testicular germ cell cancers
• 50% will have elevated β-HCG
• 60% will have elevated AFP
• 90% will have elevated β-HCG/AFP
Few cases of spuriously elevated HCG/AFP
without testicular cancer
47. Diagnosis
elevation of HCG/AFP without signs of testicular
cancer in younger than 4o yr - Extra testicular
germ cell cancer
Useful in identifying biologically distinct categories
of morphologically similar tumors.
48. Prognosis
Poor
• AFP > 500 ng/ml
• HCG > 1000 ng/ml
Monitoring
Rate of marker decline (half life) calculated weekly after initiation of
chemotherapy, used for early detection of poor response to therapy
Half life
• > 3.5 days for HCG
• > 7 days for AFP
• Increase half life Indicates very aggressive therapy is required.
49. Intermediate size protein filament found in
connective tissue
It make up the cytoskeleton in eukaryotes
along with microtubules and actin
microfilaments
Over expressed in mesodermal tumors
Sarcomas
Studied by immuno histochemistry
50. Marker for breast cancer
HER2 gene is a proto-onco gene located at the long arm of
human chromosome 17(17q21-q22)
Encodes an Epidermal Growth Factor Receptor (EGF-R)
HER2 is a cell membrane surface-bound tyrosine kinase receptor
and is normally involved in the signal transduction pathways
leading to cell growth and differentiation.
51. proto-oncogene converted to oncogene by:
• Mutation (especially point mutation) or
• Altered (over) expression
It is now routinely measured in breast cancer (IHC and
FISH) to determine the type of therapy:
• Breast cancer positive for HER-2/NEU is responsive to
treatment (Herceptin – monoclonal antibody -
Trastuzumab)
52. Tumor marker for Medullary carcinoma thyroid
32-amino acid linear polypeptide hormone
Produced by para-follicular cells (C-cells) of the
thyroid
NMR solution structure Salmon
calcitonin in SDS micelles
Cys-Gly-Asn-Leu-Ser-Thr-Cys-Met-Leu-Gly-Thr-Tyr-Thr-Gln-Asp-Phe-Asn-Lys-Phe-His-Thr-Phe-Pro-Gln-Thr-Ala-Ile-Gly-Val-Gly-Ala-Pro
53. Production regulated by CALC1 gene
regulates blood Ca2+ levels in four ways:
• Inhibits Ca2+ absorption by the intestines
• Inhibits osteoclast activity in bones
• Inhibits phosphate reabsorption by theKidney tubules
• Inhibits tubular reabsorption of Ca2+,leading to increased rates of its loss
in urine
Secretion of calcitonin is stimulated by:
• an increase in serum [Ca2+]
• Gastrin & pentagastrin
55. • The gene is located on chromosome 17 (Plus the genes
of BRCA1 and HER-2/NEU)
• Encodes a protein of 53 kDa protein involved in
protecting cells from unregulated growth
• Encodes a protein that normally result in cell cycle arrest
and induces apoptosis
• mutation: Breast cancer
56. Tumor Tumor marker
Hepatoma (HCC) AFP
Ovarian Cancer CA-125
Inherited ovarian cancer:
BRCA1
Breast Cancer CA15-3
CEA
HER-2/NEU
Estrogen and progesterone
receptors
If inherited: BRCA1, and
BRCA2 (on chromosome 13)
Medullary carcinoma thyroid Calcitonin
CEA
57. Tumor Tumor marker
Ca Pancreas CA 19-9
CEA
Colorectal carcinoma CEA
CA 19-9
pheochromocytoma Catecholamines
(VMA) in urine
Nonseminomatous testicular cancer AFP
-hCG
CEA
Vesicular mole & Choriocarcinoma -hCG
Prostate cancer PSA
58. Tumor marker for carcinoid
{enterochromaffin (Kultschitzsky) cells of the small
intestine}
main metabolite of seratonin.
24-hour urine samples combined with an acidic
additive to maintain pH below 3.
• >25 mg - strong evidence for carcinoid.
59. Neuro endocrine tumor of the adrenal medulla (originating in
chromaffin cells)
Plasma
• Catecholamines
• Chromogranin A
• Metanephrines
Urinary
• Metanephrines
• Vanillyl mandelic acid (VMA)
end-stagemetabolite of the catecholamines
60. Bence Jone protein
• Monoclonal globulin protein – in blood or urine
• Molecular weight 22 – 24 kd
• Diagnostic of Multiple myeloma
• Present in 2/3rd of Multiple myeloma cases.
61. Still at an early discovery stage
Not yet reached the clinic
It has a great potential
• DNA assays for aberrent methylation are easier & more sensitive than
those for point mutations
• Cancer specific DNA methylation patterns can be detected in tumor
derived free DNA in the blood stream & in the tumor cells shed in to the
lumen. - detection & monitoring
• DNA –methylation profiles are more chemically & biologically stable than
RNA or most proteins.
62. Targeted biologic fluid sources of DNA
• Serum/plasma
• Urine – blader cancer
• Sputum
• Saliva
High sensitivity & specificity
Applications
• Early detection
Abnormal DNA methylation patterns in histologically normal cell
• Predict response to therapy
• prognostication
63. No ideal tumor marker is known so far
Therefore, the best approach is:
• good history
• thorough physical examination.
• Use a battery of markers (>1 marker/tumor)
• Use confirmatory investigations:
Appropriate scan, Histopathology