Precision

«Precision describes the variation you see when you measure the same part repeatedly with the same device. It includes the following two types of variation:

• Repeatability
• Reproducibility: variation due to the operators and the interaction between operator and part. It is the variation of the bias observed when different operators measure the same parts using the same device.»
  

Bibliographic reference: Reliawiki. 2017. Measurement System Analysis. [online] Available at: <https://reliawiki.org/index.php/Measurement_System_Analysis> [Accessed 20 February 2022].

pMMR or dMMR

Proficient or deficient DNA (deoxyribonucleic acid) mismatch repair gene expression.

Pneumonitis of radiation

Grading systems for evaluation of radiation pneumonitis:

Source: Jain V, Berman AT. Radiation Pneumonitis: Old Problem, New Tricks. Cancers (Basel). 2018;10(7):222.
Published 2018 Jul 3. Available at: https://doi.org/10.3390/cancers10070222.

Treatment: «Corticosteroids are commonly used for the treatment of radiation pneumonitis. Prednisone is started at 1 mg/kg/day upon diagnosis and is continued for several weeks and then tapered slowly. Other agents that have been used for the treatment of radiation pneumonitis include azathioprine and cyclosporin A.» Source: Virna Ignacio Almuete. Treatment for Radiation Pneumonitis - Medscape - Jan 06, 2003. [online] Available at: <https://www.medscape.com/viewarticle/446886> [Accessed 26 May 2020].

PD-1 checkpoint inhibitors

A PD-1 (programmed cell death protein 1) inhibitor fairy tale:

How do tumors use PD-1 to cause T-cell exhaustion? Learn how overexpression of PD-1 receptors on T cells may lead to T-cell exhaustion:

Primary treatment

It is «the first treatment given for a disease. It is often part of a standard set of treatments, such as surgery followed by chemotherapy and radiation. When used by itself, primary treatment is the one accepted as the best treatment. If it doesn’t cure the disease or it causes severe side effects, other treatment may be added or used instead. Also called first-line therapy, induction therapy, and primary therapy.»

Bibliographic reference: National Cancer Institute. NCI Dictionary of Cancer Terms. Primary treatment. Available at: https://www.cancer.gov/publications/dictionaries/cancer-terms/def/primary-treatment. Accessed 2019 Mar 14.

P value

Source: Twitter.com. (2019). Twitter. [online] Available at: https://twitter.com/drnirmalraut/status/1090550945593856000?s=09 [Accessed 3 Feb. 2019].

PSAV (prostate specific antigen velocity)

Total PSA (prostate specific antigen) velocity, in ng/mL/year, is the change in total PSA values over time and it is «calculated as the running average of the rate of change during 3 consecutive visits by the equation 0.5{[(PSA2-PSA1)/(elapsed time in years)]+[(PSA3-PSA2)/(elapsed time in years)]}, where PSA1 is the first of the 3 measurements, PSA2 the second and PSA3 the third. Elapsed time refers to time between the 2 measurements [1]».

The rate of change in serum total PSA over time provides useful information and increases the specificity of PSA for cancer detection. Current recommendations for the use of PSAV include a collection of PSA levels over a period of no less than 18 months and the use of multiple values (minimum of 3) to perform the calculation. PSAV «has been best used in younger men who have elected to begin early detection programs before age 50». It «was designed to help avoid unnecessary, costly, and potentially morbid repeat biopsies in these men» [2]. «A rise in PSA of as little as 0.1 ng/ml per year is worrisome as to the long-term chance of being diagnosed with prostate cancer» [2,3]:

PSA Velocity	Prostate Cancer Risk by 10 Years
≤0.1 ng/ml/year	3%
>0.1 ng/ml/year	65%

Source: [2,3].

«Any rapid rise in PSA is worrisome both for the likelihood of developing cancer but of having more serious (high-grade prostate cancer.) A recent study [4] found that men whose PSA jumped more than 2 points in the year prior to being diagnosed had much higher death rate when treated with surgery (radical prostatectomy). Also, patients treated with radiation for prostate cancer whose PSA starts to rise do worse if the PSA doubles in less than 12 months» [2].
In patients with prostate cancer without metastases, those with a rapid PSAV and an otherwise long life expectancy should be encouraged to consider androgen deprivation therapy earlier [5].
A free online calculation can be found here: USRF (Urological Sciences Research Foundation) - PSA Velocity [6], Prostate Cancer Nomograms | Memorial Sloan Kettering Cancer Center [7], and http://www.doubling-time.com/compute-PSA-doubling-time.php [8].

Bibliographic references:

[1] Khan MA, Carter HB, Epstein JI, et al. Can prostate specific antigen derivatives and pathological parameters predict significant change in expectant management criteria for prostate cancer? J Urol. 2003 Dec;170(6 Pt 1):2274-8. Available at: https://doi.org/10.1097/01.ju.0000097124.21878.6b.
[2] PSA Velocity. Aboutcancercom. Available at: http://www.aboutcancer.com/psa_velocity.htm. Accessed June 17, 2018.
[3] Fang J, Metter EJ, Landis P, Carter HB. PSA velocity for assessing prostate cancer risk in men with PSA levels between 2.0 and 4.0 ng/ml. Urology. 2002 Jun;59(6):889-93; discussion 893-4. Available at: https://doi.org/10.1016/S0090-4295(02)01646-1.
[4] D'Amico AV, Chen MH, Roehl KA, Catalona WJ. Preoperative PSA velocity and the risk of death from prostate cancer after radical prostatectomy. N Engl J Med. 2004 Jul 8;351(2):125-35. Available at: https://doi.org/10.1056/NEJMoa032975.
[5] Mohler J, Lee R, Antonarakis E, et al. NCCN Clinical Practice Guidelines in Oncology (NCCN Guidelines) – Prostate Cancer – Version 2.2018 - March 8, 2018. Nccnorg. 2018. Available at: https://www.nccn.org/professionals/physician_gls/pdf/prostate.pdf. Accessed June 17, 2018.
[6] USRF - PSA Velocity. Usrforg. Available at: https://www.usrf.org/questionnaires/PSA_Velocity.html. Accessed June 17, 2018.
[7] Prostate Cancer Nomograms: PSA Doubling Time | Memorial Sloan Kettering Cancer Center. Mskcc.org. https://www.mskcc.org/nomograms/prostate/psa_doubling_time. Accessed October 26, 2018.
[8] PSA Doubling Time Calculator. Doubling-time.com. http://www.doubling-time.com/compute-PSA-doubling-time.php. Accessed October 26, 2018.

Pancoast syndrome or Pancoast's syndrome

«Tumor involving the upper part of the lung, with invasion of the surrounding structures as the plexus brachialis, ribs, and extending in the nodes, possibly causing a Claude-Bernard Horner syndrome. Now currently named superior pulmonary sulcus tumor [1].»

«This is accompanied by the following: severe pain in the shoulder region radiating toward the axilla and scapula, with later extension along the ulnar aspect of the arm to the hand, atrophy of hand and arm muscles, Horner syndrome (...), and compression of the blood vessels with edema [2].»

Bibliographic references:

[1] Debois JM. The Eponyms Of Oncology. Pharmacia & Upjohn; 1996.

[2] D'Silva KJ, May SK. Pancoast Syndrome: Practice Essentials, Pathophysiology, Etiology. Medscape Drugs & Diseases. 2017. Available at: https://emedicine.medscape.com/article/284011-overview. Accessed June 3, 2018.

PSA (prostate specific antigen) density

PSA density (ng/mL² or ng/mL/cc) is calculated preoperatively during the biopsy procedure by using transrectal ultrasound by dividing the maximum preoperative PSA value and prostate volume [1]. The latter is calculated based on the ellipse dimension theory formula [2] (D1 × D2 × D3 × pi/6), where D1 is the maximum transverse diameter, D2 is the maximum anteroposterior diameter, D3 is the maximum longitudinal diameter, and pi is a mathematical constant approximately equal to 3.14.

A study of a large cohort of patients (1662 patients) found a significant trend of worsening pathological features as PSA density increases [3]. Other studies [4,5] found that PSA density (using a pathological weight of the surgical specimen) was a better predictor of extracapsular disease, positive surgical margins, seminal vesicle invasion, lymph node invasion and biochemical recurrence than PSA.
«A PSAD of >0.15 ng/mL/cm³ identifies men with a higher risk of detecting prostate cancer on a screening biopsy» [6].

«It is used because an elevated PSA might not arouse suspicion in a man with a very enlarged prostate. The use of PSA density to interpret PSA results is controversial because prostate cancer might be overlooked in a man with an enlarged prostate» [7].

Bibliographic references:

[1] Sfoungaristos S, Perimenis P. Evaluating PSA Density as a Predictor of Biochemical Failure after Radical Prostatectomy: Results of a Prospective Study after a Median Follow-Up of 36 Months. ISRN Urol. 2013 May 16;2013:984951. Available at: https://doi.org/10.1155/2013/984951.

[2] Wolff JM, Boeckmann W, Mattelaer P, et al. Determination of prostate gland volume by transrectal ultrasound: correlation with radical prostatectomy specimens. Eur Urol. 1995;28(1):10-2. Available at: https://doi.org/10.1159/000475012.

[3] Kundu SD, Roehl KA, Yu X, et al. Prostate specific antigen density correlates with features of prostate cancer aggressiveness. J Urol. 2007 Feb;177(2):505-9. Available at: https://doi.org/10.1016/j.juro.2006.09.039.

[4] Freedland SJ, Wieder JA, Jack GS, et al. Improved risk stratification for biochemical recurrence after radical prostatectomy using a novel risk group system based on prostate specific antigen density and biopsy Gleason score. J Urol. 2002 Jul;168(1):110-5. Available at: http://dx.doi.org/10.1016/S0022-5347(05)64841-0.

[5] Sfoungaristos S, Perimenis P. PSA density is superior than PSA and Gleason score for adverse pathologic features prediction in patients with clinically localized prostate cancer. Can Urol Assoc J. 2012 Feb;6(1):46-50. Available at: https://doi.org/10.5489/cuaj.11079.

[6] Shah A. 53 - Low-Risk Prostate Cancer. In: Hristov B, Lin S, Christodouleas J. Radiation Oncology. 2nd ed. Philadelphia, USA: Wolters Klumer Health; 2015:366.
[7] Definition of PSA density. Phoenix5org. 2002. Available at: http://www.phoenix5.org/glossary/PSA_density.html. Accessed October 19, 2017.

PARP (poly-[adenosine diphosphate-ribose] polymerase)

Poly-(ADP)-ribose polymerase is «a family of proteins involved in a number of cellular processes involving mainly DNA [deoxyribonucleic acid] repair and programmed cell death. The PARP family comprises 17 members (10 putative). They have all very different structures and functions in the cell. One important function of PARP is assisting in the repair of single-strand DNA breaks [1]». It is «a SSB [single-strand break] detector protein» [2].
«Drugs which inhibit (...) PARP (...) are particularly effective in tumors with HR [homologous recombination] deficiencies, such as breast tumors with BCRA1 or BCRA2 [breast cancer 1 or 2] deficiencies. (...) probably (...) PARP inhibitors suppress SSB repair, resulting in greater numbers of unrepaired SSBs, which therefore have a greater chance of hitting a replication fork. Under normal circumstances, the resulting DSB [double-strand break] would be repaired by HR, so the absence or reduction of this backup pathway leads to a substantial increase in DSBs and thus cellular lethality [2].»

Bibliographic references:
[1] Tortora, G., Bergmann, L., Lindh, M., Cervantes-Ruiperez, A., Dziadziuszko, R., Eckhardt, S., Lenz, H., Normanno, N., Perez, D., Scarpa, A., Syrigos, K., Tabernero, J. and Troiani, T. (2014). ESMO glossary in molecular biology of cancer. Viganello-Lugano, Switzerland: European Society for Medical Oncology, p.127.

[2] Joiner, M. and Kogel, A. (2009). Basic clinical radiobiology. 1st ed. Boca Raton, Florida: CRC Press, p.24.

p53

It «(...) is one of the most commonly mutated tumor suppressors whose function is to regulate genes that control both cell cycle checkpoints and (...) apoptosis. Consequently, activation of p53 after irradiation can lead either to a block in proliferation or directly to cell death. (...) in unstressed normal cells, p53 is made continuously but is degraded and thus non-functional. Following DNA [deoxyribonucleic acid] damage, ATM [ataxia telangiectasia mutated] phosphorylates both p53 and MDM2 [murine double minute 2]. These events destabilize the p53-MDM2 interaction, and (...) p53 protein is no longer degraded. In addition to this stabilization, direct phosphorylation of p53 by ATM leads to its activation as a transcription factor and thus the upregulation of its many target genes [1].»

«Cells irradiated in the G1 phase are influenced by the action of p53. ATM protein is activated by double-strand DNA breaks and phosphorylates both MDM2 and p53. This leads to stabilization and activation of p53, which induces genes that can promote apoptosis (Bax [Bcl-2-associated X], Puma [p53 upregulated modulator of apoptosis]) and induces checkpoints. (...) cells are blocked at the G1/S border [1].»

Is has «(...) a mass of 53 kDa (hence its name); p53 protein is normally induced in cells having undergone DNA damage, (...); its principal effects are to stop the cell cycle and prevent the cell from undergoing mitosis; thus, DNA mutations/damage can either be repaired or a damaged cell can be eliminated from the organism, for example via apoptosis. p53 is also known as the guardian of the genome [2].»

Bibliographic references:

[1] Joiner, M. and Kogel, A. (2009). Basic clinical radiobiology. 1st ed. Boca Raton, Florida: CRC Press, p.17.

[2] Tortora, G., Bergmann, L., Lindh, M., Cervantes-Ruiperez, A., Dziadziuszko, R., Eckhardt, S., Lenz, H., Normanno, N., Perez, D., Scarpa, A., Syrigos, K., Tabernero, J. and Troiani, T. (2014). ESMO glossary in molecular biology of cancer. Viganello-Lugano, Switzerland: European Society for Medical Oncology, p.117.

Proportion

It's the relationship between the number of individuals who have a characteristic and the total population. The numerator is included in the denominator. It is different from ratio.

Putative gene

It refers to a nucleotide sequence believed to be a gene because of its open reading frame although its function and the protein it codes for has not been (fully) identified [1]. For example, putative gene 57 is the (temporary) name suggested for the gene coding for a protein produced by Bacteriophage SP01 that infects the bacterium Bacillus subtilis [2]. Another example: PTEN, a putative protein tyrosine phosphatase gene mutated in some cancers [3].

Bibliographic references:

[1] Biology-online.org. (2014). Putative - Biology-Online Dictionary. [online] Available at: http://www.biology-online.org/dictionary/Putative [Accessed 26 Jun. 2016].

[2] Stewart CR, Gaslightwala I, Hinata K, Krolikowski KA, Needleman DS, Peng AS, et al. Genes and regulatory sites of the "host-takeover module" in the terminal redundancy of Bacillus subtilis bacteriophage SPO1. Virology. 1998 Jul 5; 246 (2): 329-40. Available at: http://dx.doi.org/10.1006/viro.1998.9197.

[3] Li J, Yen C, Liaw D, Podsypanina K, Bose S, Wang SI, et al. PTEN, a putative protein tyrosine phosphatase gene mutated in human brain, breast, and prostate cancer. Science. 1997 Mar 28;275(5308):1943-7. Available at: http://dx.doi.org/10.1126/science.275.5308.1943.

PTV (planning target volume)

It includes the gross tumor volume (GTV), the clinical target volume (CTV), and a margin to account for setup error, movement, and any possible geometric variations. The volume that includes the CTV with any internal target volume (ITV), if present, as well as a setup margin to account for patient movement and daily setup uncertainties [1]. When the patient moves or internal organs change in size and shape during a fraction of treatment or between fractions (intra- or inter-fractionally), the position of the CTV may also move. Therefore, to ensure a homogeneous dose to the CTV throughout a fractionated course of irradiation, margins must be added around the CTV. These allow for physiological organ motion (internal margin) and variations in patient positioning and alignment of treatment beams (set-up margin), creating a geometric planning target volume [2]. PTV is the ultimate target volume, the primary focus of the treatment planning and delivery. Adequate dose delivered to PTV at each treatment session, presumably, assures adequate treatment of the entire disease-bearing volume, the CTV [3].

Bibliographic references:

[1] Fisher, B.,  Daugherty, L, Reiff J. E. (2013). P. In: L. Brady and T. Yaeger, ed., Encyclopedia of Radiation Oncology, 1st ed. Springer-Verlag Berlin Heidelberg, pp.585-693.

[2] Barrett, A., Dobbs, J., Morris, S. and Roques, T. ed., (2009). 2 Principles of radiotherapy planning. In: Practical Radiotherapy Planning, 4th ed. London: Hodder Arnold, an Hachette UK Company, pp.9-31.

[3] Khan, F. (2007). Chapter 1 - Introduction: Process, Equipment, and Personnel. In: F. Khan, ed., Treatment Planning in Radiation Oncology, 2nd ed. Lippincott Williams & Wilkins.