28 research outputs found
Recommended from our members
Homologous recombination DNA repair deficiency and PARP inhibition activity in primary triple negative breast cancer
- Author
- Bliss Judith M.
- Chan Stephen
- Chopra Neha
- Cutts Ros
- Daley Frances
- Davies Helen Ruth
- Degasperi Andrea
- Dodson Andrew
- Dowsett Mitch
- Evans Abigail
- Gevensleben Heidi
- Hubank Michael
- Kriplani Divya
- Nik-Zainal Serena
- Pearson Alex
- Proszek Paula
- Roylance Rebecca
- Skene Anthony
- Toms Christy
- Tovey Holly
- Turner Nicholas C.
- Tutt Andrew
- Publication venue
- 'Organisation for Economic Co-Operation and Development (OECD)'
- Publication date
- 29/05/2021
- Field of study
Funder: Breast Cancer Now (BCN); doi: https://doi.org/10.13039/100009794Abstract: Triple negative breast cancer (TNBC) encompasses molecularly different subgroups, with a subgroup harboring evidence of defective homologous recombination (HR) DNA repair. Here, within a phase 2 window clinical trial, RIO trial (EudraCT 2014-003319-12), we investigate the activity of PARP inhibitors in 43 patients with untreated TNBC. The primary end point, decreased Ki67, occured in 12% of TNBC. In secondary end point analyses, HR deficiency was identified in 69% of TNBC with the mutational-signature-based HRDetect assay. Cancers with HRDetect mutational signatures of HR deficiency had a functional defect in HR, assessed by impaired RAD51 foci formation on end of treatment biopsy. Following rucaparib treatment there was no association of Ki67 change with HR deficiency. In contrast, early circulating tumor DNA dynamics identified activity of rucaparib, with end of treatment ctDNA levels suppressed by rucaparib in mutation-signature HR-deficient cancers. In ad hoc analysis, rucaparib induced expression of interferon response genes in HR-deficient cancers. The majority of TNBCs have a defect in DNA repair, identifiable by mutational signature analysis, that may be targetable with PARP inhibitors
Recommended from our members
Homologous recombination DNA repair deficiency and PARP inhibition activity in primary triple negative breast cancer
- Author
- Bliss Judith M.
- Chan Stephen
- Chopra Neha
- Cutts Ros
- Daley Frances
- Davies Helen Ruth
- Degasperi Andrea
- Dodson Andrew
- Dowsett Mitch
- Evans Abigail
- Gevensleben Heidi
- Hubank Michael
- Kriplani Divya
- Nik-Zainal Serena
- Pearson Alex
- Proszek Paula
- Roylance Rebecca
- Skene Anthony
- Toms Christy
- Tovey Holly
- Turner Nicholas C.
- Tutt Andrew
- Publication venue
- Nature Communications
- Publication date
- 29/05/2020
- Field of study
Funder: Breast Cancer Now (BCN); doi: https://doi.org/10.13039/100009794Abstract: Triple negative breast cancer (TNBC) encompasses molecularly different subgroups, with a subgroup harboring evidence of defective homologous recombination (HR) DNA repair. Here, within a phase 2 window clinical trial, RIO trial (EudraCT 2014-003319-12), we investigate the activity of PARP inhibitors in 43 patients with untreated TNBC. The primary end point, decreased Ki67, occured in 12% of TNBC. In secondary end point analyses, HR deficiency was identified in 69% of TNBC with the mutational-signature-based HRDetect assay. Cancers with HRDetect mutational signatures of HR deficiency had a functional defect in HR, assessed by impaired RAD51 foci formation on end of treatment biopsy. Following rucaparib treatment there was no association of Ki67 change with HR deficiency. In contrast, early circulating tumor DNA dynamics identified activity of rucaparib, with end of treatment ctDNA levels suppressed by rucaparib in mutation-signature HR-deficient cancers. In ad hoc analysis, rucaparib induced expression of interferon response genes in HR-deficient cancers. The majority of TNBCs have a defect in DNA repair, identifiable by mutational signature analysis, that may be targetable with PARP inhibitors
HER2-enriched subtype and novel molecular subgroups drive aromatase inhibitor resistance and an increased risk of relapse in early ER+/HER2+ breast cancer
- Author
- Absar Mohammed
- Abson Charlotte
- Adams Jocelyn
- Adamson Douglas
- Adelekan Matthew
- Agarwal Roshan
- Alataki Anastasia
- Algurafi Hafiz
- Allerton Rozenn
- Anand Ambika
- Ashkanani Fawzia
- Babu Ed
- Ball Adrian
- Barrett Jane
- Barthelmes Ludger
- Barthkur Urmila
- Bergamino Milana A
- Bews-Hair Maria
- Bhaskar Pudhupalayam
- Bhattacharyya Madhumita
- Bliss Judith M
- Bonom Riccardo
- Bramley Maria
- Brown Victoria Alexandra
- Bundred Nigel
- Burcombe Russell
- Carr Michael
- Chakrabarti Amitabha
- Chan Charlie
- Chan Stephen
- Chandrasekharan Sankaran
- Chatterjee Sumohan
- Cheang Maggie CU
- Chin Kian
- Churn Mark
- Cleator Susan
- Coleman Rob
- Corder Allan
- Crane Peter
- Crawford Derek
- Crellin Perric
- Crowley Clare
- Cunnick Giles
- Cutress Ramsay
- Davis Ruth
- Dawson Jonathan
- Donnelly Jull
- Donnelly Peter
- Doughty Julie
- Dowsett Mitch
- Dunn Kathleen
- Dyke Gary
- Ellenbogen Simon
- Evans Abigail
- Ferguson Douglas
- Forrest Jennifer
- Fox John
- Gallegos Nicholas
- Gilbert .
- Goranova Rebecca
- Grieve Robert
- Griffith Clive
- Hadaki Maher
- Hamed Hisham
- Harding-Mackean Claudia
- Hatcher Olivia
- Hatton Matthew
- Hills Margaret
- Hinton Christopher
- Hoar Fiona
- Hogg Martin
- Holcombe Chris
- Holcombe Christopher
- Hollywood Ciaran
- Holt Simon
- Holt Simon
- Holt Steve
- Horgan Kieran
- Hwang David
- Hyett Elaine
- Iqbal Shabana
- Irvine Tracey
- Johnson Richard
- Johnson Tayo
- Johnston Stephen
- Johri Akhil
- Jones Alison
- Kelleher Muireann
- Kennedy Robert
- Kenny Frances
- Khattak Ilyas
- Kilburn Lucy
- Kishore Makam
- Kissin Mark
- Kneeshaw Peter
- Kokan Jalal
- Kothari Ashutosh
- Kovacs Tibor
- Laidlaw Ian
- Laws Siobhan
- Ledwidge Serena
- Lee Caroline
- Leonard Robert
- Lewanski Conrad
- Linforth Rick
- López-Knowles Elena
- Maxwell William
- McFall Brendan
- McIntosh Stuart
- Mehra Rakesh
- Modi Anupam
- Morani Gabriele
- Mortimer Caroline
- Muralikrishna Vummiti
- Murphy Claire
- Naik Jay Dolatrai
- Narayanan Sankaran
- Nejim Ali
- Newby Jacqueline
- Ornstein Marcus
- Pain Simon
- Parmar Jitendra
- Parton Marina
- Patel Ashraf
- Pope Vanessa
- Prasad Ramachandran
- Prof Highes-Davies
- Quigley Mary
- Ravichandran Duraisamy
- Rea Daniel
- Rees-Lee Jacqueline
- Reichert Robert
- Roberts Jonathan
- Robertson John F
- Robinson Anne
- Roylance Rebecca
- Salman Reem Ramzi
- Samra Walid
- Schuster Eugene F
- Seetharam Seema
- Sharif Muhammad
- Sharma Ravi
- Shere Michael
- Sibbering Mark
- Silva Shobha
- Sinha Prakash
- Skene Anthony
- Skene Anthony
- Smith Ian
- Smith Ian E
- Smith Simon
- Soulsby Racheal
- Sparrow Geoffrey
- Sutton Richard
- Sweetland Helen
- Thakur Kislaya
- Thekkinkattil Dinesh
- Thomson Simon
- Thorne Amanda
- Thrush Steven
- Todd Radha
- Tovey Holly
- Usman Tamoor
- Vaidya Jayant
- Vesty Sarah
- Vidya Raghavan
- Wahee Shamaela
- Walji Nawaz
- Walker Philip
- Wheatley Duncan
- Williams Michael
- Williams Nicholas
- Winter Matthew
- Winters Zoe
- Wyld Lynda
- Xiao Hui
- Publication venue
- 'Elsevier BV'
- Publication date
- 16/08/2022
- Field of study
BACKGROUND: Oestrogen receptor positive/ human epidermal growth factor receptor positive (ER+/HER2+) breast cancers (BCs) are less responsive to endocrine therapy than ER+/HER2- tumours. Mechanisms underpinning the differential behaviour of ER+HER2+ tumours are poorly characterised. Our aim was to identify biomarkers of response to 2 weeks’ presurgical AI treatment in ER+/HER2+ BCs. METHODS: All available ER+/HER2+ BC baseline tumours (n=342) in the POETIC trial were gene expression profiled using BC360™ (NanoString) covering intrinsic subtypes and 46 key biological signatures. Early response to AI was assessed by changes in Ki67 expression and residual Ki67 at 2 weeks (Ki672wk). Time-To-Recurrence (TTR) was estimated using Kaplan-Meier methods and Cox models adjusted for standard clinicopathological variables. New molecular subgroups (MS) were identified using consensus clustering. FINDINGS: HER2-enriched (HER2-E) subtype BCs (44.7% of the total) showed poorer Ki67 response and higher Ki672wk (p<0.0001) than non-HER2-E BCs. High expression of ERBB2 expression, homologous recombination deficiency (HRD) and TP53 mutational score were associated with poor response and immune-related signatures with High Ki672wk. Five new MS that were associated with differential response to AI were identified. HER2-E had significantly poorer TTR compared to Luminal BCs (HR 2.55, 95% CI 1.14–5.69; p=0.0222). The new MS were independent predictors of TTR, adding significant value beyond intrinsic subtypes. INTERPRETATION: Our results show HER2-E as a standardised biomarker associated with poor response to AI and worse outcome in ER+/HER2+. HRD, TP53 mutational score and immune-tumour tolerance are predictive biomarkers for poor response to AI. Lastly, novel MS identify additional non-HER2-E tumours not responding to AI with an increased risk of relapse
Carboplatin in BRCA1/2-mutated and triple-negative breast cancer BRCAness subgroups: the TNT Trial
- Author
- Abraham Jacinta
- Ashworth Alan
- Barrett Sophie
- Barrett-Lee Peter
- Bliss Judith M.
- Brown Robert
- Chan Stephen
- Cheang Maggie Chon U.
- Dowsett Mitchell
- Ellis Paul
- Flanagan James M.
- Fox Lisa
- Gazinska Patrycja
- Gillett Cheryl
- Grigoriadis Anita
- Gutin Alexander
- Harper-Wynne Catherine
- Harries Mark
- Hatton Matthew Q.
- Hoadley Katherine A.
- Kernaghan Sarah
- Kilburn Lucy
- Lanchbury Jerry S.
- Owen Julie
- Parikh Jyoti
- Parker Peter
- Perou Charles M.
- Pinder Sarah E.
- Rahman Nazneen
- Roylance Rebecca
- Shah Vandna
- Shaw Adam
- Smith Ian E.
- Timms Kirsten M.
- Tovey Holly
- Tutt Andrew
- Wardley Andrew M.
- Wilson Gregory
- Publication venue
- 'Springer Science and Business Media LLC'
- Publication date
- 01/01/2018
- Field of study
Germline mutations in BRCA1/2 predispose individuals to breast cancer (termed germline-mutated BRCA1/2 breast cancer, gBRCA-BC) by impairing homologous recombination (HR) and causing genomic instability. HR also repairs DNA lesions caused by platinum agents and PARP inhibitors. Triple-negative breast cancers (TNBCs) harbor subpopulations with BRCA1/2 mutations, hypothesized to be especially platinum-sensitive. Cancers in putative ‘BRCAness’ subgroups—tumors with BRCA1 methylation; low levels of BRCA1 mRNA (BRCA1 mRNA-low); or mutational signatures for HR deficiency and those with basal phenotypes—may also be sensitive to platinum. We assessed the efficacy of carboplatin and another mechanistically distinct therapy, docetaxel, in a phase 3 trial in subjects with unselected advanced TNBC. A prespecified protocol enabled biomarker–treatment interaction analyses in gBRCA-BC and BRCAness subgroups. The primary endpoint was objective response rate (ORR). In the unselected population (376 subjects; 188 carboplatin, 188 docetaxel), carboplatin was not more active than docetaxel (ORR, 31.4% versus 34.0%, respectively; P = 0.66). In contrast, in subjects with gBRCA-BC, carboplatin had double the ORR of docetaxel (68% versus 33%, respectively; biomarker, treatment interaction P = 0.01). Such benefit was not observed for subjects with BRCA1 methylation, BRCA1 mRNA-low tumors or a high score in a Myriad HRD assay. Significant interaction between treatment and the basal-like subtype was driven by high docetaxel response in the nonbasal subgroup. We conclude that patients with advanced TNBC benefit from characterization of BRCA1/2 mutations, but not BRCA1 methylation or Myriad HRD analyses, to inform choices on platinum-based chemotherapy. Additionally, gene expression analysis of basal-like cancers may also influence treatment selection
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The ATLAS inner detector trigger performance in pp collisions at 13 TeV during LHC Run 2
- Author
- Aad G
- Abbott B
- Abbott DC
- Abeling K
- Abhayasinghe DK
- Abidi SH
- AbouZeid OS
- Abraham NL
- Abramowicz H
- Abreu H
- Abud A Abed
- Abulaiti Y
- Acharya BS
- Achkar B
- Adam L
- Adamczyk L
- Adamek L
- Adelman J
- Adiguzel A
- Adorni S
- Adye T
- Affolder AA
- Afik Y
- Agapopoulou C
- Agaras MN
- Aggarwal A
- Agheorghiesei C
- Aguilar-Saavedra JA
- Agullo P Martinez
- Ahmad A
- Ahmadov F
- Ahmed WS
- Ahnen J Von
- Ai X
- Aielli G
- Akatsuka S
- Akbiyik M
- Akesson TPA
- Akilli E
- Akimov AV
- Alberghi GL
- Albert J
- Alderweireldt S
- Aleksa M
- Aleksandrov IN
- Alexa C
- Alexopoulos T
- Alfonsi A
- Alfonsi F
- Alhroob M
- Ali B
- Ali S
- Aliev M
- Alimonti G
- Allaire C
- Allbrooke BMM
- Allport PP
- Aloisio A
- Alonso F
- Alpigiani C
- Alves FL Lucio
- Alviggi MG
- Ambler A
- Ambroz L
- Amelung C
- Amidei D
- Amoroso S
- Amrouche CS
- Anastopoulos C
- Andari N
- Andeen T
- Anders JK
- Andrean SY
- Andreazza A
- Andrei V
- Anelli CR
- Angelidakis S
- Angerami A
- Anisenkov AV
- Annovi A
- Antel C
- Anthony MT
- Antipov E
- Antonelli M
- Antrim DJA
- Anulli F
- Aoki M
- Aparo MA
- Aranda C Padilla
- Aranzabal N
- Araya S Tapia
- Arcangeletti C
- Arce ATH
- Arguin J-F
- Argyropoulos S
- Arling J-H
- Armbruster AJ
- Armstrong A
- Arnaez O
- Arnold H
- Artoni G
- Asada H
- Asai K
- Asai S
- Asawatavonvanich T
- Asbah NA
- Asimakopoulou EM
- Asquith L
- Assahsah J
- Assamagan K
- Astalos R
- Astigarraga ME Pozo
- Atkin RJ
- Atkinson M
- Atlay NB
- Atmani H
- Atmasiddha PA
- Augsten K
- Austrup VA
- Avolio G
- Ayoub MK
- Azuelos G
- Babal D
- Bachacou H
- Bachas K
- Backman F
- Bagnaia P
- Bahilo JJ Lozano
- Bahrasemani H
- Bailey AJ
- Bailey VR
- Baines JT
- Bakalis C
- Baker OK
- Bakker PJ
- Bakos E
- Balaji S
- Balasubramanian R
- Baldin EM
- Balek P
- Balli F
- Balunas WK
- Balz J
- Banas E
- Bandieramonte M
- Bandyopadhyay A
- Barak L
- Barbe WM
- Barberio EL
- Barberis D
- Barbero M
- Barbour G
- Barillari T
- Barisits M-S
- Barkeloo J
- Barklow T
- Barnett BM
- Barnett RM
- Barnovska-Blenessy Z
- Baroncelli A
- Barone G
- Barr AJ
- Barreiro F
- Barron U
- Barsov S
- Bartels F
- Bartoldus R
- Bartolini G
- Barton AE
- Bartos P
- Basalaev A
- Basan A
- Bassalat A
- Basso MJ
- Basson CR
- Bates RL
- Batlamous S
- Batley John
- Batool B
- Battaglia M
- Bauce M
- Bauer F
- Bauer P
- Bawa HS
- Bayirli A
- Beacham JB
- Beau T
- Beauchemin PH
- Becherer F
- Bechtle P
- Beck HP
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- Becot C
- Beddall AJ
- Bednyakov VA
- Bee CP
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- Begalli M
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- Beisiegel F
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- Bella G
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- Bellerive A
- Bello FA Di
- Bellos P
- Beloborodov K
- Belotskiy K
- Belyaev NL
- Benchekroun D
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- Benhammou Y
- Benjamin DP
- Benoit M
- Bensinger JR
- Bentvelsen S
- Beresford L
- Beretta M
- Berge D
- Berger N
- Bergmann B
- Bergsten LJ
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- Berlingen J Montejo
- Bernardi G
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- Bobbink GJ
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- Budagov IA
- Buddenbrock SE von
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- Bulekov O
- Bullard BA
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- Burdin S
- Burgard CD
- Burger AM
- Burghgrave B
- Burr Jon
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- Burzynski JC
- Buscher V
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- Caltabiano A
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- Camelia E Alunno
- Camerlingo MT
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- Capriles FG Diaz
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- Casado MP
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- Delmastro M
- Delporte C
- Delsart PA
- Demers S
- Demichev M
- Demontigny G
- Denisov SP
- Derendarz D
- Derkaoui JE
- Derue F
- Dervan P
- Desch K
- Dette K
- Deutsch C
- Deviveiros PO
- Diaconu C
- Dias FA
- Diaz L Pedraza
- Diaz MA
- Diaz Y Delabat
- Dickinson J
- Didenko M
- Diehl EB
- Dietrich J
- Dimitrievska A
- Ding W
- Dingfelder J
- Dittmeier SJ
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- Djuvsland JI
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- Dodsworth D
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- Dominguez L Pascual
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- Donadelli M
- Donaldson C Pitman
- Donato C Di
- Donell DM Mac
- Dong B
- Donini J
- Donszelmann T Cuhadar
- Dopke J
- Doria A
- Dova MT
- Doyle AT
- Drechsler E
- Dreyer E
- Dreyer T
- Drobac AS
- Du D
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- Dubinin F
- Dubovsky M
- Dubreuil A
- Duchovni E
- Duckeck G
- Ducu OA
- Duda D
- Dudarev A
- Dudder AC
- Duflot L
- Duhrssen M
- Dulsen C
- Dumancic M
- Dumitriu AE
- Dunford M
- Dungs S
- Duperrin A
- Duren M
- Durglishvili A
- Dutta B
- Duvnjak D
- Dyckes GI
- Dyndal M
- Dysch S
- Dziedzic BS
- Eggleston MG
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- Publication venue
- EUROPEAN PHYSICAL JOURNAL C
- Publication date
- 08/03/2022
- Field of study
The design and performance of the inner detector trigger for the high level
trigger of the ATLAS experiment at the Large Hadron Collider during the 2016-18
data taking period is discussed. In 2016, 2017, and 2018 the ATLAS detector
recorded 35.6 fb−1, 46.9 fb−1, and 60.6 fb−1 respectively of
proton-proton collision data at a centre-of-mass energy of 13 TeV. In order to
deal with the very high interaction multiplicities per bunch crossing expected
with the 13 TeV collisions the inner detector trigger was redesigned during the
long shutdown of the Large Hadron Collider from 2013 until 2015. An overview of
these developments is provided and the performance of the tracking in the
trigger for the muon, electron, tau and b-jet signatures is discussed. The
high performance of the inner detector trigger with these extreme interaction
multiplicities demonstrates how the inner detector tracking continues to lie at
the heart of the trigger performance and is essential in enabling the ATLAS
physics programme
Recommended from our members
Observation of electroweak production of two jets in association with an isolated photon and missing transverse momentum, and search for a Higgs boson decaying into invisible particles at 13 TeV with the ATLAS detector
- Author
- Aad G
- Abbott B
- Abbott DC
- Abeling K
- Abhayasinghe DK
- Abidi SH
- Aboulhorma A
- Abramowicz H
- Abreu H
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- Abulaiti Y
- Acharya BS
- Achkar B
- Adam L
- Adamczyk L
- Adamek L
- Addepalli SV
- Adelman J
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- Affolder AA
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- Agapopoulou C
- Agaras MN
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- Agullo P Martinez
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- Zagazeta LF Gutierrez
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- Zhemchugov A
- Zheng Z
- Zhong D
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- Zieminska D
- Zimine NI
- Zimmermann S
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- Zormpa O
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- Publication venue
- EUROPEAN PHYSICAL JOURNAL C
- Publication date
- 03/02/2022
- Field of study
This paper presents the measurement of the electroweak production of two jets
in association with a Zγ pair with the Z boson decaying into two
neutrinos. It also presents the search for invisible or partially invisible
decays of a Higgs boson with a mass of 125 GeV produced through vector-boson
fusion with a photon in the final state. These results use data from LHC
proton-proton collisions at s = 13 TeV collected with the ATLAS
detector corresponding to an integrated luminosity of 139 fb−1. The event
signature, shared by all benchmark processes considered for measurements and
searches, is characterized by a significant amount of unbalanced transverse
momentum and a photon in the final state, in addition to a pair of forward
jets. For electroweak production of Zγ in association with two jets, the
background-only hypothesis is rejected with an observed (expected) significance
of 5.2 (5.1) standard deviations. The measured fiducial cross-section for this
process is 1.31±0.29 fb. Observed (expected) upper limit of 0.37 (0.34) at
95% confidence level is set on the branching ratio of a 125 GeV Higgs boson to
invisible particles, assuming the Standard Model production cross-section. The
signature is also interpreted in the context of decays of a Higgs boson to a
photon and a dark photon. An observed (expected) 95% CL upper limit on the
branching ratio for this decay is set at 0.018 (0.017), assuming the 125 GeV
Standard Model Higgs boson production cross-section
The ATLAS inner detector trigger performance in pp collisions at 13 TeV during LHC Run 2
- Author
- Aad G
- Abbott B
- Abbott DC
- Abeling K
- Abhayasinghe DK
- Abidi SH
- AbouZeid OS
- Abraham NL
- Abramowicz H
- Abreu H
- Abud A Abed
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- Acharya BS
- Achkar B
- Adam L
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- Adamek L
- Adelman J
- Adiguzel A
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- Adye T
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- Afik Y
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- Agullo P Martinez
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- Zorbas TG
- Zou R
- Zou W
- Zwalinski L
- Publication venue
- EUROPEAN PHYSICAL JOURNAL C
- Publication date
- 01/01/2022
- Field of study
The design and performance of the inner detector trigger for the high level
trigger of the ATLAS experiment at the Large Hadron Collider during the 2016-18
data taking period is discussed. In 2016, 2017, and 2018 the ATLAS detector
recorded 35.6 fb−1, 46.9 fb−1, and 60.6 fb−1 respectively of
proton-proton collision data at a centre-of-mass energy of 13 TeV. In order to
deal with the very high interaction multiplicities per bunch crossing expected
with the 13 TeV collisions the inner detector trigger was redesigned during the
long shutdown of the Large Hadron Collider from 2013 until 2015. An overview of
these developments is provided and the performance of the tracking in the
trigger for the muon, electron, tau and b-jet signatures is discussed. The
high performance of the inner detector trigger with these extreme interaction
multiplicities demonstrates how the inner detector tracking continues to lie at
the heart of the trigger performance and is essential in enabling the ATLAS
physics programme
Identifying Biomarkers to Pair with Targeting Treatments within Triple Negative Breast Cancer for Improved Patient Stratification
- Publication venue
- 'MDPI AG'
- Publication date
- Field of study
Managing non-proportionality of hazards (PH) within TNT: a randomised phase III trial of carboplatin compared to docetaxel for patients with metastatic or recurrent locally advanced triple negative (TN) or brca1/2 breast cancer (BC)
- Author
- Publication venue
- 'Springer Science and Business Media LLC'
- Publication date
- Field of study
Multi-candidate immunohistochemical markers to assess radiation response and prognosis in prostate cancer: results from the CHHiP trial of radiotherapy fractionation
- Author
- Publication venue
- 'Elsevier BV'
- Publication date
- 16/01/2023
- Field of study
BACKGROUND: Protein markers of cellular proliferation, hypoxia, apoptosis, cell cycle checkpoints, growth factor signalling and inflammation in localised prostate tumours have previously shown prognostic ability. A translational substudy within the CHHiP trial of radiotherapy fractionation evaluated whether these could improve prediction of prognosis and assist treatment stratification following either conventional or hypofractionated radiotherapy. METHODS: Using case:control methodology, patients with biochemical or clinical failure after radiotherapy (BCR) were matched to patients without recurrence according to established prognostic factors (Gleason score, presenting PSA, tumour-stage) and fractionation schedule. Immunohistochemical (IHC) staining of diagnostic biopsy sections was performed and scored for HIF1α, Bcl-2, Ki67, Geminin, p16, p53, p-chk1 and PTEN. Univariable and multivariable conditional logistic regression models, adjusted for matching strata and age, estimated the prognostic value of each IHC biomarker, including interaction terms to determine BCR prediction according to fractionation. FINDINGS: IHC results were available for up to 336 tumours. PTEN, Geminin, mean Ki67 and max Ki67 were prognostic after adjusting for multiple comparisons and were fitted in a multivariable model (n = 212, 106 matched pairs). Here, PTEN and Geminin showed significant prediction of prognosis. No marker predicted BCR according to fractionation. INTERPRETATION: Geminin or Ki67, and PTEN, predicted response to radiotherapy independently of established prognostic factors. These results provide essential independent external validation of previous findings and confirm a role for these markers in treatment stratification. FUNDING: 10.13039/501100000289Cancer Research UK (BIDD) grant (A12518), 10.13039/501100000289Cancer Research UK (C8262/A7253), Department of Health, 10.13039/501100000771Prostate Cancer UK, 10.13039/100008719Movember Foundation, NIHR Biomedical Research Centre at 10.13039/100012139Royal Marsden/ICR